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1
Wallin, R. "Vitamin K antagonism of coumarin anticoagulation. A dehydrogenase pathway in rat liver is responsible for the antagonistic effect." Biochemical Journal 236, no. 3 (June 15, 1986): 685–93. http://dx.doi.org/10.1042/bj2360685.
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In the liver, it appears that there are two different pathways for vitamin K reduction. One pathway is irreversibly inhibited by coumarin anticoagulant drugs. The other pathway has been shown in the present study to be composed of enzymes that are not effected by physiological ‘in vivo’ concentrations of these drugs. This pathway appears to be responsible for the antidotal effect of vitamin K in overcoming coumarin poisoning. In rat liver the pathway has been shown to be composed of DT-diaphorase (EC.1.6.99.2) and a microsomal dehydrogenase(s). The activity of the microsomal dehydrogenase(s) was 3.6-fold higher with NADH than with NADPH present in the test system. It appears that this enzyme is the physiologically important enzyme in the pathway. In contrast with DT-diaphorase, this enzyme(s) is shown to be tightly associated with the mirosomal membrane. The enzyme(s) is not identical with either of the quinone-reducing enzymes cytochrome P-450 reductase or cytochrome-b5 reductase. Our data thus postulate the existence of an as-yet-unidentified microsomal dehydrogenase that appears to have an important function in the pathway.
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Voronin, Mikhail V., Yulia V. Vakhitova, Inna P. Tsypysheva, Dmitry O. Tsypyshev, Inna V. Rybina, Rustam D. Kurbanov, Elena V. Abramova, and Sergei B. Seredenin. "Involvement of Chaperone Sigma1R in the Anxiolytic Effect of Fabomotizole." International Journal of Molecular Sciences 22, no. 11 (May 21, 2021): 5455. http://dx.doi.org/10.3390/ijms22115455.
Full textAbstract:
Sigma-1 receptor (chaperone Sigma1R) is an intracellular protein with chaperone functions, which is expressed in various organs, including the brain. Sigma1R participates in the regulation of physiological mechanisms of anxiety (Su, T. P. et al., 2016) and reactions to emotional stress (Hayashi, T., 2015). In 2006, fabomotizole (ethoxy-2-[2-(morpholino)-ethylthio]benzimidazole dihydrochloride) was registered in Russia as an anxiolytic (Seredenin S. and Voronin M., 2009). The molecular targets of fabomotizole are Sigma1R, NRH: quinone reductase 2 (NQO2), and monoamine oxidase A (MAO-A) (Seredenin S. and Voronin M., 2009). The current study aimed to clarify the dependence of fabomotizole anxiolytic action on its interaction with Sigma1R and perform a docking analysis of fabomotizole interaction with Sigma1R. An elevated plus maze (EPM) test revealed that the anxiolytic-like effect of fabomotizole (2.5 mg/kg i.p.) administered to male BALB/c mice 30 min prior EPM exposition was blocked by Sigma1R antagonists BD-1047 (1.0 mg/kg i.p.) and NE-100 (1.0 mg/kg i.p.) pretreatment. Results of initial in silico study showed that fabomotizole locates in the active center of Sigma1R, reproducing the interactions with the site’s amino acids common for established Sigma1R ligands, with the ΔGbind value closer to that of agonist (+)-pentazocine in the 6DK1 binding site.
3
Umezawa, Kiwamu, Kouta Takeda, Takuya Ishida, Naoki Sunagawa, Akiko Makabe, Kazuo Isobe, Keisuke Koba, et al. "A Novel Pyrroloquinoline Quinone-Dependent 2-Keto-d-Glucose Dehydrogenase from Pseudomonas aureofaciens." Journal of Bacteriology 197, no. 8 (February 2, 2015): 1322–29. http://dx.doi.org/10.1128/jb.02376-14.
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A gene encoding an enzyme similar to a pyrroloquinoline quinone (PQQ)-dependent sugar dehydrogenase from filamentous fungi, which belongs to new auxiliary activities (AA) family 12 in the CAZy database, was cloned fromPseudomonas aureofaciens. The deduced amino acid sequence of the cloned enzyme showed only low homology to previously characterized PQQ-dependent enzymes, and multiple-sequence alignment analysis showed that the enzyme lacks one of the three conserved arginine residues that function as PQQ-binding residues in known PQQ-dependent enzymes. The recombinant enzyme was heterologously expressed in anEscherichia coliexpression system for further characterization. The UV-visible (UV-Vis) absorption spectrum of the oxidized form of the holoenzyme, prepared by incubating the apoenzyme with PQQ and CaCl2, revealed a broad peak at approximately 350 nm, indicating that the enzyme binds PQQ. With the addition of 2-keto-d-glucose (2KG) to the holoenzyme solution, a sharp peak appeared at 331 nm, attributed to the reduction of PQQ bound to the enzyme, whereas no effect was observed upon 2KG addition to authentic PQQ. Enzymatic assay showed that the recombinant enzyme specifically reacted with 2KG in the presence of an appropriate electron acceptor, such as 2,6-dichlorophenol indophenol, when PQQ and CaCl2were added.1H nuclear magnetic resonance (1H-NMR) analysis of reaction products revealed 2-keto-d-gluconic acid (2KGA) as the main product, clearly indicating that the recombinant enzyme oxidizes the C-1 position of 2KG. Therefore, the enzyme was identified as a PQQ-dependent 2KG dehydrogenase (Pa2KGDH). Considering the high substrate specificity, the physiological function ofPa2KGDH may be for production of 2KGA.
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Kalneniece, Kristīne, Toms Kusiņš, Inga Balode, Līva Mazkalniņa, Kārlis Švirksts, Māra Grūbe, Gunta Kizane, Vasīlijs Bankovskis, Andrejs Grīnbergs, and Olga Muter. "Effect of Isothiocyanates on the Activity of Lactobacillus plantarum Exposed to Irradiation." Key Engineering Materials 850 (June 2020): 219–24. http://dx.doi.org/10.4028/www.scientific.net/kem.850.219.
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Two isothiocyanates, i.e., sulforaphane (SFA) and sulforaphene (SFE), are suggested to be used as an alternative chemopreventive diet. This study was focused on the effect of SFA and SFE on Lactobacillus plantarum, which has been subjected to the irradiation (2-50 Gy). The cultures grown in De Man, Rogosa and Sharpe (MRS) and Tryptone Soya Broth (TSB) were compared in terms of bacteria physiological activity under tested conditions. Broth composition notably influenced the bacteria growth kinetic parameters, as well as culture response to the oxidative stress. Activity of L. plantarum cells after irradiation was evaluated by their dehydrogenase (DHA) and quinone-reductase (QR) activities. The enzyme activity was quantified in living cells. Bacterial cultures obtained in MRS and TSB broth, demonstrated contrasting characteristics in their enzyme activities. The MRS-grown culture did not show any QR activity, whereas the TSB-grown cells showed a non-linear response towards gamma-irradiation with a maximum inhibition being at 10 Gy. Addition of SFA or SFE in concentration of 1 µg/mL to the cultures before irradiation exposure recovered the QR activity from 23% in a non-amended variant up to 102% and 121%, respectively, taking the non-irradiated non-amended variant as 100%.
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Cooley, Jason W., and Wim F. J. Vermaas. "Succinate Dehydrogenase and Other Respiratory Pathways in Thylakoid Membranes of Synechocystis sp. Strain PCC 6803: Capacity Comparisons and Physiological Function." Journal of Bacteriology 183, no. 14 (July 15, 2001): 4251–58. http://dx.doi.org/10.1128/jb.183.14.4251-4258.2001.
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ABSTRACT Respiration in cyanobacterial thylakoid membranes is interwoven with photosynthetic processes. We have constructed a range of mutants that are impaired in several combinations of respiratory and photosynthetic electron transport complexes and have examined the relative effects on the redox state of the plastoquinone (PQ) pool by using a quinone electrode. Succinate dehydrogenase has a major effect on the PQ redox poise, as mutants lacking this enzyme showed a much more oxidized PQ pool. Mutants lacking type I and II NAD(P)H dehydrogenases also had more oxidized PQ pools. However, in the mutant lacking type I NADPH dehydrogenase, succinate was essentially absent and effective respiratory electron donation to the PQ pool could be established after addition of 1 mM succinate. Therefore, lack of the type I NADPH dehydrogenase had an indirect effect on the PQ pool redox state. The electron donation capacity of succinate dehydrogenase was found to be an order of magnitude larger than that of type I and II NAD(P)H dehydrogenases. The reason for the oxidized PQ pool upon inactivation of type II NADH dehydrogenase may be related to the facts that the NAD pool in the cell is much smaller than that of NADP and that the NAD pool is fully reduced in the mutant without type II NADH dehydrogenase, thus causing regulatory inhibition. The results indicate that succinate dehydrogenase is the main respiratory electron transfer pathway into the PQ pool and that type I and II NAD(P)H dehydrogenases regulate the reduction level of NADP and NAD, which, in turn, affects respiratory electron flow through succinate dehydrogenase.
6
Lacombe, Julie, and Mathieu Ferron. "VKORC1L1, An Enzyme Mediating the Effect of Vitamin K in Liver and Extrahepatic Tissues." Nutrients 10, no. 8 (July 26, 2018): 970. http://dx.doi.org/10.3390/nu10080970.
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Vitamin K is an essential nutrient involved in the regulation of blood clotting and tissue mineralization. Vitamin K oxidoreductase (VKORC1) converts vitamin K epoxide into reduced vitamin K, which acts as the co-factor for the γ-carboxylation of several proteins, including coagulation factors produced by the liver. VKORC1 is also the pharmacological target of warfarin, a widely used anticoagulant. Vertebrates possess a VKORC1 paralog, VKORC1-like 1 (VKORC1L1), but until very recently, the importance of VKORC1L1 for protein γ-carboxylation and hemostasis in vivo was not clear. Here, we first review the current knowledge on the structure, function and expression pattern of VKORC1L1, including recent data establishing that, in the absence of VKORC1, VKORC1L1 can support vitamin K-dependent carboxylation in the liver during the pre- and perinatal periods in vivo. We then provide original data showing that the partial redundancy between VKORC1 and VKORC1L1 also exists in bone around birth. Recent studies indicate that, in vitro and in cell culture models, VKORC1L1 is less sensitive to warfarin than VKORC1. Genetic evidence is presented here, which supports the notion that VKORC1L1 is not the warfarin-resistant vitamin K quinone reductase present in the liver. In summary, although the exact physiological function of VKORC1L1 remains elusive, the latest findings clearly established that this enzyme is a vitamin K oxidoreductase, which can support γ-carboxylation in vivo.
7
Bradley, C. A., and K. A. Ames. "Effect of Foliar Fungicides on Corn with Simulated Hail Damage." Plant Disease 94, no. 1 (January 2010): 83–86. http://dx.doi.org/10.1094/pdis-94-1-0083.
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Quinone outside inhibitor (QoI) foliar fungicides can be effective at reducing foliar diseases in corn (Zea mays), and they have been shown to provide physiological benefits experimentally in other crops in the absence of disease. A new supplemental label for pyraclostrobin that was approved in January 2009 by the United States Environmental Protection Agency (EPA) states that corn plants applied with pyraclostrobin may have better tolerance to damage caused by hail. To determine the effects of QoI foliar fungicides on hail-damaged corn, field research trials were conducted near Champaign, IL in 2007 and 2008. Hail damage was simulated with a gasoline-powered string-mower at the V12 growth stage, which caused injury to leaves and defoliation. At VT, the foliar fungicides azoxystrobin and pyraclostrobin were applied to corn. Control treatments included a nontreated control and a nondamaged control. The simulated hail damage significantly (P ≤ 0.05) increased gray leaf spot severity (caused by Cercospora zeae-maydis) in 2007 but not in 2008. Simulated hail damage also significantly reduced yield compared with the nondamaged control in both 2007 and 2008. Foliar fungicides significantly reduced disease severity compared with the nontreated control in 2007 but not in 2008; however, foliar fungicides did not significantly improve yield in either the damaged or nondamaged plots compared with the nontreated controls. Results from our research trials indicated that foliar fungicides provided very little benefit to corn injured by simulated hail; thus, growers should consider factors other than hail damage when making fungicide application decisions for corn.
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Schnabel, G., and C. H. Crisosto. "Seasonal Applications of a Pyraclostrobin and Boscalid Mixture Do Not Impact Same-year Peach Fruit Quality Attributes." HortTechnology 18, no. 4 (January 2008): 678–84. http://dx.doi.org/10.21273/horttech.18.4.678.
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Quinone outside inhibitor (QoI) fungicides can improve the yield and quality of cereal crops in the absence of disease pressure through the so called “greening effect,” but little is known about the potential beneficial effects on deciduous tree fruit crops. In a multiyear and multicultivar study carried out in South Carolina (2005 and 2006) and California (2006), we examined the potential influence of the QoI fungicide pyraclostrobin on antioxidant activity and commercially important peach (Prunus persica) fruit quality attributes, including fruit size, coloration, firmness, soluble solids concentration, and yield. Experimental orchards were sprayed according to commercial guidelines to manage insect pests and diseases. A pyraclostrobin + boscalid mixture was applied up to five times per season starting 1 week after the physiological stage of “shuck off” until 1 to 2 weeks before harvest. Fruit size was measured weekly between “shuck off” and harvest, whereas the other fruit quality attributes were determined at harvest. Results indicate no consistent impact of the pyraclostrobin + boscalid mixture on same-year fruit size development or other fruit quality attributes in orchards with no or very little disease pressure. To our knowledge, this is the first in-depth evaluation of the potential effects of a QoI fungicide on commercially important tree fruit quality attributes.
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Soltani, Sepideh, Shahin Sowlati-Hashjin, Conrard Giresse Tetsassi Feugmo, and Mikko Karttunen. "Structural Investigation of DHICA Eumelanin Using Density Functional Theory and Classical Molecular Dynamics Simulations." Molecules 27, no. 23 (December 1, 2022): 8417. http://dx.doi.org/10.3390/molecules27238417.
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Eumelanin is an important pigment, for example, in skin, hair, eyes, and the inner ear. It is a highly heterogeneous polymer with 5,6-dihydroxyindole-2-carboxylic acid (DHICA) and 5,6-dihydroxyindole (DHI) building blocks, of which DHICA is reported as the more abundant in natural eumelanin. The DHICA-eumelanin protomolecule consists of three building blocks, indole-2-carboxylic acid-5,6-quinone (ICAQ), DHICA and pyrrole-2,3,5-tricarboxylic acid (PTCA). Here, we focus on the self-assembly of DHICA-eumelanin using multi-microsecond molecular dynamics (MD) simulations at various concentrations in aqueous solutions. The molecule was first parameterized using density functional theory (DFT) calculations. Three types of systems were studied: (1) uncharged DHICA-eumelanin, (2) charged DHICA-eumelanin corresponding to physiological pH, and (3) a binary mixture of both of the above protomolecules. In the case of uncharged DHICA-eumelanin, spontaneous aggregation occurred and water molecules were present inside the aggregates. In the systems corresponding to physiological pH, all the carboxyl groups are negatively charged and the DHICA-eumelanin model has a net charge of −4. The effect of K+ ions as counterions was investigated. The results show high probability of binding to the deprotonated oxygens of the carboxylate anions in the PTCA moiety. Furthermore, the K+ counterions increased the solubility of DHICA-eumelanin in its charged form. A possible explanation is that the charged protomolecules favor binding to the K+ ions rather than aggregating and binding to other protomolecules. The binary mixtures show aggregation of uncharged DHICA-eumelanins; unlike the charged systems with no aggregation, a few charged DHICA-eumelanins are present on the surface of the uncharged aggregation, binding to the K+ ions.
10
Spector, Alan C., and Steven J. St. John. "Role of taste in the microstructure of quinine ingestion by rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 6 (June 1, 1998): R1687—R1703. http://dx.doi.org/10.1152/ajpregu.1998.274.6.r1687.
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The microstructure of the licking behavior of water-deprived rats presented with either water or quinine during 45-min single-bottle tests was analyzed. The chorda tympani (CT) and glossopharyngeal (GL) nerves, which innervate the taste buds of the tongue, were transected in deeply anesthetized rats to discern their contribution to the behavioral pattern of quinine drinking. Rats were presurgically habituated to the testing protocol and postsurgically tested first with water and then novel 0.2 mM quinine-HCl in a subsequent session. The substantial decrease in intake observed in sham-operated controls ( n = 16) when quinine was the stimulus was entirely a function of a decrease in lick volume and burst size (a run of licks with interlick intervals <1 s). Contrary to the intake-suppressing effects of quinine, pause duration decreased and burst number increased. Combined transection of the CT and GL ( n = 6) strikingly opposed all of these quinine-induced behavioral changes, whereas CT transection ( n = 7) was without effect and GL transection ( n = 8) had an intermediate influence. These results suggest that taste acts more on neural circuits governing burst termination as opposed to burst initiation, which, in turn, appears to be more sensitive to signals related to physiological state. These findings are discussed in terms of other known nerve transection effects on quinine responsiveness, and the implications of the microstructural results are considered with respect to probabilistic as opposed to deterministic control of licking behavior.
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Giza, B. K., and T. R. Scott. "Intravenous insulin infusions in rats decrease gustatory-evoked responses to sugars." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 252, no. 5 (May 1, 1987): R994—R1002. http://dx.doi.org/10.1152/ajpregu.1987.252.5.r994.
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Physiological factors that affect food intake have been shown to influence taste-evoked activity in the rat's central nervous system. Insulin appears to have a bimodal effect on feeding, inhibiting intake when its rise is within the normal physiological range, but, with further increases, causing hyperphagia. We studied the effect of low intravenous doses (0.5 U/kg) of regular insulin on taste-evoked responses in the nucleus tractus solitarius. Taste activity was elicited by application to the tongue of glucose, fructose, NaCl, HCl, and quinine. We monitored responses before and after intrajugular injections of insulin or a control vehicle. Taste responsiveness to glucose and fructose was significantly reduced for the period 7-22 min following the injection. Activity representing NaCl, HCl, and quinine was unaffected. The suppression of responsiveness to sweet stimuli could decrease the hedonic appeal of tastants and so serve as a mechanism by which physiological doses of insulin could contribute to a reduction in feeding.
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Ito, Shosuke, Hitomi Tanaka, Makoto Ojika, Kazumasa Wakamatsu, and Manickam Sugumaran. "Oxidative Transformations of 3,4-Dihydroxyphenylacetaldehyde Generate Potential Reactive Intermediates as Causative Agents for Its Neurotoxicity." International Journal of Molecular Sciences 22, no. 21 (October 29, 2021): 11751. http://dx.doi.org/10.3390/ijms222111751.
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Neurogenerative diseases, such as Parkinson’s disease, are associated, not only with the selective loss of dopamine (DA), but also with the accumulation of reactive catechol-aldehyde, 3,4-dihydroxyphenylacetaldehyde (DOPAL), which is formed as the immediate oxidation product of cytoplasmic DA by monoamine oxidase. DOPAL is well known to exhibit toxic effects on neuronal cells. Both catecholic and aldehyde groups seem to be associated with the neurotoxicity of DOPAL. However, the exact cause of toxicity caused by this compound remains unknown. Since the reactivity of DOPAL could be attributed to its immediate oxidation product, DOPAL-quinone, we examined the potential reactions of this toxic metabolite. The oxidation of DOPAL by mushroom tyrosinase at pH 5.3 produced conventional DOPAL-quinone, but oxidation at pH 7.4 produced the tautomeric quinone-methide, which gave rise to 3,4-dihydroxyphenylglycolaldehyde and 3,4-dihydroxybenzaldehyde as products through a series of reactions. When the oxidation reaction was performed in the presence of ascorbic acid, two additional products were detected, which were tentatively identified as the cyclized products, 5,6-dihydroxybenzofuran and 3,5,6-trihydroxybenzofuran. Physiological concentrations of Cu(II) ions could also cause the oxidation of DOPAL to DOPAL-quinone. DOPAL-quinone exhibited reactivity towards the cysteine residues of serum albumin. DOPAL-oligomer, the oxidation product of DOPAL, exhibited pro-oxidant activity oxidizing GSH to GSSG and producing hydrogen peroxide. These results indicate that DOPAL-quinone generates several toxic compounds that could augment the neurotoxicity of DOPAL.
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Zabalza, Ana, Ainhoa Zulet-González, Maria Barco-Antoñanzas, Mikel V. Eceiza, Miriam Gil-Monreal, and Mercedes Royuela. "Physiological Approach to the Use of the Natural Compound Quinate in the Control of Sensitive and Resistant Papaver rhoeas." Plants 9, no. 9 (September 16, 2020): 1215. http://dx.doi.org/10.3390/plants9091215.
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Quinate (1,3,4,5-tetrahydroxycyclohexanecarboxylate) is a compound synthesized in plants through a side-branch of the shikimate biosynthesis pathway, which is accumulated after glyphosate and acetolactate synthase inhibiting herbicides (ALS-inhibitors) and has phytotoxic potential. The objective of this study was to evaluate the phytotoxicity of quinate on several weed species. Among the species evaluated, Cynodon dactylon, Bromus diandrus, Lolium rigidum, Sinapis alba, and Papaver rhoeas, P. rhoeas was the most sensitive, and its growth was controlled with quinate concentrations above 100 mM at the phenological stage of 6–8 true leaves. A physiological study, including the shikimate pathway and the physiological markers of ALS-inhibitors (carbohydrates and amino acids), was performed in the sensitive and resistant plants treated with sulfonylureas or quinate. The typical physiological effects of ALS-inhibitors were detected in the sensitive population (free amino acid and carbohydrate accumulation) and not detected in the resistant population. The mode of action of quinate appeared to be related to general perturbations in their carbon/nitrogen metabolism rather than to specific changes in the shikimate pathway. These results suggest the possibility of using quinate in the weed control management of P. rhoeas.
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Callies, C., T. G. Cooper, and C. H. Yeung. "Channels for water efflux and influx involved in volume regulation of murine spermatozoa." REPRODUCTION 136, no. 4 (October 2008): 401–10. http://dx.doi.org/10.1530/rep-08-0149.
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The nature of the membrane channels mediating water transport in murine spermatozoa adjusting to anisotonic conditions was investigated. The volume of spermatozoa subjected to physiologically relevant hypotonic conditions either simultaneously, or after isotonic pre-incubation, with putative water transport inhibitors was monitored. Experiments in which quinine prevented osmolyte efflux, and thus regulatory volume decrease (RVD), revealed whether water influx or efflux was being inhibited. There was no evidence that sodium-dependent solute transporters or facilitative glucose transporters were involved in water transport during RVD of murine spermatozoa since phloretin, cytochalasin B and phloridzin had no effect on volume regulation. However, there was evidence that Hg2+- and Ag+-sensitive channels were involved in water transport and the possibility that they include aquaporin 8 is discussed. Toxic effects of these heavy metals were ruled out by evidence that mitochondrial poisons had no such effect on volume regulation.
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Hoffman, David L., and Paul S. Brookes. "Oxygen Sensitivity of Mitochondrial Reactive Oxygen Species Generation Depends on Metabolic Conditions." Journal of Biological Chemistry 284, no. 24 (April 14, 2009): 16236–45. http://dx.doi.org/10.1074/jbc.m809512200.
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The mitochondrial generation of reactive oxygen species (ROS) plays a central role in many cell signaling pathways, but debate still surrounds its regulation by factors, such as substrate availability, [O2] and metabolic state. Previously, we showed that in isolated mitochondria respiring on succinate, ROS generation was a hyperbolic function of [O2]. In the current study, we used a wide variety of substrates and inhibitors to probe the O2 sensitivity of mitochondrial ROS generation under different metabolic conditions. From such data, the apparent Km for O2 of putative ROS-generating sites within mitochondria was estimated as follows: 0.2, 0.9, 2.0, and 5.0 μm O2 for the complex I flavin site, complex I electron backflow, complex III QO site, and electron transfer flavoprotein quinone oxidoreductase of β-oxidation, respectively. Differential effects of respiratory inhibitors on ROS generation were also observed at varying [O2]. Based on these data, we hypothesize that at physiological [O2], complex I is a significant source of ROS, whereas the electron transfer flavoprotein quinone oxidoreductase may only contribute to ROS generation at very high [O2]. Furthermore, we suggest that previous discrepancies in the assignment of effects of inhibitors on ROS may be due to differences in experimental [O2]. Finally, the data set (see supplemental material) may be useful in the mathematical modeling of mitochondrial metabolism.
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Fan, Lijuan, Ruihua Huang, Chengwu Wu, Yang Cao, Taoran Du, Guang Pu, Huan Wang, Wuduo Zhou, Pinghua Li, and Sung Woo Kim. "Defatted Rice Bran Supplementation in Diets of Finishing Pigs: Effects on Physiological, Intestinal Barrier, and Oxidative Stress Parameters." Animals 10, no. 3 (March 8, 2020): 449. http://dx.doi.org/10.3390/ani10030449.
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Rice bran is a waste product with low cost and high fiber content, giving it an added advantage over corn and soybean meal, which have to be purchased and always at a relatively higher cost. Under the background of increased attention to sustainable agriculture, it is significant to find alternative uses for this byproduct. A total of 35 finishing pigs were allotted to five dietary treatments: a control group with basal diet and four experimental diets where corn was equivalently substituted by 7%, 14%, 21%, and 28% defatted rice bran (DFRB), respectively. With increasing levels of DFRB, the neutrophil to lymphocyte ratio (NLR) linearly decreased (p < 0.05). In the jejunum, the mRNA level of nuclear factor erythroid-2 related factor-2 (Nrf2) exhibited a quadratic response (p < 0.01) with incremental levels of DFRB. In the colon, the mRNA levels of mucin 2 (MUC2), Nrf2, and NAD(P)H: quinone oxidoreductase 1 (NQO1) were upregulated (linear, p < 0.05) and heme oxygenase-1 (HO-1) was upregulated (linear, p < 0.01). Overall, using DFRB to replace corn decreased the inflammatory biomarkers of serum and showed potential function in modulating the intestinal barrier by upregulating the mRNA expression levels of MUC2 and downregulating that of Nrf2, NQO1, and HO-1 in the colon.
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Min, Zhihui, Jiebai Zhou, Ruolin Mao, Bo Cui, Yunfeng Cheng, and Zhihong Chen. "Pyrroloquinoline Quinone Administration Alleviates Allergic Airway Inflammation in Mice by Regulating the JAK-STAT Signaling Pathway." Mediators of Inflammation 2022 (October 29, 2022): 1–18. http://dx.doi.org/10.1155/2022/1267841.
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The current asthma therapies are inadequate for many patients with severe asthma. Pyrroloquinoline quinone (PQQ) is a naturally-occurring redox cofactor and nutrient that can exert a multitude of physiological effects, including anti-inflammatory and antioxidative effects. We sought to explore the effects of PQQ on allergic airway inflammation and reveal the underlying mechanisms. In vitro, the effects of PQQ on the secretion of epithelial-derived cytokines by house dust mite- (HDM-) incubated 16-HBE cells and on the differentiation potential of CD4+ T cells were investigated. In vivo, PQQ was administered to mice with ovalbumin- (OVA-) induced asthma, and lung pathology and inflammatory cell infiltration were assessed. The changes in T cell subsets and signal transducers and activators of transcription (STATs) were evaluated by flow cytometry. Pretreatment with PQQ significantly decreased HDM-stimulated thymic stromal lymphopoietin (TSLP) production in a dose-dependent manner in 16-HBE cells and inhibited Th2 cell differentiation in vitro. Treatment with PQQ significantly reduced bronchoalveolar lavage fluid (BALF) inflammatory cell counts in the OVA-induced mouse model. PQQ administration also changed the secretion of IFN-γ and IL-4 as well as the percentages of Th1, Th2, Th17, and Treg cells in the peripheral blood and lung tissues, along with inhibition the phosphorylation of STAT1, STAT3, and STAT6 while promoting that of STAT4 in allergic airway inflammation model mice. PQQ can alleviate allergic airway inflammation in mice by improving the immune microenvironment and regulating the JAK-STAT signaling pathway. Our findings suggest that PQQ has great potential as a novel therapeutic agent for inflammatory diseases, including asthma.
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DiNicolantonio, James J., Mark F. McCarty, and James H. O'Keefe. "Nutraceutical activation of Sirt1: a review." Open Heart 9, no. 2 (December 2022): e002171. http://dx.doi.org/10.1136/openhrt-2022-002171.
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The deacetylase sirtuin 1 (Sirt1), activated by calorie restriction and fasting, exerts several complementary effects on cellular function that are favourable to healthspan; it is often thought of as an ‘anti-aging’ enzyme. Practical measures which might boost Sirt1 activity are therefore of considerable interest. A number of nutraceuticals have potential in this regard. Nutraceuticals reported to enhance Sirt1 synthesis or protein expression include ferulic acid, tetrahydrocurcumin, urolithin A, melatonin, astaxanthin, carnosic acid and neochlorogenic acid. The half-life of Sirt1 protein can be enhanced with the natural nicotinamide catabolite N1-methylnicotinamide. The availability of Sirt1’s obligate substrate NAD+ can be increased in several ways: nicotinamide riboside and nicotinamide mononucleotide can function as substrates for NAD+ synthesis; activators of AMP-activated kinase—such as berberine—can increase expression of nicotinamide phosphoribosyltransferase, which is rate limiting for NAD+ synthesis; and nutraceutical quinones such as thymoquinone and pyrroloquinoline quinone can boost NAD+ by promoting oxidation of NADH. Induced ketosis—as via ingestion of medium-chain triglycerides—can increase NAD+ in the brain by lessening the reduction of NAD+ mediated by glycolysis. Post-translational modifications of Sirt1 by O-GlcNAcylation or sulfonation can increase its activity, suggesting that administration of glucosamine or of agents promoting hydrogen sulfide synthesis may aid Sirt1 activity. Although resveratrol has poor pharmacokinetics, it can bind to Sirt1 and activate it allosterically—as can so-called sirtuin-activating compound drugs. Since oxidative stress can reduce Sirt1 activity in multiple ways, effective antioxidant supplementation that blunts such stress may also help preserve Sirt1 activity in some circumstances. Combination nutraceutical regimens providing physiologically meaningful doses of several of these agents, capable of activating Sirt1 in complementary ways, may have considerable potential for health promotion. Such measures may also amplify the benefits of sodium-glucose cotransporter-2 (SGLT2) inhibitors in non-diabetic disorders, as these benefits appear to reflect upregulation of Sirt1 and AMP-activated protein kinase activities.
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Nakamura, Tomoko, Takeshi Akiyoshi, Naoko Tanaka, Kazumasa Shinozuka, Sumio Matzno, Toshikatsu Nakabayashi, Kenji Matsuyama, Makoto Kashiwayanagi, and Takahiro Uchida. "Effect of Quinine Solutions on Intracellular Ca2+ Levels in Neuro-2a Cells—Conventional Physiological Method for the Evaluation of Bitterness—." Biological & Pharmaceutical Bulletin 26, no. 11 (2003): 1637–40. http://dx.doi.org/10.1248/bpb.26.1637.
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Ximenes, Valdecir F., Ghassan J. Maghzal, Rufus Turner, Yoji Kato, Christine C. Winterbourn, and Anthony J. Kettle. "Serotonin as a physiological substrate for myeloperoxidase and its superoxide-dependent oxidation to cytotoxic tryptamine-4,5-dione." Biochemical Journal 425, no. 1 (December 14, 2009): 285–93. http://dx.doi.org/10.1042/bj20090776.
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During inflammatory events, neutrophils and platelets interact to release a variety of mediators. Neutrophils generate superoxide and hydrogen peroxide, and also discharge the haem enzyme myeloperoxidase. Among numerous other mediators, platelets liberate serotonin (5-hydroxytryptamine), which is a classical neurotransmitter and vasoactive amine that has significant effects on inflammation and immunity. In the present study, we show that serotonin is a favoured substrate for myeloperoxidase because other physiological substrates for this enzyme, including chloride, did not affect its rate of oxidation. At low micromolar concentrations, serotonin enhanced hypochlorous acid production by both purified myeloperoxidase and neutrophils. At higher concentrations, it almost completely blocked the formation of hypochlorous acid. Serotonin was oxidized to a dimer by myeloperoxidase and hydrogen peroxide. It was also converted into tryptamine-4,5-dione, especially in the presence of superoxide. This toxic quinone was produced by stimulated neutrophils in a reaction that required myeloperoxidase. In plasma, stimulated human neutrophils oxidized serotonin to its dimer using the NADPH oxidase and myeloperoxidase. We propose that myeloperoxidase will oxidize serotonin at sites of inflammation. In doing so, it will impair its physiological functions and generate a toxic metabolite that will exacerbate inflammatory tissue damage. Consequently, oxidation of serotonin by myeloperoxidase may profoundly influence inflammatory processes.
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Paco Pérez, Víctor, Marcelo Gonzales Torrico, Ermindo Barrientos, and Felipe S. Carevic. "Influencia bacteriana y fúngica en la mineralización de estiércol bovino: evidencia sobre la fertilidad del suelo en el cultivo de quinua (Chenopodium quinoa Willd.)." Revista de Investigaciones Altoandinas - Journal of High Andean Research 24, no. 1 (February 21, 2022): 9–16. http://dx.doi.org/10.18271/ria.2022.358.
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Organic residues in soil are often degraded by the dynamic action of soil life. The objective of the present study was to determine the bacterial and fungal influence on the mineralization of bovine manure (BM) in soil. The research was carried out at the Centro Experimental Agropecuario de Condoriri, Oruro, Bolivia, at an altitude of 3,830 m asl. BM was applied to the pots at concentrations of 0.9, 1.9, 3.3, 4.2, 5.0, 5.6 and 6.7%, which were homogenized with river sand separately. 5 to 10 seeds of C. quinoa were manually sown in the pots. Soil samples were collected from the pots for microbiological analysis every 30 days, while macronutrients were collected at the end of plant physiological maturity. Bacteria were evaluated in Plate Count Agar (PCA) culture of 10-5 dilutions and fungi in Potato Dextrose Agar (PDA) of 10-2 solutions. The results indicate that alkaline pH does not reduce the population of bacteria and fungi. It was found that, at higher microbial population, nitrogen (N) has higher mineralization than other essential minerals. On the other hand, it was observed that the higher the degree of application of BM and the higher the soil moisture concentration, the more favorable the effects on the increase of bacterial and fungal populations. It is concluded that BM mineralization depends on high concentrations of bacterial and fungal populations as well as on soil moisture.
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Ishibashi, Toru. "Therapeutic Efficacy of Molecular Hydrogen: A New Mechanistic Insight." Current Pharmaceutical Design 25, no. 9 (July 9, 2019): 946–55. http://dx.doi.org/10.2174/1381612825666190506123038.
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Background: Molecular hydrogen (H2) is now recognized as a therapeutic gas for the treatment of numerous diseases including neurodegenerative diseases, metabolic disorders, and inflammatory diseases. Nonpolar, neutral H2 is assumed to have health benefits facilitated by its passive diffusion across the human body immediately after administration and is considered a safe therapeutic inert gas that does not interfere with physiological enzymatic reactions. The effects of H2 on mammalian cells are assumed to be based on non-enzymatic reactions with reactive oxygen species (ROS) exhibiting extremely high reactivity. However, many reports on therapeutic applications of H2 have the limitation to regard H2 only as a scavenger for the hydroxyl radical and peroxynitrite. Methods: Apart from this proposed principle, a new possible mechanism of H2 activation and consumption in mammalian cells is considered in this review, which is specifically focused on the mitochondrial complex I that has a close evolutionary relationship with energy-converting, membrane-bound [NiFe]-hydrogenases (MBH). Notably, the possibility that H2 may function as both electron and proton donor in the ubiquinone-binding chamber of complex I is discussed. Results: H2 is proposed to act as the rectifier of the mitochondrial electron flow in the disordered or pathological state when the accumulation of electrons leads to ROS production, specifically during the re-supply of O2 after hypoxia in the mitochondria. Conclusion: Furthermore, H2 is proposed to convert the quinone intermediates to the fully reduced ubiquinol, thereby increasing the antioxidant capacity of the quinone pool as well as preventing the generation of ROS.
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Kovacic, Peter, and Ratnasamy Somanathan. "Clinical Physiology and Mechanism of Dizocilpine (MK-801): Electron Transfer, Radicals, Redox Metabolites and Bioactivity." Oxidative Medicine and Cellular Longevity 3, no. 1 (2010): 13–22. http://dx.doi.org/10.4161/oxim.3.1.10028.
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Dizocilpine (MK-801), an extensively investigated drug possessing secondary amine and benzenoid functions, displays a wide array of biological properties, including anticonvulsant and anesthetic. There is scant discussion of biomechanism. A relevant, important finding is formation of oxidative metabolites in the hydroxylamine and phenolic categories. Analogy to cocaine metabolites suggests participation of redox entities, such as, hydroxylamine, nitroxide and nitrosonium, which can lead to electron transfer and radical formation. There is also similarity to metabolism by 3,3′-iminodipropionitrile and phencyclidine. Alternatively, the phenolic metabolites are well-known precursors of ET quinones. The review documents various physiological effects, mainly involving the central nervous system. Also of interest are the pro- and anti-oxidant properties. Considerable attention has been paid to MK-801 as an antagonist of the N-methyl-D-aspartate receptor in the glutamate category. This aspect is often associated with effects on the central nervous system. The review also provides recent literature dealing with MK-801/NMDA receptor in various areas of bioactivity. Studies were made of MK-801 involvement in working memory processing. Deficits in behavior were noted after administration of the drug. Treatment of mice with dizocilpine induced learning impairment. The influence of MK-801 on fear has been investigated. The substance is known to exert an analgesic effect in pain control. A number of reports deal with anesthetic properties.
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Adeyemi, O. I., O. O. Ige, M. A. Akanmu, and O. E. Ukponmwan. "In vivo anti-malarial activity of propranolol against experimental Plasmodium berghei ANKA infection in mice." African Journal of Clinical and Experimental Microbiology 21, no. 4 (August 25, 2020): 333–39. http://dx.doi.org/10.4314/ajcem.v21i4.10.
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Background: Malaria is a mosquito-borne infectious disease caused by Plasmodium spp, which is widespread in tropical and subtropical regions of the world. The objective of this study is to evaluate in vivo antimalarial activity of propranolol against experimental Plasmodium berghei ANKA (PbA) infection in a mouse model.Methods: A total of 36 mice weighing between 15 to 18g were randomly divided into six groups of six mice each. Mice in the first group (SAL) were non-infected with P. berghei but received normal saline (control), second group (PbA) were mice infected without treatment (control), third group (PRL) were non-infected mice treated with propranolol at the dose of 7.5 mg/kg/bid, fourth group (PbA+PRL) were mice infected and treated with same dose of propranolol, fifth group (QUN) were non-infected mice treated with quinine at a dose of 20 mg/kg stat, then 10 mg/kg bid, and sixth group (PbA+QUN) were infected mice treated with quinine. Parasitaemia, physiological conditions (cognitive function, temperature) and lethality of infected mice were monitored over 7-day period to assess the antimalarial activity of propranolol and quinine. The Y-maze paradigm was used to assess cognitive impairment induced by PbA infection. The effects of propranolol on malaria indices and cognitive impairment were compared with that of quinine and the control using T-test statistical method.Results: Mortality of mice at day 7 in the infected group without treatment (PbA) was 100% (6/6) while mortality was 50% (3/6) in infected group treated with propranolol (PbA+PRL) and 33.3% (2/6) in infected group treated with quinine (PbA+QUN) (OR=2.000, p=1.000). No mortality was recorded in any of the three groups of uninfected mice. Propranolol reduced parasitaemia to a trough level of 1.40±0.07 three days after treatment, comparable to trough level of 1.39±0.0633 by quinine but did not reverse PbA-induced hypothermia, which quinine did.Conclusion: Propranolol demonstrated in vivo antimalarial activity against experimental PbA infection in mice comparable to that of quinine.
Keywords: malaria, propranolol, quinine, Plasmodium, cerebral malaria
French Title: Activité antipaludique in vivo du propranolol contre l'infection expérimentale par Plasmodium berghei ANKA chez la souris
Contexte: Le paludisme est une maladie infectieuse transmise par les moustiques causée par Plasmodium spp, qui est répandue dans les régions tropicales et subtropicales du monde. L'objectif de cette étude est d'évaluer l'activité antipaludique in vivo du propranolol contre une infection expérimentale à Plasmodium berghei ANKA (PbA) dans un modèle murin.
Méthodes: Un total de 36 souris pesant entre 15 et 18 g ont été réparties au hasard en six groupes de six souris chacun. Les souris du premier groupe (SAL) n'étaient pas infectées par P. berghei mais ont reçu une solution saline normale (contrôle), le deuxième groupe (PbA) était des souris infectées sans traitement (contrôle), le troisième groupe (PRL) était des souris non infectées traitées par propranolol à la dose de 7,5mg/kg/bid, le quatrième groupe (PbA+PRL) étaient des souris infectées et traitées avec la même dose de propranolol, le cinquième groupe (QUN) étaient des souris non infectées traitées avec de la quinine à une dose de 20mg/kg stat, puis 10mg/kg bid et le sixième groupe (PbA+QUN) étaient des souris infectées traitées avec de la quinine. La parasitémie, les conditions physiologiques (fonction cognitive, température) et la létalité des souris infectées ont été surveillées sur une période de 7 jours pour évaluer l'activité antipaludique du propranolol et de la quinine. Le paradigme du labyrinthe en Y a été utilisé pour évaluer les troubles cognitifs induits par l'infection au PbA. Les effets du propranolol sur les indices du paludisme et les troubles cognitifs ont été comparés à ceux de la quinine et du témoin à l'aide de la méthode statistique du test T.
Résultats: La mortalité des souris au jour 7 dans le groupe infecté sans traitement (PbA) était de 100% (6/6) tandis que la mortalité était de 50% (3/6) dans le groupe infecté traité avec du propranolol (PbA+PRL) et 33,3% ( 2/6) dans le groupe infecté traité par la quinine (PbA+QUN) (OR=2.000, p=1.000). Aucune mortalité n'a été enregistrée dans aucun des trois groupes de souris non infectées. Le propranolol a réduit la parasitémie à un niveau minimum de 1,40±0,07 trois jours après le traitement, comparable au niveau minimum de 1,39±0,0633 de la quinine, mais n'a pas inversé l'hypothermie induite par le PbA, ce que la quinine a fait.
Conclusion: le propranolol a démontré une activité antipaludique in vivo contre l'infection expérimentale au PbA chez la souris comparable à celle de la quinine.
Mots-clés: paludisme, propranolol, quinine, Plasmodium, paludisme cérébral
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Hanaa H. Mohamed and Raghad M. Mirry. "THE ALLELOPATHIC EFFECT OF MAIZE AND SORGHUM ON SOME PHYSIOLOGICAL TERISTICS OF WHEAT AND BROAD BEAN USING HYDROPONICS." journal of the college of basic education 25, no. 103 (June 23, 2019): 90–118. http://dx.doi.org/10.35950/cbej.v25i103.4548.
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Two experiments were conducted to test the allelopathic potential of aqueous extracts concentrations of maize (Zea mays L.) and sorghum (Sorghum bicolor L.) on some physiological characteristics of wheat (Triticum aestivum L.) and broad bean (Vicia faba L.) plants in two cultures. The effective allelochemicals available in extracts of maize and sorghum have been isolated and identified. The experiments included two factors, the Main plots were the growing culture (Sand culture and Soil culture) and the Sub-plots were five concentrations of (0,25,50,75 and 100%) the aqueous extracts of the whole plants (root and shoot for maize (in first experiment) and sorghum (in the second one), Results indicated that:
Most of the studied characteristics in wheat and broad bean decreased in sand culture when treated with the aqueous extracts of maize and sorghum.
Increasing the aqueous extracts of maize to 100% decreased the plant content of soluble carbohydrate, chlorophyll a, chlorophyll b, protein to 0.29 ,0.39, 0.39 and 0.28 % in wheat, and to 0.28 , 0.46 , 0.53 and 0.46 % in broad bean. While Increasing the aqueous extracts of sorghum to 100% decreased the plant content of soluble carbohydrate, chlorophyll a, chlorophyll b, protein to 0.34 and 0.56 and 0.64 and 0.39 % in wheat, and to 0.41 and 0.47 and 0.44 and 0.20 % in broad bean, respectively compared to control treatment (0%).
Chromatographic analysis revealed the presence of 8 compounds in aqueous extracts of maize. The isolated compounds are phenolic in nature and known to have potential phytotoxicity as syringic, gallic, caffeic, vanillic, ferulic, coumaric, catechol and hydroxybenzoic. While Chromatographic analysis revealed the existence of 10 compounds in aqueous extracts of sorghum, 8 of them similar to what found in maize in addition to quinon, benzaquinon
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Pienkowski, Martin, and Mats Ulfendahl. "Differential Effects of Salicylate, Quinine, and Furosemide on Guinea Pig Inner and Outer Hair Cell Function Revealed by the Input–Output Relation of the Auditory Brainstem Response." Journal of the American Academy of Audiology 22, no. 02 (February 2011): 104–12. http://dx.doi.org/10.3766/jaaa.22.2.5.
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Background: Sensory hearing loss is predominantly caused by the destruction of cochlear outer hair cells (OHCs), inner hair cells (IHCs), or spiral ganglion cells (SGCs). There have been a number of attempts to differentiate between these etiologies of hearing loss, using various psychoacoustic and physiologic paradigms. Purpose: Here we investigate the potential of the auditory brainstem response (ABR) input/output function for such differential diagnosis. On the basis of the saturation of the OHC-based cochlear amplifier, it was hypothesized that selective impairment of OHCs would reduce ABR amplitudes at low to moderate but not at high sound levels. Selective impairment of IHCs or SGCs would reduce ABR amplitudes more or less uniformly across sound level. Finally, a mix of OHC and IHC or SGC impairment would reduce ABR amplitudes at all sound levels but less so at high levels depending on the relative contribution of OHC impairment to the hearing loss. Research Design: To test these hypotheses, normal-hearing adult guinea pigs were intravenously injected with either salicylate, furosemide, or quinine, under ketamine anesthesia. ABRs, as well as distortion-product otoacoustic emissions (DPOAEs), were measured as a function of the sound stimulus level before and after drug injection. Results: Following salicylate injection, ABR amplitudes were reduced only at low–moderate stimulus levels. Following furosemide or quinine injection, ABR amplitudes were reduced at all levels but less so at high ones. This is in accord with the expectation that acute salicylate administration selectively affects the OHCs, while furosemide and quinine affect both OHCs and IHCs/SGCs. Such differential diagnosis was not possible solely on the basis of DPOAE amplitudes, which were unchanged at high stimulus levels after the injection of each of the three drugs. Comparison of ABR and DPOAE threshold shifts could also differentiate the effects of salicylate from those of furosemide and quinine but could not, for example, unequivocally point to salicylate's selective impairment of OHCs. Conclusions: ABR amplitudes appear suitable for differentiating between damage to OHCs and IHCs/SGCs, at least in a controlled experimental setting where pre- and postmanipulation data are available. This could be useful for noninvasively testing the effects of drugs or acoustic overstimulation on the cochlea, at least in the laboratory. Clinical applicability would seem to be limited by the high variability in ABR amplitudes among normal-hearing humans but might be feasible in the future if regular ABR testing entered into routine clinical practice.
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Borisov, Vitaliy B., and Elena Forte. "Impact of Hydrogen Sulfide on Mitochondrial and Bacterial Bioenergetics." International Journal of Molecular Sciences 22, no. 23 (November 24, 2021): 12688. http://dx.doi.org/10.3390/ijms222312688.
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This review focuses on the effects of hydrogen sulfide (H2S) on the unique bioenergetic molecular machines in mitochondria and bacteria—the protein complexes of electron transport chains and associated enzymes. H2S, along with nitric oxide and carbon monoxide, belongs to the class of endogenous gaseous signaling molecules. This compound plays critical roles in physiology and pathophysiology. Enzymes implicated in H2S metabolism and physiological actions are promising targets for novel pharmaceutical agents. The biological effects of H2S are biphasic, changing from cytoprotection to cytotoxicity through increasing the compound concentration. In mammals, H2S enhances the activity of FoF1-ATP (adenosine triphosphate) synthase and lactate dehydrogenase via their S-sulfhydration, thereby stimulating mitochondrial electron transport. H2S serves as an electron donor for the mitochondrial respiratory chain via sulfide quinone oxidoreductase and cytochrome c oxidase at low H2S levels. The latter enzyme is inhibited by high H2S concentrations, resulting in the reversible inhibition of electron transport and ATP production in mitochondria. In the branched respiratory chain of Escherichia coli, H2S inhibits the bo3 terminal oxidase but does not affect the alternative bd-type oxidases. Thus, in E. coli and presumably other bacteria, cytochrome bd permits respiration and cell growth in H2S-rich environments. A complete picture of the impact of H2S on bioenergetics is lacking, but this field is fast-moving, and active ongoing research on this topic will likely shed light on additional, yet unknown biological effects.
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Fernández-Aparicio, Mónica, Marco Masi, Alessio Cimmino, and Antonio Evidente. "Effects of Benzoquinones on Radicles of Orobanche and Phelipanche Species." Plants 10, no. 4 (April 11, 2021): 746. http://dx.doi.org/10.3390/plants10040746.
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The holoparasitic broomrape weeds (Orobanche and Phelipanche species) cause severe yield losses throughout North Africa, the Middle East, and Southern and Eastern Europe. These parasitic weeds form an haustorium at the tip of their radicles to infect the crop upon detection of the host-derived haustorium-inducing factors. Until now, the haustorial induction in the broomrapes remains less studied than in other parasitic plant species. Known haustorium-inducing factors active in hemiparasites, such as Striga and Triphysaria species, were reported to be inefficient for the induction of haustoria in broomrape radicles. In this work, the haustorium-inducing activity of p-benzoquinone and 2,6-dimethoxy-p-benzoquinone (BQ and DMBQ) on radicles of three different broomrapes, namely Orobanche cumana, Orobanche minor and Phelipanche ramosa, is reported. Additional allelopathic effects of benzoquinones on radicle growth and radicle necrosis were studied. The results of this work suggest that benzoquinones play a role in the induction of haustorium in broomrapes. Although dependent on the broomrape species assayed and the concentration of quinones used in the test, the activity of BQ appeared to be stronger than that of DMBQ. The redox property represented by p-benzoquinone, which operates in several physiological processes of plants, insects and animals, is invoked to explain this different activity. This work confirms the usefulness of benzoquinones as haustorium-inducing factors for holoparasitic plant research. The findings of this work could facilitate future studies in the infection process, such as host-plant recognition and haustorial formation.
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Belcastro, Philip A. "Pedagogical Patronizing of the Pharmacodynamic Promises of Illicit Drugs." Journal of Drug Education 22, no. 1 (March 1992): 9–13. http://dx.doi.org/10.2190/j9kw-krlm-gp55-agvc.
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A review of popular drug education textbooks and curricula indicated most juxtapose the physiologic effects of licitly manufactured drugs under headings representing illicitly prepared drugs. This misrepresentation ignores the literature, which is undivided, in reporting that illicit drugs contain adulterants and substitutes such as: sodium acetate, sodium cyclamate, dolomite, acetaminophen, gypsum, mannitol, inositol, lidocaine, amydricaine, benzocaine, caffeine, ephedrine, intercaine, phenylpropanolamine, piperocaine, procainamide, azopyridine, bromodiphenhydramine, ibuprofen, methaqualone, phenobarital trazodone, acetylcodine, codeine, quinine, quinidine, thallium, arsenic and strychnine. The temptation to extrapolate the results of licitly pure drug lots administered at precisely measured doses to represent the pharmacodynamics of illegally prepared drug lots administered at indiscernible doses must be avoided in drug educational resources. There is a pressing need to correct the factual base, both implied and suggestive, of drug education resources regarding the purity and toxicity of illicitly manufactured and purchased drugs.
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LOSKOVICH, Maria V., Vera G. GRIVENNIKOVA, Gary CECCHINI, and Andrei D. VINOGRADOV. "Inhibitory effect of palmitate on the mitochondrial NADH:ubiquinone oxidoreductase (complex I) as related to the active–de-active enzyme transition." Biochemical Journal 387, no. 3 (April 26, 2005): 677–83. http://dx.doi.org/10.1042/bj20041703.
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Palmitate rapidly and reversibly inhibits the uncoupled NADH oxidase activity catalysed by activated complex I in inside-out bovine heart submitochondrial particles (IC50 extrapolated to zero enzyme concentration is equal to 9 μM at 25 °C, pH 8.0). The NADH:hexa-ammineruthenium reductase activity of complex I is insensitive to palmitate. Partial (∼50%) inhibition of the NADH:external quinone reductase activity is seen at saturating palmitate concentration and the residual activity is fully sensitive to piericidin. The uncoupled succinate oxidase activity is considerably less sensitive to palmitate. Only a slight stimulation of tightly coupled respiration with NADH as the substrate is seen at optimal palmitate concentrations, whereas complete relief of the respiratory control is observed with succinate as the substrate. Palmitate prevents the turnover-induced activation of the de-activated complex I (IC50 extrapolated to zero enzyme concentration is equal to 3 μM at 25 °C, pH 8.0). The mode of action of palmitate on the NADH oxidase is qualitatively temperature-dependent. Rapid and reversible inhibition of the complex I catalytic activity and its de-active to active state transition are seen at 25 °C, whereas the time-dependent irreversible inactivation of the NADH oxidase proceeds at 37 °C. Palmitate drastically increases the rate of spontaneous de-activation of complex I in the absence of NADH. Taken together, these results suggest that free fatty acids act as specific complex I-directed inhibitors; at a physiologically relevant temperature (37 °C), their inhibitory effects on mitochondrial NADH oxidation is due to perturbation of the pseudo-reversible active–de-active complex I transition.
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Tazzeo, Tracy, Genevieve Bates, Horia Nicolae Roman, Anne-Marie Lauzon, Mukta D. Khasnis, Masumi Eto, and Luke J. Janssen. "Caffeine relaxes smooth muscle through actin depolymerization." American Journal of Physiology-Lung Cellular and Molecular Physiology 303, no. 4 (August 15, 2012): L334—L342. http://dx.doi.org/10.1152/ajplung.00103.2012.
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Caffeine is sometimes used in cell physiological studies to release internally stored Ca2+. We obtained evidence that caffeine may also act through a different mechanism that has not been previously described and sought to examine this in greater detail. We ruled out a role for phosphodiesterase (PDE) inhibition, since the effect was 1) not reversed by inhibiting PKA or adenylate cyclase; 2) not exacerbated by inhibiting PDE4; and 3) not mimicked by submillimolar caffeine nor theophylline, both of which are sufficient to inhibit PDE. Although caffeine is an agonist of bitter taste receptors, which in turn mediate bronchodilation, its relaxant effect was not mimicked by quinine. After permeabilizing the membrane using β-escin and depleting the internal Ca2+ store using A23187, we found that 10 mM caffeine reversed tone evoked by direct application of Ca2+, suggesting it functionally antagonizes the contractile apparatus. Using a variety of molecular techniques, we found that caffeine did not affect phosphorylation of myosin light chain (MLC) by MLC kinase, actin-filament motility catalyzed by MLC kinase, phosphorylation of CPI-17 by either protein kinase C or RhoA kinase, nor the activity of MLC-phosphatase. However, we did obtain evidence that caffeine decreased actin filament binding to phosphorylated myosin heads and increased the ratio of globular to filamentous actin in precontracted tissues. We conclude that, in addition to its other non-RyR targets, caffeine also interferes with actin function (decreased binding by myosin, possibly with depolymerization), an effect that should be borne in mind in studies using caffeine to probe excitation-contraction coupling in smooth muscle.
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Afanas'ev, Igor. "Signaling of Reactive Oxygen and Nitrogen Species in Diabetes Mellitus." Oxidative Medicine and Cellular Longevity 3, no. 6 (2010): 361–73. http://dx.doi.org/10.4161/oxim.3.6.14415.
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Disorder of physiological signaling functions of reactive oxygen species(ROS) superoxide and hydrogen peroxide and reactive nitrogen species (RNS) nitric oxide and peroxynitrite is an important feature of diabetes mellitus type 1 and type 2. It is now known that hyperglycemic conditions of cells are associated with the enhanced levels of ROS mainly generated by mitochondria and NADPH oxidase. It has been established that ROS stimulate many enzymatic cascades under normal physiological conditions, but hyperglycemia causes ROS overproduction and the deregulation of ROS signaling pathways initiating the development of diabetes mellitus. On the other hand the deregulation of RNS signaling leads basically to a decrease in NO formation with subsequent damaging disorders. In the present work we will consider the pathological changes of ROS and RNS signaling in enzyme/gene regulated processes catalyzed by protein kinases C and B (Akt/B), phosphatidylinositol 3′-kinase (PI3-kinase), extracellular signal-regulated kinase 1/2 (ERK1/2) and some others. Furthermore we will discuss a particularly important role of several ROS-regulated genes and adapter proteins such as the p66shc, FOXO3a and Sirt2. The effects of low and high ROS levels in diabetes will be also considered. Thus the regulation of damaging ROS levels in diabetes by antioxidants and free radical scavengers must be one of promising treatment of this disease, however, because of the inability of traditionalantioxidative vitamin E and C to interact with superoxide and hydrogen peroxide,new free radical scavengers such as flavonoids, quinones and synthetic mimetics of superoxide dismutase (SOD) should be intensively studied.
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Kshirsagar, Suhas G., and Rammohan V. Rao. "Antiviral and Immunomodulation Effects of Artemisia." Medicina 57, no. 3 (February 27, 2021): 217. http://dx.doi.org/10.3390/medicina57030217.
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Background and Objectives: Artemisia is one of the most widely distributed genera of the family Astraceae with more than 500 diverse species growing mainly in the temperate zones of Europe, Asia and North America. The plant is used in Chinese and Ayurvedic systems of medicine for its antiviral, antifungal, antimicrobial, insecticidal, hepatoprotective and neuroprotective properties. Research based studies point to Artemisia’s role in addressing an entire gamut of physiological imbalances through a unique combination of pharmacological actions. Terpenoids, flavonoids, coumarins, caffeoylquinic acids, sterols and acetylenes are some of the major phytochemicals of the genus. Notable among the phytochemicals is artemisinin and its derivatives (ARTs) that represent a new class of recommended drugs due to the emergence of bacteria and parasites that are resistant to quinoline drugs. This manuscript aims to systematically review recent studies that have investigated artemisinin and its derivatives not only for their potent antiviral actions but also their utility against the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Materials and Methods: PubMed Central, Scopus and Google scholar databases of published articles were collected and abstracts were reviewed for relevance to the subject matter. Conclusions: The unprecedented impact that artemisinin had on public health and drug discovery research led the Nobel Committee to award the Nobel Prize in Physiology or Medicine in 2015 to the discoverers of artemisinin. Thus, it is clear that Artemisia’s importance in indigenous medicinal systems and drug discovery systems holds great potential for further investigation into its biological activities, especially its role in viral infection and inflammation.
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Hemalatha C N, Mehurnisha K, Preethi B, Keerthana V, and Harikrishnan N. "Antioxidant Activity of Kiwi Fruit (Actindia Chinensis)." International Journal of Research in Pharmaceutical Sciences 11, no. 4 (December 5, 2020): 6810–17. http://dx.doi.org/10.26452/ijrps.v11i4.3637.
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Actinidia chinensis (kiwi fruit), also known as golden fruit, has its origin in China. All the plant parts of Actinidia chinensis such as fruit, leaves, vine, and root were used in food products and also used as medicine in China. The Worldwide distribution of the kiwi (Actinidia chinensis) is due to its Nutritional property, economic value and the presence of the various phytoconstituents such as terpenoids, quinones, flavones, phenyl proteinoids and steroids. It is also rich in antioxidant and dietary fibres which are utilized for the production of cellulose and hemicellulose. The Nutritional composition of the Kiwi fruit has distinguishing amount of vitamin C and also several other compounds such as Minerals, Vitamin E and Carotenoids and these are used to protect DNA. It has a high amount of medicinal and Nutritional value and also provides various health benefits. In traditional medicine of China, Kiwi fruit is also used in the treatment of Edema, Pyorrhea, gingivitis, Hepatitis, maintenance of blood glucose level, asthma, fight against muscular degenerative diseases and reduces the risk of blood clots and also used in Cancer treatment. Recently researchers have updated that Kiwi fruit has beneficial Physiological effect on the human body through clinical studies. It has been proven that Kiwi has Anti-Oxidant property and relieves Oxidative stress which was the Major cause of Diseases. This article is an overview of kiwi fruit, its nutritional benefits and its antioxidant effect.
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Chen, Xi, Bingxian Yang, Wei Huang, Tantan Wang, Yaohan Li, Zhuoheng Zhong, Lin Yang, Shouxin Li, and Jingkui Tian. "Comparative Proteomic Analysis Reveals Elevated Capacity for Photosynthesis in Polyphenol Oxidase Expression-Silenced Clematis terniflora DC. Leaves." International Journal of Molecular Sciences 19, no. 12 (December 5, 2018): 3897. http://dx.doi.org/10.3390/ijms19123897.
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Polyphenol oxidase (PPO) catalyzes the o-hydroxylation of monophenols and oxidation of o-diphenols to quinones. Although the effects of PPO on plant physiology were recently proposed, little has been done to explore the inherent molecular mechanisms. To explore the in vivo physiological functions of PPO, a model with decreased PPO expression and enzymatic activity was constructed on Clematis terniflora DC. using virus-induced gene silencing (VIGS) technology. Proteomics was performed to identify the differentially expressed proteins (DEPs) in the model (VC) and empty vector-carrying plants (VV) untreated or exposed to high levels of UV-B and dark (HUV-B+D). Following integration, it was concluded that the DEPs mainly functioned in photosynthesis, glycolysis, and redox in the PPO silence plants. Mapman analysis showed that the DEPs were mainly involved in light reaction and Calvin cycle in photosynthesis. Further analysis illustrated that the expression level of adenosine triphosphate (ATP) synthase, the content of chlorophyll, and the photosynthesis rate were increased in VC plants compared to VV plants pre- and post HUV-B+D. These results indicate that the silence of PPO elevated the plant photosynthesis by activating the glycolysis process, regulating Calvin cycle and providing ATP for energy metabolism. This study provides a prospective approach for increasing crop yield in agricultural production.
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Cho, Young K., Cheng-Shu Li, and David V. Smith. "Taste Responses of Neurons of the Hamster Solitary Nucleus Are Enhanced by Lateral Hypothalamic Stimulation." Journal of Neurophysiology 87, no. 4 (April 1, 2002): 1981–92. http://dx.doi.org/10.1152/jn.00765.2001.
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Gustatory responses in the brain stem are modifiable by several physiological factors, including blood insulin and glucose, intraduodenal lipids, gastric distension, and learning, although the neural substrates for these modulatory effects are not known. Stimulation of the lateral hypothalamus (LH) produces increases in food intake and alterations in taste preference behavior, whereas damage to this area has opposite effects. In the present study, we investigated the effects of LH stimulation on the neural activity of taste-responsive cells in the nucleus of the solitary tract (NST) of the hamster. Bipolar stimulating electrodes were bilaterally implanted in the LH, and the responses of 99 neurons in the NST, which were first characterized for their taste sensitivities, were tested for their response to both ipsilateral and contralateral LH stimulation. Half of the taste-responsive cells in the NST (49/99) were modulated by LH stimulation. Contralateral stimulation was more often effective (41 cells) than ipsilateral (13 cells) and always excitatory; 10 cells were excited bilaterally. Six cells were inhibited by ipsilateral stimulation. A subset of these cells ( n = 13) was examined for the effects of microinjection of dl-homocysteic acid (DLH), a glutamate receptor agonist, into the LH. The effects of electrical stimulation were completely mimicked by DLH, indicating that cell somata in and around the LH are responsible for these effects. Other cells ( n = 14) were tested for the effects of electrical stimulation of the LH on the responses to stimulation of the tongue with 0.032 M sucrose, NaCl, and quinine hydrochloride, and 0.0032 M citric acid. Responses to taste stimuli were more than doubled by the excitatory influence of the LH. These data show that the LH, in addition to its role in feeding and metabolism, exerts descending control over the processing of gustatory information through the brain stem.
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Li, Cheng-Shu, Young K. Cho, and David V. Smith. "Modulation of Parabrachial Taste Neurons by Electrical and Chemical Stimulation of the Lateral Hypothalamus and Amygdala." Journal of Neurophysiology 93, no. 3 (March 2005): 1183–96. http://dx.doi.org/10.1152/jn.00828.2004.
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The lateral hypothalamus (LH) and the central nucleus of the amygdala (CeA) exert an influence on ingestive behavior and are reciprocally connected to gustatory and viscerosensory areas, including the nucleus of the solitary tract (NST) and the parabrachial nuclei (PbN). We investigated the effects of LH and CeA stimulation on the activity of 101 taste-responsive neurons in the hamster PbN. Eighty three of these neurons were antidromically activated by stimulation of these sites; 57 were antidromically driven by both. Of these 83 neurons, 21 were also orthodromically activated—8 by the CeA and 3 by the LH. Additional neurons were excited ( n = 5) or inhibited ( n = 8) by these forebrain nuclei but not antidromically activated. Taste stimuli were: 0.032 M sucrose, 0.032 M sodium chloride (NaCl), 0.032 M quinine hydrochloride (QHCl), and 0.0032 M citric acid. Among the 34 orthodromically activated neurons, more sucrose-best neurons were excited than inhibited, whereas the opposite occurred for citric-acid- and QHCl-best cells. Neurons inhibited by the forebrain responded significantly more strongly to citric acid and QHCl than cells excited by these sites. The effects of electrical stimulation were mimicked by microinjection of dl-homocysteic acid, indicating that cells at these forebrain sites were responsible for these effects. These data demonstrate that many individual PbN gustatory neurons project to both the LH and CeA and that these areas modulate the gustatory activity of a subset of PbN neurons. This neural substrate is likely involved in the modulation of taste activity by physiological and experiential factors.
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Doss, Jennifer, Jude Jonassaint, Nirmish Shah, Marilyn J. Telen, and Jen-Tsan A. Chi. "Effects of Sulforaphane Obtained from Broccoli Sprout Homogenate in Patients with Sickle Cell Disease (SCD)." Blood 124, no. 21 (December 6, 2014): 4931. http://dx.doi.org/10.1182/blood.v124.21.4931.4931.
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Abstract BACKGROUND Sickle cell disease (SCD) is the most common hemoglobinopathy worldwide, characterized by chronic complications due to ongoing vaso-occlusion and hemolysis. Previous studies have shown that red cells from individuals with sickle cell disease (HbSS) have reduced NRF2 expression levels, which contribute to decreased oxidative stress capacity and increased hemolysis (Sangokoya, et al. 2010 Blood). Additionally, Macari and Lowry have shown that in vitro NRF2 activation of erythroid progenitors results in induction of anti-oxidant stress response genes, as well as increased percent fetal hemoglobin (HbF), which is known to prevent sickling (2011 Blood). Therefore, we hypothesize that NRF2 activation in SCD patients has potential therapeutic benefits by simultaneously inducing HbF and increasing the anti-oxidative stress capacity of red cells. We proposed to activate NRF2 by using sulforaphane (SFN), a well-known natural product enriched in broccoli sprouts. We conducted an open-label, dose-escalation clinical trial for SCD patients to investigate the safety and physiological effects of NRF2 activation by SFN through ingestion of a broccoli sprout homogenate (BSH). METHODS Male and female adult patients (> 18 years) with either HbSS or HbSߺ thalassemia were enrolled at the Duke Comprehensive Sickle Cell Center adult clinic. Exclusion criteria: RBC transfusion or a change in hydroxyurea dose in the last three months, ongoing pregnancy, diabetes, or renal insufficiency (BUN >21 mg/dL and/or creatinine >1.4 mg/dL). Inclusion criteria: Hematocrit (Hct) ≥ 20% and Hb > 6.0 g/dL. Recruited subjects were instructed to avoid additional SFN-containing foods before and during the study period. Subjects ingested a thawed preparation of BSH once daily for 21 days to allow for repopulation of red cells during therapy. Tolerability, toxicity, and physiological effects of NRF2 activation were determined at pre-treatment baseline (day 0), on the last day of ingestion (day 21), and after a wash-out period (day 49). Five patients were recruited for each dose (50g, 100g), with the smaller dose having elicited no safety concerns. RESULTS No safety concerns were noted among the subjects at either dose. In both cohorts, there were no significant differences in the adverse events, pain scores, complete blood counts, complete metabolic profile, reticulocyte count, and LDH levels when comparing days 0 and 21. In the 50g cohort, there was an overall but not statistically significant increase of average HbF from 14.5% to 14.9% (p=0.0786) in all five patients from Day 0 to Day 21; analyses are incomplete for the higher dose. We also observed a trend of NRF2 mRNA target gene induction, including heme oxygenase-1 (HO-1), NAD(P)H dehydrogenase (quinone 1, NQO1), and globin mRNAs, at day 21 vs day 0, which returned to baseline levels at day 49. In the 50g cohort, we observed a 66% increase of ho-1 and 44% increase of nqo1 mRNA levels at day 21 vs. baseline. In the 100g cohort, we observed a 14% increase of ho-1 and 42% increase of nqo1mRNA levels at day 21 vs. baseline. CONCLUSION Our pilot trial suggests that NRF2 activation by BSH may increase NRF2 expression programs and induce fetal hemoglobin. We aim to enroll more patients at escalating doses, as participants present a wide range of clinical variability and may show variable response. Additionally, the lack of statistical significance at the lowest doses along with a lack of safety concerns strongly compel us to pursue more potent NRF2 inducers to elicit more robust physiological changes for additional clinical trials. Disclosures No relevant conflicts of interest to declare.
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Maroco, João P., M. Lucília Rodrigues, Carlos Lopes, and M. Manuela Chaves. "Limitations to leaf photosynthesis in field-grown grapevine under drought — metabolic and modelling approaches." Functional Plant Biology 29, no. 4 (2002): 451. http://dx.doi.org/10.1071/pp01040.
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The effects of a slowly-imposed drought stress on gas-exchange, chlorophyll a fluorescence, biochemical and physiological parameters of Vitis vinifera L. leaves (cv. Aragonez, syn. Tempranillo) growing in a commercial vineyard (South Portugal) were evaluated. Relative to well-watered plants (predawn water potential, ΨPD = –0.13 ± 0.01 MPa), drought-stressed plants (ΨPD = –0.97 ± 0.01 MPa) had lower photosynthetic rates (ca 70%), stomatal conductance, and PSII activity (associated with a higher reduction of the quinone A pool and lower efficiency of PSII open centres). Stomatal limitation to photosynthesis was increased in drought-stressed plants relative to well-watered plants by ca 44%. Modelled responses of net photosynthesis to internal CO2 indicated that drought-stressed plants had significant reductions in maximum Rubisco carboxylation activity (ca 32%), ribulose-1,5-bisphosphate regeneration (ca 27%), and triose phosphate (triose-P) utilization rates (ca 37%) relative to well-watered plants. There was good agreement between the effects of drought on modelled biochemical parameters, and in vitro activities of key enzymes of carbon metabolism, namely Rubisco, glyceraldehyde-3-phosphate dehydrogenase, ribulose-5-phosphate kinase and fructose-1,6-bisphosphate phosphatase. Quantum yields measured under both ambient (35 Pa) and saturating CO2 (100 Pa) for drought-stressed plants were decreased relative to well-watered plants, as well as maximum photosynthetic rates measured at light and CO2 saturating conditions (three times ambient CO2 levels). Although stomatal closure was a strong limitation to CO2 assimilation under drought, comparable reductions in electron transport, CO2 carboxylation, and utilization of triose-P capacities were also adaptations of the photosynthetic machinery to dehydration that slowly developed under field conditions. Results presented in this study confirm that modelling photosynthetic responses based on gas-exchange data can be successfully used to predict metabolic limitations to photosynthesis.
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Gorka, Alexander P., John N. Alumasa, Katy S. Sherlach, Lauren M. Jacobs, Katherine B. Nickley, Jonathan P. Brower, Angel C. de Dios, and Paul D. Roepe. "Cytostatic versus Cytocidal Activities of Chloroquine Analogues and Inhibition of Hemozoin Crystal Growth." Antimicrobial Agents and Chemotherapy 57, no. 1 (October 31, 2012): 356–64. http://dx.doi.org/10.1128/aac.01709-12.
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ABSTRACTWe report an improved, nonhazardous, high-throughput assay forin vitroquantification of antimalarial drug inhibition of β-hematin (hemozoin) crystallization performed under conditions that are more physiological relative to previous assays. The assay uses the differential detergent solubility of crystalline and noncrystalline forms of heme and is optimized via the use of lipid catalyst. Using this assay, we quantify the effect of pH on the crystal growth-inhibitory activities of current quinoline antimalarials, evaluate the catalytic efficiencies of different lipids, and test for a possible correlation between hemozoin inhibition by drugs versus their antiplasmodial activity. Consistent with several previous reports, we found a good correlation between hemozoin inhibition potency versus cytostatic antiplasmodial potency (50% inhibitory concentration) for a series of chloroquine (CQ) analogues. However, we found no correlation between hemozoin inhibition potency and cytocidal antiplasmodial potency (50% lethal dose) for the same drugs, suggesting that cellular targets for these two layers of 4-aminoquinoline drug activity differ. This important concept is also explored further for QN and its stereoisomers in the accompanying paper (A. P. Gorka, K. S. Sherlach, A. C. de Dios, and P. D. Roepe, Antimicrob. Agents Chemother. 57:365–374, 2013).
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Rheault, Mark R., Donna M. Debicki, and Michael J. O'Donnell. "Characterization of tetraethylammonium uptake across the basolateral membrane of the Drosophila Malpighian (renal) tubule." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 2 (August 2005): R495—R504. http://dx.doi.org/10.1152/ajpregu.00109.2005.
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Basolateral transport of the prototypical type I organic cation tetraethylammonium (TEA) by the Malpighian tubules of Drosophila melanogaster was studied using measurements of basolateral membrane potential (Vbl) and uptake of [14C]-labeled TEA. TEA uptake was metabolically dependent and saturable (maximal rate of mediated TEA uptake by all potential transport processes, reflecting the total transport capacity of the membrane, 0.87 pmol·tubule−1·min−1; concentration of TEA at 0.5 of the maximal rate of TEA uptake value, 24 μM). TEA uptake in Malpighian tubules was inhibited by a number of type I (e.g., cimetidine, quinine, and TEA) and type II (e.g., verapamil) organic cations and was dependent on Vbl. TEA uptake was reduced in response to conditions that depolarized Vbl (high-K+ saline, Na+-free saline, NaCN) and increased in conditions that hyperpolarized Vbl (low-K+ saline). Addition of TEA to the saline bathing Malpighian tubules rapidly depolarized the Vbl, indicating that TEA uptake was electrogenic. Blockade of K+ channels with Ba2+ did not block effects of TEA on Vbl or TEA uptake indicating that TEA uptake does not occur through K+ channels. This is the first study to provide physiological evidence for an electrogenic carrier-mediated basolateral organic cation transport mechanism in insect Malpighian tubules. Our results also suggest that the mechanism of basolateral TEA uptake by Malpighian tubules is distinct from that found in vertebrate renal tubules.
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Hur, Chang-Gi, Eun-Jin Kim, Seong-Keun Cho, Young-Woo Cho, Sook-Young Yoon, Hyun-Min Tak, Chang-Woon Kim, Changyong Choe, Jaehee Han, and Dawon Kang. "K+ efflux through two-pore domain K+ channels is required for mouse embryonic development." REPRODUCTION 143, no. 5 (May 2012): 625–36. http://dx.doi.org/10.1530/rep-11-0225.
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Numerous studies have suggested that K+ channels regulate a wide range of physiological processes in mammalian cells. However, little is known about the specific function of K+ channels in germ cells. In this study, mouse zygotes were cultured in a medium containing K+ channel blockers to identify the functional role of K+ channels in mouse embryonic development. Voltage-dependent K+ channel blockers, such as tetraethylammonium and BaCl2, had no effect on embryonic development to the blastocyst stage, whereas K2P channel blockers, such as quinine, selective serotonin reuptake inhibitors (fluoxetine, paroxetine, and citalopram), gadolinium trichloride, anandamide, ruthenium red, and zinc chloride, significantly decreased blastocyst formation (P<0.05). RT-PCR data showed that members of the K2P channel family, specifically KCNK2, KCNK10, KCNK4, KCNK3, and KCNK9, were expressed in mouse oocytes and embryos. In addition, their mRNA expression levels, except Kcnk3, were up-regulated by above ninefold in morula-stage embryos compared with 2-cell stage embryos (2-cells). Immunocytochemical data showed that KCNK2, KCNK10, KCNK4, KCNK3, and KCNK9 channel proteins were expressed in the membrane of oocytes, 2-cells, and blastocysts. Each siRNA injection targeted at Kcnk2, Kcnk10, Kcnk4, Kcnk3, and Kcnk9 significantly decreased blastocyst formation by ∼38% compared with scrambled siRNA injection (P<0.05). The blockade of K2P channels acidified the intracellular pH and depolarized the membrane potential. These results suggest that K2P channels could improve mouse embryonic development through the modulation of gating by activators.
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Cirilli, Ilenia, Patrick Orlando, Fabio Marcheggiani, Phiwayinkosi V. Dludla, Sonia Silvestri, Elisabetta Damiani, and Luca Tiano. "The Protective Role of Bioactive Quinones in Stress-induced Senescence Phenotype of Endothelial Cells Exposed to Cigarette Smoke Extract." Antioxidants 9, no. 10 (October 16, 2020): 1008. http://dx.doi.org/10.3390/antiox9101008.
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Endothelial dysfunction represents the initial stage in atherosclerotic lesion development which occurs physiologically during aging, but external factors like diet, sedentary lifestyle, smoking accelerate it. Since cigarette smoking promotes oxidative stress and cell damage, we developed an in vitro model of endothelial dysfunction using vascular cells exposed to chemicals present in cigarette smoke, to help elucidate the protective effects of anti-inflammatory and antioxidant agents, such as ubiquinol and vitamin K, that play a fundamental role in vascular health. Treatment of both young and senescent Human Umbilical Vein Endothelial Cells (HUVECs) for 24 h with cigarette smoke extract (CSE) decreased cellular viability, induced apoptosis via reactive oxygen species (ROS) imbalance and mitochondrial dysfunction and promoted an inflammatory response. Moreover, the senescence marker SA-β-galactosidase was observed in both young CSE-exposed and in senescent HUVECs suggesting that CSE exposure accelerates aging in endothelial cells. Supplementation with 10 µM ubiquinol and menaquinone-7 (MK7) counteracted oxidative stress and inflammation, resulting in improved viability, decreased apoptosis and reduced SA-β-galactosidase, but were ineffective against CSE-induced mitochondrial permeability transition pore opening. Other K vitamins tested like menaquinone-4 (MK4) and menaquinone-1 (K1) were less protective. In conclusion, CSE exposure was able to promote a stress-induced senescent phenotype in young endothelial cells likely contributing to endothelial dysfunction in vivo. Furthermore, the molecular changes encountered could be offset by ubiquinol and menaquinone-7 supplementation, the latter resulting the most bioactive K vitamin in counteracting CSE-induced damage.
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Marsova, Maria, Maya Odorskaya, Maria Novichkova, Valentina Polyakova, Serikbay Abilev, Elena Kalinina, Alexander Shtil, Elena Poluektova, and Valery Danilenko. "The Lactobacillus brevis 47 f Strain Protects the Murine Intestine from Enteropathy Induced by 5-Fluorouracil." Microorganisms 8, no. 6 (June 9, 2020): 876. http://dx.doi.org/10.3390/microorganisms8060876.
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We report that the results of our study indicate that Lactobacillus brevis 47 f strain isolated from the faeces of a healthy individual prevents the manifestations of experimental mucositis induced by treatment of Balb/c mice with the anticancer drug 5-fluorouracil (5 FU; 100 mg/kg i.p. × 3 days). The presence of damage to the intestine and the colon was determined by a morphometric analysis of specimens including the height of villi, the amount of goblet cells and infiltrating mononuclear cells, and the expression of the proliferative Ki-67 antigen. Changes in the lipid peroxidation in the blood and the intestine were determined by severalfold increase of the concentration of malonic dialdehyde. Oral administration of L. brevis 47 f strain prior to 5 FU decreased the drug-induced morphological and biochemical changes to their respective physiological levels; the ability of intestinal epitheliocytes to express Ki-67 was partially restored. These effects of L. brevis 47 f strain were more pronounced or similar to those of the reference compound Rebamipid, a quinoline derivative known to protect the gut from drug-induced toxicity. Thus, the new lactobacilli strain attenuates the severity of 5 FU-induced enteropathy.
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Yang, Shih-Chun, Ching-Yun Hsu, Wei-Ling Chou, Jia-You Fang, and Shih-Yi Chuang. "Bioactive Agent Discovery from the Natural Compounds for the Treatment of Type 2 Diabetes Rat Model." Molecules 25, no. 23 (December 3, 2020): 5713. http://dx.doi.org/10.3390/molecules25235713.
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Diabetes mellitus is a well-known chronic metabolic disease that poses a long-term threat to human health and is characterized by a relative or absolute lack of insulin, resulting in hyperglycemia. Type 2 diabetes mellitus (T2DM) typically affects many metabolic pathways, resulting in β-cell dysfunction, insulin resistance, abnormal blood glucose levels, inflammatory processes, excessive oxidative reactions, and impaired lipid metabolism. It also leads to diabetes-related complications in many organ systems. Antidiabetic drugs have been approved for the treatment of hyperglycemia in T2DM; these are beneficial for glucose metabolism and promote weight loss, but have the risk of side effects, such as nausea or an upset stomach. A wide range of active components, derived from medicinal plants, such as alkaloids, flavonoids, polyphenol, quinones, and terpenoids may act as alternative sources of antidiabetic agents. They are usually attributed to improvements in pancreatic function by increasing insulin secretions or by reducing the intestinal absorption of glucose. Ease of availability, low cost, least undesirable side effects, and powerful pharmacological actions make plant-based preparations the key player of all available treatments. Based on the study of therapeutic reagents in the pathogenesis of humans, we use the appropriate animal models of T2DM to evaluate medicinal plant treatments. Many of the rat models have characteristics similar to those in humans and have the advantages of ease of genetic manipulation, a short breeding span, and access to physiological and invasive testing. In this review, we summarize the pathophysiological status of T2DM rat models and focus on several bioactive compounds from herbal medicine with different functional groups that exhibit therapeutic potential in the T2DM rat models, in turn, may guide future approach in treating diabetes with natural drugs.
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Yakoviichuk, O. V., O. O. Danchenko, M. M. Danchenko, A. S. Fedorko, and I. O. Kulyk. "ЖИРНОКИСЛОТНИЙ СКЛАД МІОКАРДУ ГУСЕЙ ЗА ДІЇ ВІКАСОЛУ." Scientific Issue Ternopil Volodymyr Hnatiuk National Pedagogical University. Series: Biology 77, no. 3 (September 24, 2019): 32–38. http://dx.doi.org/10.25128/2078-2357.19.3.4.
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In science vicasol is known to be relative to the energy and antioxidant systems of tissues closely related to the biosynthesis and oxidation of fatty acids. This effect may cause changes in the fatty acid composition of tissues, and numerous works on the positive effect of quinones and their derivatives on the myocardial function, suggest that the proper dose and feeding can increase the stability and productivity of poultry. The given was aims to study the effect of vicasol on the fatty acid composition of goose myocardium.
Myocardium was chosen as a biological object. Biological material was collected every 7 days throughout the period from the 21st to the 35th day of ontogeny, characterized by the state of physiological tension of geese. Feeding of geese with vicasol at a dose of 0.7 mg / kg body weight began with the 3rd day of ontogeny. Fatty acid analysis in myocardial tissues was performed by gas-liquid chromatography, pre-fabric samples were processed with the method by Palmer (1971) to obtain tissue lipid extracts.
According to the results of the study, due to various changes in the content of the entire spectrum of fatty acids of the tissue during the experiment - the use of vicasol causes a slight increase in the unsaturation and the total content of unsaturated fatty acids in the myocardium of geese. These fluctuations are realized depending on the physiological state of the body. where vicasol can stimulate both the biosynthesis processes of individual fatty acids and their mitochondrial and microsomal oxidation, as evidenced by multidirectional reliable changes in the content of their entire spectrum. In particular, on the 21st day, the content of docosopentaenoic acid increased by 36.3% whereas the content of docosohexaenoic and linolenic acids decreased by an average of 21–24%, on the 28th day the content of eicosatetraic and docosahexaenoic acids increased whereas the content of the linoleic acids dropped by 22.6% in control groups. On the 35th day, the content of basic unsaturated fatty acids: palmitooleic, linoleic, linolenic and docosohexaenoic acids increased in the tissue under the influence of vicasol with complete depletion of docosopentaenoic acid. These fluctuations in fatty acid composition cause a slight increase in the total content of unsaturated fatty acids and increase the unsaturation of myocardial lipids on the 28th and 35th days of ontogeny of geese. Based on previous results regarding the antioxidant state of myocardium affected by vicasol and the given findings, which prove changes in the content of the entire spectrum of fatty acids during the selected ontogeny, vicasol can be used in poultry farming as a tool to improve the quality and the resilience of poultry.
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Bachheti, Rakesh Kumar, Limenew Abate Worku, Yilma Hunde Gonfa, Meseret Zebeaman, Deepti, D. P. Pandey, and Archana Bachheti. "Prevention and Treatment of Cardiovascular Diseases with Plant Phytochemicals: A Review." Evidence-Based Complementary and Alternative Medicine 2022 (July 4, 2022): 1–21. http://dx.doi.org/10.1155/2022/5741198.
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Cardiovascular diseases (CVDs) are the world’s leading killers, accounting for 30% deaths. According to the WHO report, CVDs kill 17.9 million people per year, and there will be 22.2 million deaths from CVD in 2030. The death rates rise as people get older. Regarding gender, the death rate of women by CVD (51%) is higher than that of men (42%). To decrease and prevent CVD, most people rely on traditional medicine originating from the plant (phytochemicals) in addition to or in preference to commercially available drugs to recover from their illness. The CVD therapy efficacy of 92 plants, including 15 terrestrial plants, is examined. Some medicinal plants well known to treat CVD are, Daucus carota, Nerium oleander, Amaranthus Viridis, Ginkgo biloba, Terminalia arjuna, Picrorhiza kurroa, Salvia miltiorrhiza, Tinospora cordifolia, Mucuna pruriens, Hydrocotyle asiatica, Bombax ceiba, and Andrographis paniculate. The active phytochemicals found in these plants are flavonoids, polyphenols, plant sterol, plant sulphur compounds, and terpenoids. A general flavonoid mechanism of action is to prevent low-density lipoprotein oxidation, which promotes vasodilatation. Plant sterols prevent CVD by decreasing cholesterol absorption in the blood. Plant sulphur compound also prevent CVD by activation of nuclear factor-erythroid factor 2-related factor 2 (Nrf2) and inhibition of cholesterol synthesis. Quinone decreases the risk of CVD by increasing ATP production in mitochondria while terpenoids by decreasing atherosclerotic lesion in the aortic valve. Although several physiologically active compounds with recognized biological effects have been found in various plants because of the increased prevalence of CVD, appropriate CVD prevention and treatment measures are required. More research is needed to understand the mechanism and specific plants’ phytochemicals responsible for treating CVD.
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OuYang, Fangqun, Yang Ou, Tianqin Zhu, Jianwei Ma, Sanping An, Jun Zhao, Junhui Wang, Lisheng Kong, Hanguo Zhang, and Mulualem Tigabu. "Growth and Physiological Responses of Norway Spruce (Picea abies (L.) H. Karst) Supplemented with Monochromatic Red, Blue and Far-Red Light." Forests 12, no. 2 (January 30, 2021): 164. http://dx.doi.org/10.3390/f12020164.
Full textAbstract:
Monochromatic red light (R) supplementation is more efficient than blue light (B) in promoting Norway spruce (Picea abies (L.) H. Karst) growth. Transcriptome analysis has revealed that R and B may regulate stem growth by regulating phytohormones and secondary metabolites; however, the effects of light qualities on physiological responses and related gene expression in Norway spruce require further study. In the present study, three-year-old Norway spruce seedlings received sunlight during the daytime were exposed to monochromatic B (460 mm), monochromatic R (660 nm), monochromatic far-red light (FR, 730 nm), and a combination of three monochromatic lights (control, R:FR:B = 7:1:1) using light-emitting diode (LED) lamps for 12 h after sunset for 90 day. Growth traits, physiological responses, and related gene expression were determined. The results showed that light quality significantly affected Norway spruce growth. The stem height, root collar diameter, and current-year shoot length of seedlings treated with R were 2%, 10% and 12% higher, respectively, than those of the control, whereas seedlings treated with B and FR showed significantly lower values of these parameters compared with that of the control. The net photosynthetic rate (Pn) of seedlings under R treatment was 10% higher than that of the control, whereas the Pn values of seedlings treated with FR and B were 22% and 33%, respectively, lower than that of the control. The ratio of phosphoenolpyruvate carboxylase to ribulose-1,5-bisphosphate carboxylase/oxygenase (PEPC/Rubisco) of seedlings after the R treatment (0.581) was the highest and 3.98 times higher than that of the seedlings treated with B. Light quality significantly affected the gibberellic acid (GAs) levels, which was 13% higher in seedlings treated with R (6.4 g/100 ng) than that of the control, whereas, the GAs level of seedlings treated with B and FR was 17% and 19% lower, respectively, than that of the control. In addition, seedlings treated with R achieved the lowest ratio of leaf chlorophyll content to fresh weight (8.7). Compared to the R and control treatments, seedlings received FR treatment had consistently lower values of the quantum yield of electron transport beyond QA− (primary quinone, ϕEo) and efficiency, with which a trapped exciton moves an electron into the electron transport chain beyond QA− (ψo), while higher values of the relatively variable fluorescence at the J step and normalized relatively variable fluorescence at the K step (Wk). The values of ϕEo, ψO, VJ and Wk in seedlings treated with B were similar to those in the control group. The expression of genes associated with light signal transduction, such as PHYTOCHROME C (PHYC), ELONGATED HYPOCOTYL5 (HY5), CONSTITUTIVE PHOTOMORPHOGENIC 1-2 (COP1-2), and PHYTOCHROMEINTERACTING FACTOR 3 (PIF3), was significantly higher in seedlings under B treatment than those under other light treatments. Nevertheless, significant differences were not observed in the expression of COP1-2, HY5, and PIF3 between the R treatment and the control. The expression value of COP1-2 was significantly lower in R than FR light treatments. In conclusion, compared with the control, R promotes, whereas B and FR inhibit Norway spruce growth, which was accompanied by physiological changes and genes expression regulation that may be relate to a changing phytochrome photostationary state (PSS) with the supplemental R in seedlings.
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Li, Cheng-Shu, and David V. Smith. "Glutamate Receptor Antagonists Block Gustatory Afferent Input to the Nucleus of the Solitary Tract." Journal of Neurophysiology 77, no. 3 (March 1, 1997): 1514–25. http://dx.doi.org/10.1152/jn.1997.77.3.1514.
Full textAbstract:
Li, Cheng-Shu and David V. Smith. Glutamate receptor antagonists block gustatory afferent input to the nucleus of the solitary tract. J. Neurophysiol. 77: 1514–1525, 1997. The effects of excitatory amino acid (EAA) receptor antagonists in blocking the synaptic transmission between gustatory fibers of the chorda tympani (CT) nerve and taste-responsive neurons within the nucleus of the solitary tract (NST) were examined electrophysiologically in urethan-anesthetized hamsters. Single neurons in the NST were recorded extracellularly and drugs were microinjected into the vicinity of the cell with the use of a multibarrel pipette assembly. The activity of each cell was recorded in response to lingual stimulation with 0.032 M NaCl, 0.032 M sucrose, 0.0032 M citric acid, 0.032 M quinine hydrochloride, and/or 25-μA anodal current pulses. Once a cell was identified as a taste-responsive neuron, one or more EAA receptor antagonists were administered by microinjection. Approximately 27 nl of 50 mM kynurenic acid (KYN), a broad-spectrum EAA receptor antagonist; 0.5 or 2.0 mM dl-2-amino-5-phosphonovalerate (APV), an N-methyl-d-aspartate (NMDA) receptor antagonist; 0.05 or 0.5 mM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptor antagonist; or phosphate-buffered physiological saline was applied to the neuron. Responses to chemical stimulation of the anterior tongue were obtained before and after drug administration and again after recovery; responses to anodal current stimulation (0.1 Hz) were obtained continually throughout the drug administration protocol. Microinjection of KYN completely and reversibly abolished responses elicited by both anodal current and chemical stimulation of the anterior tongue. The excitatory responses of cells in the NST to chemical and electrical stimulation of the anterior tongue were also completely and reversibly blocked by CNQX, implicating the involvement of an AMPA/kainate receptor. Microinjection of APV was generally less effective and partially reduced the responses of some taste-responsive NST cells to chemical stimulation of the anterior tongue. There were no effects following microinjection of a 27-nl bolus of phosphate-buffered saline. None of these EAA receptor antagonists had a differential effect on responses to different taste stimuli. The responses to all tastants were completely blocked by both KYN and CNQX; there was no apparent relationship between the response to any particular tastant and the limited effects of APV. These data implicate glutamate as an excitatory neurotransmitter between CT gustatory fibers and taste-responsive NST cells and suggest that it acts primarily on AMPA/kainate receptors, with some contribution from NMDA receptors. This conclusion is strengthened by other data obtained from in vitro slice preparations, which show that responses of cells in the rostral NST to solitary tract stimulation are blocked by both NMDA and AMPA/kainate receptor antagonists.
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Nyakudya, Trevor T., Thulani Tshabalala, Rachael Dangarembizi, Kennedy H. Erlwanger, and Ashwell R. Ndhlala. "The Potential Therapeutic Value of Medicinal Plants in the Management of Metabolic Disorders." Molecules 25, no. 11 (June 9, 2020): 2669. http://dx.doi.org/10.3390/molecules25112669.
Full textAbstract:
Metabolic syndrome (MetS) is a prevalent, multifactorial and complex disease that is associated with an increased risk of developing diabetes and other major cardiovascular complications. The rise in the global prevalence of MetS has been attributed to genetic, epigenetic, and environmental factors. The adoption of sedentary lifestyles that are characterized by low physical activity and the consumption of high-energy diets contributes to MetS development. Current management criteria for MetS risk factors involve changes in lifestyle and the use of pharmacological agents that target specific biochemical pathways involved in the metabolism of nutrients. Pharmaceutical drugs are usually expensive and are associated with several undesirable side effects. Alternative management strategies of MetS risk factors involve the use of medicinal plants that are considered to have multiple therapeutic targets and are easily accessible. Medicinal plants contain several different biologically active compounds that provide health benefits. The impact of phytochemicals present in local medicinal plants on sustainable health and well-being of individuals has been studied for many years and found to involve a plethora of complex biochemical, metabolic, and physiological mechanisms. While some of these phytochemicals are the basis of mainstream prescribed drugs (e.g., metformin, reserpine, quinine, and salicin), there is a need to identify more medicinal plants that can be used for the management of components of MetS and to describe their possible mechanisms of action. In this review, we assess the potential health benefits of South African ethnomedicinal plants in protecting against the development of health outcomes associated with MetS. We aim to provide the state of the current knowledge on the use of medicinal plants and their therapeutically important phytochemicals by discussing the current trends, with critical examples from recent primary references of how medicinal plants are being used in South African rural and urban communities.