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1
Frame, Mary D. S. "Conducted signals within arteriolar networks initiated by bioactive amino acids." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 3 (1999): H1012—H1021. http://dx.doi.org/10.1152/ajpheart.1999.276.3.h1012.
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Our purpose was to determine the specificity of l-arginine (l-Arg)-induced conducted signals for intra- vs. extracellular actions ofl-Arg. Diameter and red blood cell velocities were measured for arterioles [18 ± 1.6 (SE) μm] in the cremaster muscle of pentobarbital sodium-anesthetized (Nembutal, 70 mg/kg) hamsters ( n = 53). Remote (conducted) responses were viewed ∼1,000 μm upstream from the local (micropipette) application. Six amino acids were tested:l-arginine,l-cystine,l-leucine,l-lysine,l-histidine, andl-aspartate (100 μM each). Only l-Arg induced a remote dilation; l-lysine andl-aspartate had no effect, and the others each induced a significant remote constriction. There is a second conducted signal initiated byl-arginine that preconditions the arteriolar network and upregulates a direct response ofl-arginine to dilate the remote site. This was blocked by inhibition ofl-arginine uptake at the local (preconditioning) site (100 μMl-histidine or 1 mM phenformin). Arginine-glycine-aspartate (100 μM)-induced remote dilations (+3.2 ± 0.3 μm) were not mimicked by a peptide control and were prevented by anti- integrin αv monoclonal antibody. Remote dilations were greater in animals with a higher wall shear stress for arginine-glycine-aspartate ( r 2 = 0.92) but not for l-arginine ( r 2 = 0.12). Thusl-arginine initiates separate conducted signals related to system y+ transport, integrins, and baseline flow.
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Kuvaeva, Z. I., D. V. Lopatik, M. M. Markovich, L. G. Vinokurova, and O. P. Popova. "Synthesis of L-ornithine L-aspartate from L-arginine." Pharmaceutical Chemistry Journal 46, no. 8 (2012): 495–97. http://dx.doi.org/10.1007/s11094-012-0833-x.
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Yamamoto, Tatsuo, and Naohito Shimoyama. "Role of Nitric Oxide in the Development of Thermal Hyperesthesia Induced by Sciatic Nerve Constriction Injury in the Rat." Anesthesiology 82, no. 5 (1995): 1266–73. http://dx.doi.org/10.1097/00000542-199505000-00022.
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Background Nitric oxide (NO) has been shown to be involved in mediating nociceptive information transmission in the spinal cord. It is known that the N-methyl-D-aspartate receptor plays an important role in the development of the spinal facilitation evoked by a protracted small afferent input and that this effect is mediated at least in part by NO. Recently, it has been found that N-methyl-D-aspartate receptor-mediated spinal facilitation is crucial in the development of thermal hyperesthesia evoked by a nerve constriction injury. In the current study, we investigated the role of NO in the development of thermal hyperesthesia after a nerve constriction injury. Methods The Bennett and Xie model (four loose chromic gut ligations around the rat sciatic nerve) was used to examine the development of thermal hyperesthesia. An NO synthase inhibitor (N omega-nitro-L-arginine or N omega-nitro-L-arginine methyl ester hydrochloride), rat hemoglobin, or L-arginine was administered intrathecally 10 min before the nerve injury (pretreatment study) or 15 min after the nerve injury (posttreatment study). Results Pretreatment but not posttreatment administration of NO synthase inhibitor significantly delayed the development of thermal hyperesthesia. The effect of NO synthase inhibitor was reversed by the coadministration of L-arginine but not by the coadministration of D-arginine. Pretreatment with rat hemoglobin also delayed the development of thermal hyperesthesia. L-Arginine itself had no effect on the development of thermal hyperesthesia. Conclusions NO may play an important role in the development of N-methyl-D-aspartate receptor-mediated spinal facilitation after a nerve constriction injury.
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Joung, Seung-Sam, and Sung-Keun Choi. "The effects of administration of L-arginine and L-aspartate on energy substrate utilization and endurance performance during exercise." Korean Journal of Sports Science 27, no. 5 (2018): 1591–604. http://dx.doi.org/10.35159/kjss.2018.10.27.5.1591.
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Bentsa, T. M., and O. A. Pastukhova. "Clinical efficacy of L-arginin aspartate in complex treatment of patients with essential arterial hypertension with concomitant type 2 diabetes mellitus." Infusion & Chemotherapy, no. 3.1 (October 11, 2020): 10–11. http://dx.doi.org/10.32902/2663-0338-2020-3.1-06.
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Objective. Investigate directly the clinical efficacy of L-arginine aspartate in the treatment of patients with essential arterial hypertension (EAG) and type 2 diabetes mellitus (DM).
 Materials and methods. The study included 43 patients with EAG II in combination with type 2 DM. The mean age of patients was 55,7±0,6 years, of which 20 (46,5 %) were men and 23 (53,5 %) were women. The duration of the disease on the EAG averaged 8,4±0,4 years, on type 2 DM – 6,5±0,5 years. A comprehensive clinical, laboratory and instrumental examination was carried out. All patients were divided into two groups. Patients in both groups received ramipril 5-10 mg a day in combination with amlodipine 5-10 mg a day and antidiabetic drugs (metformin, gliclazide or a combination thereof) as basic therapy. Patients in group 2 (n=22) were additionally prescribed the drug L-arginine aspartate orally 3 g 3 times a day for 4 weeks. The course of treatment was repeated after 2 months.
 Results and discussion. In group 2 there was a more pronounced tendency to decrease the average daily and night blood pressure levels, in particular diastolic (3,2 and 2,9 mm Hg; p>0,05) and heart rate (by 17,3 %; p<0,05). The use of L-arginine aspartate significantly improved systolic (ejection fraction increased by 7,1 % vs 4,4 % in group 1; p<0,05) and left ventricular (LV) diastolic function (Em/Am increased by 48,8 % vs 34,7 % in group 1; p<0,05), a decrease in the size of the left atrium (10,2 % vs 8,3 % in group 1; p<0,05) and the reversal of LV hypertrophy (index LV myocardial mass decreased by 20,1 % against 15,9 % in group 1; p<0,05). Additional administration of L-arginine aspartate also led to a decrease in fasting and postprandial plasma glucose (4,9 % and 7,0 %; p<0,05, respectively) than the use of basic therapy alone. At the same time in group 2 there was a decrease in microalbuminuria by 27,6 % (p<0,05) and an increase in glomerular filtration rate by 11,4 % (p>0,05).
 Conclusions. L-arginine aspartate should be used in patients with EAG in combination with type 2 DM and microalbuminuria to increase the cardio- and nephroprotective efficacy of basic therapy.
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Cole, S. C., P. A. Yaghmaie, P. J. Butterworth, and R. J. Yon. "Inactivation of wheat-germ aspartate transcarbamoylase by the arginine-specific reagent phenylglyoxal." Biochemical Journal 233, no. 1 (1986): 303–6. http://dx.doi.org/10.1042/bj2330303.
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Wheat-germ aspartate transcarbamoylase (EC 2.1.3.2) was inactivated by phenylglyoxal in a first-order process, provided that the inactivation time did not exceed 10 min. Apparent first-order rate constants were linearly dependent on phenylglyoxal concentration, indicating a bimolecular reaction between a single active-centre residue and phenylglyoxal, with second-order constant of 0.023 mM-1 X min-1. A plot of apparent first-order rate constant versus pH showed a steep rise above pH 9.5, indicating that the essential residue has a pKa value of 10.5 or higher, consistent with an arginine residue. Saturating concentrations of the following ligands provided a degree of protection (percentages in parentheses) against 1 mM-phenylglyoxal: N-phosphonoacetyl-L-aspartate, a bisubstrate analogue (94%); carbamoyl phosphate (75%); UMP, an end-product inhibitor (53%). Succinate (an analogue of L-aspartate) alone gave no protection, but in combination with carbamoyl phosphate raised the protection to 92%, in agreement with the known binding order of the two substrates. These results indicate that the essential arginine residue is close to the carbamoyl phosphate site, probably oriented towards the aspartate site. Attempts to desensitize the UMP-binding site by reaction with phenylglyoxal, while protecting the active centre, were unsuccessful. The essential active-centre arginine residue is compared with a similar residue in the Escherichia coli enzyme.
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Kohan, D. E., and G. F. Schreiner. "Interleukin 1 modulation of renal epithelial glucose and amino acid transport." American Journal of Physiology-Renal Physiology 254, no. 6 (1988): F879—F886. http://dx.doi.org/10.1152/ajprenal.1988.254.6.f879.
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We have investigated the effect of immune factors on glucose and amino acid transport by proximal tubular epithelium. Proximal tubular cells were obtained by enzymatic digestion of mouse renal cortex and grown to confluent monolayers. alpha-[14C]methylglucoside (AMG), D-[3H]-aspartate, L-[3H]leucine, and L-[3H]arginine uptake were assayed. Proximal tubular epithelium coincubated with supernatants derived from lipopolysaccharide (LPS)-stimulated mouse peritoneal macrophages had a twofold increase in AMG and aspartate uptake that was sodium dependent, was prevented by cycloheximide or actinomycin D, and was not associated with changes in cell growth or differentiation. Chromatographic separation of the macrophage supernatant yielded one fraction, mol wt 16,000-20,000, that enhanced AMG and aspartate uptake and contained interleukin 1 (IL 1) determined by bioassay. Recombinant IL 1 (mol wt 17,500) reproduced changes in AMG and aspartate uptake seen with macrophage supernatants. In contrast, neither macrophage supernatants nor IL 1 affected sodium-independent leucine or arginine transport. IL 1 directly increased 22Na transport into proximal tubular cells. These data indicate that macrophages, via IL 1 secretion, are capable of modulation of sodium-linked solute transport in proximal tubular epithelium.
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Burnat, Mireia, Antonia Herrero, and Enrique Flores. "Compartmentalized cyanophycin metabolism in the diazotrophic filaments of a heterocyst-forming cyanobacterium." Proceedings of the National Academy of Sciences 111, no. 10 (2014): 3823–28. http://dx.doi.org/10.1073/pnas.1318564111.
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Heterocyst-forming cyanobacteria are multicellular organisms in which growth requires the activity of two metabolically interdependent cell types, the vegetative cells that perform oxygenic photosynthesis and the dinitrogen-fixing heterocysts. Vegetative cells provide the heterocysts with reduced carbon, and heterocysts provide the vegetative cells with fixed nitrogen. Heterocysts conspicuously accumulate polar granules made of cyanophycin [multi-L-arginyl-poly (L-aspartic acid)], which is synthesized by cyanophycin synthetase and degraded by the concerted action of cyanophycinase (that releases β-aspartyl-arginine) and isoaspartyl dipeptidase (that produces aspartate and arginine). Cyanophycin synthetase and cyanophycinase are present at high levels in the heterocysts. Here we created a deletion mutant of geneall3922encoding isoaspartyl dipeptidase in the model heterocyst-forming cyanobacteriumAnabaenasp. strain PCC 7120. The mutant accumulated cyanophycin and β-aspartyl-arginine, and was impaired specifically in diazotrophic growth. Analysis of anAnabaenastrain bearing an All3922-GFP (green fluorescent protein) fusion and determination of the enzyme activity in specific cell types showed that isoaspartyl dipeptidase is present at significantly lower levels in heterocysts than in vegetative cells. Consistently, isolated heterocysts released substantial amounts of β-aspartyl-arginine. These observations imply that β-aspartyl-arginine produced from cyanophycin in the heterocysts is transferred intercellularly to be hydrolyzed, producing aspartate and arginine in the vegetative cells. Our results showing compartmentalized metabolism of cyanophycin identify the nitrogen-rich molecule β-aspartyl-arginine as a nitrogen vehicle in the unique multicellular system represented by the heterocyst-forming cyanobacteria.
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Lyalyukova, E. A., M. A. Livzan, A. V. Lyalyukov, and A. N. Sudakova. "L-ornithine-L-aspartate in patients with non-alcoholic fatty liver disease." RMJ, no. 10 (2024): 27–31. https://doi.org/10.32364/2225-2282-2024-10-5.
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Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic hepatic disorder marked by excessive lipid accumulation in hepatocytes. Current evidence underscores the multifactorial etiology of NAFLD, involving insulin resistance, lipotoxicity, neurohumoral alterations accompanied by elevated proinflammatory cytokine and adipokine release, activation of innate immunity, dysbiosis of the gut microbiota, increased intestinal permeability, and genetic susceptibility. Recent studies have identified hyperammonemia as a pivotal factor in NAFLD pathogenesis. Ammonia accumulation in the liver maintains inflammatory processes, stellate cell activation, and initiates fibrogenesis, heightening the risk of progression to cirrhosis and hepatocellular carcinoma. Furthermore, systemic hyperammonemia detrimentally impacts other organ systems, notably contributing to cognitive deficits and sarcopenia. Hence, it is pathophysiologically rational to administer L-ornithine-L-aspartate to individuals with NAFLD. This compound not only possesses hypoammonemic effects but also exhibits hepatoprotective, hypoazotemic, and detoxifying actions. The beneficial effects of L-ornithine-L-aspartate are also attributed to the metabolic conversion of L-ornithine and L-aspartate into L-glutamine, L-arginine, and glutathione, which are potent antioxidants safeguarding hepatocytes against lipid peroxidation and enhancing hepatic microcirculation. Collectively, these mechanisms contribute to the efficacy of L-ornithine-L-aspartate in mitigating the extent of steatosis, inflammation, and even hepatic fibrosis in NAFLD patients. Keywords: non-alcoholic fatty liver disease, L-ornithine-L-aspartate, hyperammonemia, metabolic syndrome, oxidative stress. For citation: Lyalyukova E.A., Livzan M.A., Lyalyukov A.V., Sudakova A.N. L-ornithine-L-aspartate in patients with non-alcoholic fatty liver disease. RMJ. 2024;10:27–31. DOI: 10.32364/2225-2282-2024-10-5
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Lefin, Nicolás, Javiera Miranda, Iris Munhoz Costa, et al. "Optimized Amino Acid-Enhanced Medium for Efficient L-Asparaginase II Production in E. coli: From Shake Flask to Bioreactor." Fermentation 11, no. 5 (2025): 239. https://doi.org/10.3390/fermentation11050239.
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L-asparaginase (L-ASNase) is a key enzyme in the treatment of leukemia and lymphoma, with high demand in cancer therapies. Advances in recombinant protein production have improved yields and reduced costs, enabling large-scale production. However, optimizing culture conditions remains crucial for maximizing production. This study focused on optimizing the production of double mutant L-ASNase expressed in Escherichia coli BL21 (DE3) by supplementing media with amino acids. Five amino acids were evaluated at a shake flask scale using the design of experiments, with arginine and aspartate showing the most positive effects. Under optimized conditions (14.5 mM arginine, 12.7 mM aspartate, and 0 mM cysteine), the activity model reached 12,513 U L−1, experimentally validated at 10,089 U L−1. The maximum specific cell growth rate was µx,max = 0.74 h−1, with substrate–biomass conversion factor Yx/s = 1.16 g/g and cell–product conversion factor Yp/x = 13,891 U/gcell. Amino acid supplementation resulted in a ten-fold increase in L-ASNase activity. Finally, at the bioreactor scale, adding amino acids and the inducer at the end of the exponential phase increased activity by 135% compared to conventional MD, demonstrating its potential for industrial-scale production.
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Kurhaluk, Natalia. "Nitric Oxide-Dependent Regulation of Oxygen-Related Processes in a Rat Model of Lead Neurotoxicity: Influence of the Hypoxia Resistance Factor." Cellular Physiology and Biochemistry 58, no. 5 (2024): 597–629. http://dx.doi.org/10.33594/000000734.
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Background/Aims: Lead exposure is known to induce oxidative stress and neurotoxicity. Nitric oxide (NO) plays an important role in modulating oxidative stress, with L-arginine as a precursor of NO and Nω-nitro-L-arginine (L-NNA) as an inhibitor of NO synthase, an enzyme that catalyses the production of nitric oxide (NO) from L-arginine. Methods: This study investigated the differential effects of L-arginine and L-NNA on markers of oxidative stress and biochemical changes in brain tissue from rats with different levels of resistance to hypoxia exposed to lead nitrate. Rats with either low or high resistance to hypoxia were exposed to lead nitrate (oral 3.6 mg lead nitrate/kg b.w. per day for 30 days) and treated with L-arginine (600 mg/kg b.w., i.p., 30 min before and after exposure to lead nitrate) or L-NNA (35 mg/kg b.w., i.p., 30 min before and after exposure to lead nitrate). Brain tissue samples were analysed for lipid peroxidation, oxidative modification of proteins, and activity of antioxidant enzymes, including superoxide dismutase, catalase, glutathione reductase, and peroxidase, and total antioxidant status (TAS). We also examined the biomarkers of biochemical pathways involving the activity of alanine and aspartate aminotransferases, succinate dehydrogenase (SDH), and α-ketoglutarate dehydrogenase (KGDH). In addition, the trend observed was supported by assessments of the acetylcholine levels and acetylcholinesterase activity (ACh-AChE system) in brain tissue. Results: In rats with low resistance to hypoxia, the L-arginine treatment significantly reduced lipid peroxidation and oxidative protein modification but increased antioxidant enzyme activity, suggesting a protective effect against lead-induced oxidative stress. Conversely, in rats with high resistance to hypoxia, L-NNA had a protective effect, reducing lead-induced oxidative damage and decreasing lipid peroxidation, whereas L-arginine exacerbated oxidative stress and impaired antioxidant defences. These findings were supported by corresponding changes in the acetylcholine-acetylcholinesterase system, reflecting the observed patterns of lead-induced oxidative stress and neurotoxicity. The study shows that L-arginine exerts a protective effect by reducing lead-induced oxidative damage via an improvement in TAS. Our study shows that lead nitrate exposure significantly increases ala-nine and aspartate aminotransferase activity in brain tissue, with L-arginine exacerbating and L-NNA reversing this effect. The lead nitrate exposure also affected the activities of SDH and KGDH, which are important for cellular energy production and hypoxia resistance, with L-arginine altering SDH activity depending on the level of resistance and L-NNA enhancing both SDH and KGDH activities. These trends were further validated by alterations in the ACh-AChE system, highlighting the differential role of NO-dependent mechanisms in modulating lead-induced neurotoxicity based on hypoxia resistance. Conclusion: These findings suggest potential targeted therapeutic strategies based on the oxidative stress profile and highlight the potential of nitric oxide system modulators in counteracting lead-induced biochemical alterations and the dynamics of the ACh-AChE system depending on the individual physiological reactivity of organisms.
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Huang, Yajuan, Xige He, Yunfei Han, et al. "Age-Related Meat Flavor Precursors of Naturally Grazed Sunit Sheep: Metabolomics and Transcriptomics Approaches." Foods 14, no. 9 (2025): 1616. https://doi.org/10.3390/foods14091616.
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This study elucidated the regulatory mechanisms of age-related meat flavor precursors in naturally grazed Sunit sheep of different ages (6, 18, and 30 months) by analyzing their metabolite and mRNA profiles. The longissimus dorsi muscle was sampled from each group and subjected to metabolomics and transcriptomics analyses. A total of 395 differential metabolites (DMs) and 1482 differentially expressed genes (DEGs) were detected across the age groups. As the age increased, the expression levels of GOT1 and GLUL increased, activating arginine biosynthesis and alanine, aspartate, and glutamate metabolism pathways, which promoted the accumulation of umami compounds (L-glutamate and L-glutamine). Meanwhile, the expression level of LPIN1 increased with age, promoting glycerophospholipid metabolism and contributing to the development of lipid-related aroma. FADS1 and FADS2 expressed the highest levels at age Mth_18. This pattern influenced the unsaturated fatty acid biosynthesis pathway and consequently had a regulatory effect on the DHA levels. An amino acid metabolic regulatory network that involved arginine biosynthesis, alanine, aspartate and glutamate metabolisms, and arginine and proline metabolisms was established. This study provided insights into the variations in meat flavor precursors among sheep of different ages and elucidated the underlying regulatory mechanisms.
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Acquaviva, Rosaria, Raffaele Lanteri, Giovanni Li Destri, et al. "Beneficial effects of rutin and l-arginine coadministration in a rat model of liver ischemia-reperfusion injury." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 3 (2009): G664—G670. http://dx.doi.org/10.1152/ajpgi.90609.2008.
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Reperfusion following liver ischemia results in oxidative stress leading to liver injury. The aim of this study was to investigate the combined effects of two antioxidant agents, rutin and l-arginine, in rat liver ischemia-reperfusion (I/R). Male Wistar rats were divided into five groups: 1) sham operated, 2) I/R, 3) I/R + rutin, 4) I/R + l-arginine, and 5) I/R + rutin + l-arginine. Plasmatic and hepatic levels of alanine transaminase (ALT), aspartate transaminase (AST), lipid peroxides (LOOH), and thiol groups (RSH) were examined, as well as DNA fragmentation and liver histopathology. Furthermore, to elucidate the pathophysiological processes involved in the antioxidant mechanism(s) of rutin and l-arginine, we assessed the expression of inducible (iNOS) and endothelial nitric oxide synthase (eNOS) isoforms and heme oxygenase-1 (HO-1), both playing key roles in the biochemical cascade of liver injury. Significant increase in plasmatic ALT and AST activities were observed in untreated I/R rats compared with sham-operated animals, whereas treatment with rutin or l-arginine in I/R rats reduced hepatic damage. Interestingly, combined therapy with rutin and l-arginine resulted in a further reduction of plasmatic ALT and AST activities compared with rutin or l-arginine alone. These results were further confirmed by the analysis of DNA fragmentation, LOOH, RSH groups, and liver histopathology, which showed the highest protective effects following the coadministration of rutin and l-arginine. Finally, the combined therapy protocol resulted in a significant induction of liver HO-1 and a concomitant reduction of iNOS expression that may both be responsible for the beneficial effects of the proposed pharmacological protocol.
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Hou, Entai, Na Sun, Fuchang Zhang, et al. "Malate and Aspartate Increase L-Arginine and Nitric Oxide and Attenuate Hypertension." Cell Reports 19, no. 8 (2017): 1631–39. http://dx.doi.org/10.1016/j.celrep.2017.04.071.
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Sweiry, J. H., M. Munoz, and G. E. Mann. "Cis-inhibition and trans-stimulation of cationic amino acid transport in the perfused rat pancreas." American Journal of Physiology-Cell Physiology 261, no. 3 (1991): C506—C514. http://dx.doi.org/10.1152/ajpcell.1991.261.3.c506.
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Transport of cationic amino acids in the isolated perfused rat pancreas was studied using dual-isotope dilution techniques. At 50 microM substrate concentration, unidirectional tracer uptakes for L-arginine (56 +/- 1%), L-lysine (49 +/- 2%), and L-ornithine (44 +/- 3%) were followed by rapid tracer efflux. In the presence of Na+, influx of L-arginine [Michaelis constant (Km) = 1.74 +/- 0.15 mM, maximum velocity (Vmax) = 1.97 +/- 0.07 mumol.min-1.g-1] and L-lysine (Km = 2.48 +/- 0.17 mM, Vmax = 2.42 +/- 0.08 mumol.min-1.g-1) was mediated by a common transport system, sensitive to cis-inhibition by L-ornithine, 2,4-L-diaminobutyric acid, D-lysine, and D-arginine. Substrates for system A [alpha-(methylamino)isobutyric acid] and an anionic carrier (L-aspartate) were poor cis-inhibitors of L-arginine entry. Removal of Na+ resulted in a 40% reduction in cationic amino acid influx. After cell loading (20 min), L-[3H]-lysine cleared predominantly from a slowly exchanging pool with a rate constant of 5.97 +/- 0.67 min. An influx/efflux permeability ratio of 14.5 +/- 1.6 was determined, and efflux of L-lysine was trans-stimulated by vascular challenges with cationic or large neutral amino acids. The specificity, relative Na+ independence, and exchange properties of this saturable cationic amino acid transporter in the pancreatic epithelium resemble those reported for system y+ in cultured fibroblasts and hepatocytes.
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Mamani-Huanca, Maricruz, Sandra Marcia Muxel, Stephanie Maia Acuña, Lucile Maria Floeter-Winter, Coral Barbas, and Ángeles López-Gonzálvez. "Metabolomic Reprogramming of C57BL/6-Macrophages during Early Infection with L. amazonensis." International Journal of Molecular Sciences 22, no. 13 (2021): 6883. http://dx.doi.org/10.3390/ijms22136883.
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Leishmania survival inside macrophages depends on factors that lead to the immune response evasion during the infection. In this context, the metabolic scenario of the host cell–parasite relationship can be crucial to understanding how this parasite can survive inside host cells due to the host’s metabolic pathways reprogramming. In this work, we aimed to analyze metabolic networks of bone marrow-derived macrophages from C57BL/6 mice infected with Leishmania amazonensis wild type (La-WT) or arginase knocked out (La-arg−), using the untargeted Capillary Electrophoresis-Mass Spectrometry (CE-MS) approach to assess metabolomic profile. Macrophages showed specific changes in metabolite abundance upon Leishmania infection, as well as in the absence of parasite-arginase. The absence of L. amazonensis-arginase promoted the regulation of both host and parasite urea cycle, glycine and serine metabolism, ammonia recycling, metabolism of arginine, proline, aspartate, glutamate, spermidine, spermine, methylhistidine, and glutathione metabolism. The increased L-arginine, L-citrulline, L-glutamine, oxidized glutathione, S-adenosylmethionine, N-acetylspermidine, trypanothione disulfide, and trypanothione levels were observed in La-WT-infected C57BL/6-macrophage compared to uninfected. The absence of parasite arginase increased L-arginine, argininic acid, and citrulline levels and reduced ornithine, putrescine, S-adenosylmethionine, glutamic acid, proline, N-glutamyl-alanine, glutamyl-arginine, trypanothione disulfide, and trypanothione when compared to La-WT infected macrophage. Moreover, the absence of parasite arginase leads to an increase in NO production levels and a higher infectivity rate at 4 h of infection. The data presented here show a host-dependent regulation of metabolomic profiles of C57BL/6 macrophages compared to the previously observed BALB/c macrophages infected with L. amazonensis, an important fact due to the dual and contrasting macrophage phenotypes of those mice. In addition, the Leishmania-arginase showed interference with the urea cycle, glycine, and glutathione metabolism during host–pathogen interactions.
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Bekpinar, Seldag, Seval Develi-Is, Yesim Unlucerci, Zeynep Kusku-Kiraz, Mujdat Uysal, and Figen Gurdol. "Modulation of arginine and asymmetric dimethylarginine concentrations in liver and plasma by exogenous hydrogen sulfide in LPS-induced endotoxemia." Canadian Journal of Physiology and Pharmacology 91, no. 12 (2013): 1071–75. http://dx.doi.org/10.1139/cjpp-2013-0114.
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Plasma levels of asymmetric dimethylarginine (ADMA) are known to be elevated under pathological conditions, but reports on intracellular ADMA levels are scarce. In this study, we investigated whether lipopolysaccharide (LPS)-induced endotoxemia alters the intra- and extra-cellular partition of l-arginine and ADMA. The effect of H2S pretreatment was also researched. Wistar rats were given sodium hydrogen sulfide (NaHS, 1 mg·(kg body mass)−1) one hour before the LPS injections (20 mg·kg−1). Six hours after the LPS treatment, the animals were sacrificed. Myeloperoxidase (MPO) and dimethylarginine dimethylaminohydrolase (DDAH) activities and levels of hypoxia-inducible factor (HIF)-1α were measured in the liver. ADMA and arginine levels were determined using HPLC. LPS injection caused liver injury, as evidenced by the activities of alanine transaminase, aspartate transaminase, and arginase. LPS increased l-arginine content and decreased DDAH activity in the rat liver. MPO activity and HIF-1α levels indicated inflammation and hypoxia. Despite the accumulation of ADMA in the plasma, the level remained unchanged in the liver. NaHS pretreatment restored both the DDAH activity and intracellular l-arginine levels. It is concluded that increased H2S generation has a potency to restore hepatic l-arginine levels and ADMA handling in endotoxemia. Extra- and intra-cellular partitions of ADMA seem to depend on transport proteins as well as the DDAH activity.
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Wang, Wenyan, Bradley W. Poland, Richard B. Honzatko, and Herbert J. Fromm. "Identification of Arginine Residues in the Putative L-Aspartate Binding Site ofEscherichiacoliAdenylosuccinate Synthetase." Journal of Biological Chemistry 270, no. 22 (1995): 13160–63. http://dx.doi.org/10.1074/jbc.270.22.13160.
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Pinilla, Leonor, Dolores González, Manuel Tena-Sempere, Rafaela Aguilar, and Enrique Aguilar. "Effects of N-methyl-d-aspartate and kainic acid on prolactin secretion in prepubertal female rats." European Journal of Endocrinology 135, no. 4 (1996): 464–68. http://dx.doi.org/10.1530/eje.0.1350464.
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Pinilla L, González D, Tena-Sempere M, Aguilar R, Aguilar E. Effects of N-methyl-d-aspartate and kainic acid on prolactin secretion in prepubertal female rats. Eur J Endocrinol 1996;135:464–8. ISSN 0804–4643 The control of prolactin (PRL) secretion by N-methyl-d-aspartate (NMDA) and kainic acid (KA), agonists of NMDA and kainate receptors, and the interactions between NMDA and KA with nitric oxide (NO) were analysed in prepubertal female rats. For this purpose, serum PRL concentrations and hypothalamic and pituitary dopamine (DA) and serotonin (5-HT) concentrations were measured in females injected with NMDA, KA or two blockers of NO synthase: Nw-nitro-l-arginine methyl ester (NAME) and Nw-nitro-l-arginine (NA). Also, the effects of combined administration of NMDA and KA with the blockers of NO synthase were analyzed. We found that PRL release was inhibited 15 min after NMDA and KA administration, an effect probably mediated through the release of hypothalamic DA, as shown by the higher pituitary DA concentrations after NMDA or KA administration. The inhibitory effect of NMDA was preceded by an increase in serum PRL levels, observed at 5 and 10 min after NMDA administration. Nw-Nitro-l-arginine methyl ester alone inhibited prolactin secretion, and both NAME and NA abolished the inhibitory effect of KA, but not that of NMDA. We conclude that administration of NMDA exerted a dual action on PRL secretion: initially DA release was inhibited, leading to an increase in PRL secretion that in turn stimulated DA release and decreased serum PRL concentrations. Kainic acid also inhibited PRL secretion by releasing DA, an effect blocked by NO synthase inhibitors. Enrique Aguilar, Department of Physiology, Faculty of Medicine, University of Córdoba, E-14004, Spain
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Levillain, O., A. Hus-Citharel, F. Morel, and L. Bankir. "Localization of arginine synthesis along rat nephron." American Journal of Physiology-Renal Physiology 259, no. 6 (1990): F916—F923. http://dx.doi.org/10.1152/ajprenal.1990.259.6.f916.
Full textAbstract:
Arginine production was measured in isolated rat nephron segments. Segments were incubated with 0.3 mM aspartate and 0.1 mM L-[ureido-14C]-citrulline in a sealed chamber. Arginase and urease were added to the medium to hydrolyze arginine and to release 14CO2, which was trapped in KOH and counted. Arginine synthesis was found only in the proximal tubule, with decreasing intensity from proximal convoluted (PCT) to proximal straight tubule (PST). Results were as follows (in fmol.min-1.mm tubule length-1): PCT, 122 +/- 15; cortical PST, 71 +/- 6; outer medullary PST, 41 +/- 4; all other segments, less than 6. Arginine synthesis changed almost proportionally with precursor concentration of less than or equal to 0.4 mM. We had shown previously that PST but not PCT was able to hydrolyze arginine into urea and ornithine. In this study arginine was further hydrolyzed in cortical (40%) and medullary (64%) PST but not in PCT. These observations suggest that the arginine formed in PCT contributes to the maintenance of the whole body arginine pool, whereas most of the arginine formed in PST might contribute, by its conversion to urea, to the process of urine concentration.
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Butterworth, Roger F., and Ali Canbay. "Hepatoprotection by L-Ornithine L-Aspartate in Non-Alcoholic Fatty Liver Disease." Russian Journal of Gastroenterology, Hepatology, Coloproctology 29, no. 1 (2019): 24–30. http://dx.doi.org/10.22416/1382-4376-2019-29-1-24-30.
Full textAbstract:
Background.Non-alcoholic fatty liver disease (NAFLD) is the leading chronic hepatic condition worldwide and new approaches to management and treatment are limited.Summary.L-ornithine L-aspartate (LOLA) has hepatoprotective properties in patients with fatty liver of diverse etiology and results of a multicenter randomized clinical trial reveal that 12 weeks treatment with oral LOLA (6–9 g/d) results in a dose-related reduction in activities of liver enzymes and triglycerides together with significant improvements of liver/spleen CT ratios. A preliminary report described improvements of hepatic microcirculation in patients with nonalcoholic steatohepatitis (NASH) following treatment with LOLA. Mechanisms responsible for the beneficial effects of LOLA in NAFLD/NASH involve, in addition to its established ammonia-lowering effect, metabolic transformations of the LOLA-constituent amino acids L-ornithine and L-aspartate into L-glutamine, L-arginine, and glutathione. These metabolites have well-established actions implicated in the prevention of lipid peroxidation, improvement of hepatic microcirculation in addition to anti-inflammatory, and anti-oxidant properties.Key messages.(1) LOLA is effective for the treatment of key indices in NAFLD/NASH. (2) Mechanisms other than LOLA’s ammonia-lowering action have been postulated. (3) Further assessments in the clinical setting are now required.
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Travagli, R. A., and R. A. Gillis. "Nitric oxide-mediated excitatory effect on neurons of dorsal motor nucleus of vagus." American Journal of Physiology-Gastrointestinal and Liver Physiology 266, no. 1 (1994): G154—G160. http://dx.doi.org/10.1152/ajpgi.1994.266.1.g154.
Full textAbstract:
The purpose of our study was to explore whether nitric oxide was involved as an intercellular messenger in the dorsal motor nucleus of the vagus (DMV). To achieve this purpose we examined DMV motoneurons of the rat in vitro with the use of the extracellular cell-attached recording technique. The motoneurons, in general, exhibit a spontaneous discharge and when exposed to NO-producing drugs (i.e., 3-300 microM L-arginine and 10-100 microM S-nitroso-N-acetylpenicillamine) exhibit a concentration-related increase in their spontaneous firing rate. Because NO activates soluble guanylate cyclase and increases guanosine 3',5'-cyclic monophosphate (cGMP), we tested dibutyryl-cGMP (30-300 microM) and found that it also excites DMV neurons. Perfusion of the DMV neurons with N omega-nitro-L-arginine (300 microM), an inhibitor of NO synthase (NOS), and with NO scavenger, reduced hemoglobin (1 microM), counteracted the excitatory effect of L-arginine and N-methyl-D-aspartate (NMDA). Perfusion of the preparation with LY-83583 (10 microM), an inhibitor of guanylate cyclase, also counteracted the effects of L-arginine and NMDA. These data indicate that NOS is present in DMV neurons, and that the excitatory effect of NMDA on these neurons is due in part to formation of NO and the resulting accumulation of cGMP in DMV neurons.
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Butterworth, Roger F., and Ali Canbay. "Hepatoprotection by L-Ornithine L-Aspartate in Non-Alcoholic Fatty Liver Disease." Digestive Diseases 37, no. 1 (2018): 63–68. http://dx.doi.org/10.1159/000491429.
Full textAbstract:
Background: Non-alcoholic fatty liver disease (NAFLD) is the leading chronic hepatic condition worldwide and new approaches to management and treatment are limited. Summary: L-ornithine L-aspartate (LOLA) has hepatoprotective properties in patients with fatty liver of diverse etiology and results of a multicenter randomized clinical trial reveal that 12 weeks treatment with oral LOLA (6–9 g/d) results in a dose-related reduction in activities of liver enzymes and triglycerides together with significant improvements of liver/spleen CT ratios. A preliminary report described improvements of hepatic microcirculation in patients with non-alcoholic steatohepatitis (NASH) following treatment with LOLA. Mechanisms responsible for the beneficial effects of LOLA in NAFLD/NASH involve, in addition to its established ammonia-lowering effect, metabolic transformations of the LOLA-constituent amino acids L-ornithine and L-aspartate into L-glutamine, L-arginine, and glutathione. These metabolites have well-established actions implicated in the prevention of lipid peroxidation, improvement of hepatic microcirculation in addition to anti-inflammatory, and anti-oxidant properties. Key Messages: (1) LOLA is effective for the treatment of key indices in NAFLD/NASH. (2) Mechanisms other than LOLA’s ammonia-lowering action have been postulated. (3) Further assessments in the clinical setting are now required.
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Alexander, Guillermo M., Erin Reichenberger, B. Lee Peterlin, Marielle J. Perreault, John R. Grothusen, and Robert J. Schwartzman. "Plasma Amino Acids Changes in Complex Regional Pain Syndrome." Pain Research and Treatment 2013 (November 4, 2013): 1–10. http://dx.doi.org/10.1155/2013/742407.
Full textAbstract:
Complex regional pain syndrome (CRPS) is a severe chronic pain condition that most often develops following trauma. Blood samples were collected from 220 individuals, 160 CRPS subjects, and 60 healthy pain-free controls. Plasma amino acid levels were compared and contrasted between groups. L-Aspartate, L-glutamate, and L-ornithine were significantly increased, whereas L-tryptophan and L-arginine were significantly decreased in CRPS subjects as compared to controls. In addition, the L-kynurenine to L-tryptophan ratio demonstrated a significant increase, whereas the global arginine bioavailability ratio (GABR) was significantly decreased in the CRPS subjects. The CRPS subjects demonstrated a significant correlation between overall pain and the plasma levels of L-glutamate and the L-kynurenine to L-tryptophan ratio. CRPS subjects also showed a correlation between the decrease in plasma L-tryptophan and disease duration. This study shows that CRPS subjects exhibit significant changes in plasma levels of amino acids involved in glutamate receptor activation and in amino acids associated with immune function as compared to healthy pain-free controls. A better understanding of the role plasma amino acids play in the pathophysiology of CRPS may lead to novel treatments for this crippling condition.
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Kato, K., and C. F. Zorumski. "Nitric oxide inhibitors facilitate the induction of hippocampal long-term potentiation by modulating NMDA responses." Journal of Neurophysiology 70, no. 3 (1993): 1260–63. http://dx.doi.org/10.1152/jn.1993.70.3.1260.
Full textAbstract:
1. The effects of the competitive nitric oxide (NO) synthase inhibitor, L-nitroarginine (L-NOArg), on synaptically activated N-methyl-D-aspartate (NMDA) currents and the induction of long-term potentiation (LTP) were studied in the CA1 region of rat hippocampal slices. 2. Application of 10 microM L-NOArg increased the amplitude of NMDA currents by approximately 50% in the presence of 2 mM extracellular Mg2+. This augmentation occurred within minutes of L-NOArg administration and was readily reversible on removal of the drug. L-arginine (100 microM) overcame the enhancement produced by L-NOArg. 3. At 5-100 microM, 10-25-min applications of L-NOArg facilitated the induction of LTP produced by a single 100 Hz X 300 ms tetanus. In control slices, the 100 Hz X 300 ms tetanus was insufficient to induce LTP. The development of LTP in L-NOArg-treated slices was inhibited by 50 microM D-2-amino-5-phosphonovalerate (D-APV), and the effects of L-NOArg were overcome by 10-fold higher concentrations of L-arginine but not by D-arginine. 4. Hemoglobin, an agent that binds NO extracellularly, also facilitated NMDA currents and the development of LTP when administered at 10 microM. 5. These results suggest that tonically released NO modulates the threshold for LTP in the CA1 hippocampal region and are consistent with prior studies indicating that untimely activation of NMDA receptors and release of NO inhibit LTP.
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Posokhova, S. P., S. V. Nikolaeva, and K. O. Nitoсhko. "Preeclampy prevention issues in women with obesity." HEALTH OF WOMAN, no. 4(150) (May 30, 2020): 61–66. http://dx.doi.org/10.15574/hw.2020.150.61.
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The objective: evaluation of the effectiveness of the prevention of preeclampsia in pregnant women with obesity using L-arginine during pregnancy Materials and methods. Materials and methods. The main group consisted of 38 obese women (1st century – 15th, 2nd century – 12th, 3rd century – 11), who were prescribed complex prevention of preeclampsia: from 12 weeks of pregnancy 150 mg of aspirin once a day, and from 16 weeks the solution L-arginine (Тivortin aspartate) 5 ml (1 g) 4 times a day for 2 months. The comparison group included 30 pregnant women with obesity of the II-III stage who did not receive preventive treatment. The control group consisted of 30 healthy pregnant women. By the beginning of prophylactic treatment and in the dynamics of all obese pregnant women, the level of pregnancy-associated plasma protein A (PAPP-A), placental growth factor (PlGF), arginine and leptin was determined in blood serum. Results. In pregnant women with obesity, already in the first trimester a significantly higher level of leptin is observed compared to the main group and the level of placental growth factor is significantly lower, which are significant triggers for the development of preeclampsia and other gestational complications. After the prophylactic treatment of pregnant women of the main group with L-arginine for 2 months (at 16–24 weeks), the following trends were observed: the level of L-arginine did not change, was constant. Leptin levels differed depending on the degree of obesity, but did not have a high critical value. A positive trend was the growth of placental growth factor in women of the main group, which indicated normal placentation and the prevention of early preeclampsia. Conclusions. Thus, in pregnant women of the main group, after comprehensive prevention of the development of preeclampsia with aspirin and L-arginine (Тivortin) for 2 months, the incidence of severe severe preeclampsia decreased by 4.4 times, which is a favorable factor in maintaining a woman’s health and reducing perinatal losses. Additional L-arginine in the diet reduced the frequency of preeclampsia in pregnant women with obesity, contributing to vasodilation due to increased production of nitric oxide, may be one of the positive factors of pathogenetic treatment. Keywords: pregnancy, obesity, preeclampsia, leptin, nitric oxide, L-arginine.
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Gavrylenko, V. E. "Evaluation of complex treatment of patients with postoperative hypothyroidism and non-alcoholic fatty liver disease." Infusion & Chemotherapy, no. 3.1 (October 11, 2020): 20. http://dx.doi.org/10.32902/2663-0338-2020-3.1-16.
Full textAbstract:
Objective. To evaluate the effectiveness of comprehensive treatment of patients with postoperative hypothyroidism (PH) and non-alcoholic fatty liver disease (NAFLD).
 Materials and methods. 40 patients (20 men and 20 women) aged 42±6 years with PH and NAFLD were examined. Patients were divided into two groups: main (n=20) and control (n=20). Prior to the study and after 1 month, the level of total cholesterol (TH), triglycerides (TG), low-density lipoprotein (LDL), alanine aminotransferase (ALT), aspartate aminotransferase (AST) was determined. Patients in both groups were prescribed levothyroxine sodium (125-175 μg a day). Additionally, the 1st group of patients received arginine hydrochloride 42 mg/ml according to the scheme 200 ml a day per 15 days, the next 15 days L-arginine aspartate 200 mg/ml 5 ml a day. And the control group received only levothyroxine sodium.
 Results. The level of TH in 1st group decreased from 7.1±0.8 to 6.7±0.4 mmol/l, and in 2nd – from 7.2±0.7 to 6.97±0.35 mmol/l. In the 1st group TG decreased from 3.9±0.4 to 3.5±0.3 mmol/l, and in the 2nd – from 3.8±0.5 to 3.7±0.1 mmol/l. LDL in 1st group decreased from 5.9±1.4 to 5.5±1.2 mmol/l, in the 2nd – from 5.8±1.3 to 5.7±1.4 mmol/l. The level of ALT in 1st group decreased from 47.5±1.82 to 40.1±1.73 IU/l, the level of AST – from 41.3±1.52 to 39.8±1.33 IU/l, in no changes in AST and ALT levels were observed in the control group.
 Conclusions. Comprehensive treatment of patients with PH and NAFLD contributed to the improvement of liver transaminases (reduction of AST, ALT), as well as the normalization of the lipid profile (reduction of TC, TG and LDL).
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Kakoki, Masao, Hyung-Suk Kim, Cora-Jean S. Edgell, Nobuyo Maeda, Oliver Smithies, and David L. Mattson. "Amino acids as modulators of endothelium-derived nitric oxide." American Journal of Physiology-Renal Physiology 291, no. 2 (2006): F297—F304. http://dx.doi.org/10.1152/ajprenal.00417.2005.
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To examine the mechanisms whereby amino acids modulate nitric oxide (NO) production and blood flow in the renal vasculature, chemiluminescence techniques were used to quantify NO in the renal venous effluent of the isolated, perfused rat kidney as different amino acids were added to the perfusate. The addition of 10−4 or 10−3 M cationic amino acids (l-ornithine, l-lysine, or l-homoarginine) or neutral amino acids (l-glutamine, l-leucine, or l-serine) to the perfusate decreased NO and increased renal vascular resistance. Perfusion with anionic amino acids (l-glutamate or l-aspartate) had no effect on either parameter. The effects of the cationic and neutral amino acids were reversed with 10−3 M l-arginine and prevented by deendothelialization or NO synthase inhibition. The effects of the neutral amino acids but not the cationic amino acids were dependent on extracellular sodium. Cationic and neutral amino acids also decreased calcimycin-induced NO, as assessed by DAF-FM-T fluorescence, in cultured EA.hy926 endothelial cells. Inhibition of system y+ or y+L by siRNA for the cationic amino acid transporter 1 or the CD98/4F2 heavy chain diminished the NO-depleting effects of these amino acids. Finally, transport studies in cultured cells demonstrated that cationic or neutral amino acids in the extracellular space stimulate efflux of l-arginine out of the cell. Thus the present experiments demonstrate that cationic and neutral amino acids can modulate NO production in endothelial cells by altering cellular l-arginine transport through y+ and y+L transport mechanisms.
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Taran, O. A., and S. V. Demianiuk. "Optimization of the management tactics for women with fetal loss syndrome and high-risk thrombophilias in history at the preconception stage." UKRAINIAN JOURNAL OF PERINATOLOGY AND PEDIATRICS, no. 1(101) (March 28, 2025): 24–30. https://doi.org/10.15574/pp.2025.1(101).2430.
Full textAbstract:
One of the most significant medico-social problems in modern obstetrics is the reduction of reproductive losses, which underlie pregnancy loss, with a prevalence of up to 55%, reaching 80% in the first trimester. Aim - to evaluate the effectiveness of an optimized preconception preparation program using folates, a complex of vitamins, vitamin D, and L-arginine aspartate in women with fetal loss syndrome and high-risk thrombophilias in history. Materials and methods. A prospective controlled clinical study was conducted involving 49 women aged 25 to 42 years with fetal loss syndrome and high-risk thrombophilias in history, divided into two groups. In the control group (n=26), the pre-gravid period was accompanied by standard management, whereas in the main group (n=23), in addition to enoxaparin and acetylsalicylic acid, additional therapy was administered, including folic acid preparations, a complex of vitamins and minerals with the biologically active fourth-generation folate – quatrefolic, vitamin D, and L-arginine aspartate. From the moment of the desired pregnancy diagnosis, the structure and frequency of pregnancy and childbirth complications were studied. Statistical data processing was performed using the SPSS 21 program. Results. It was established that the administration of folates, a complex of vitamins, vitamin D, and L-arginine aspartate at the stage of comprehensive preconception preparation in women with fetal loss syndrome and high-risk thrombophilias in history is associated with a reduction in the frequency of threatened abortion, vitamin D deficiency, anemia during the first trimester, threatened miscarriage, de novo hypertensive disorders, placental dysfunction with fetal growth restriction in the second and third trimesters of pregnancy. Conclusions. The proposed pre-gravid preparation and therapy tactics in women with fetal loss syndrome and high-risk thrombophilias in history demonstrated a tendency to increase the number of preserved desired pregnancies from 76.9% to 91.3%. The research was carried out in accordance with the principles of the Helsinki Declaration. The study protocol was approved by the Local Ethics Committee of participating institution. The informed consent of the patient was obtained for conducting the studies. No conflict of interest was declared by the authors.
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QAFAITI, MICHAEL, and GROVER C. STEPHENS. "Distribution of Amino Acids to Internal Tissues After Epidermal Uptake in the Annelid Glycera Dibranchiata." Journal of Experimental Biology 136, no. 1 (1988): 177–91. http://dx.doi.org/10.1242/jeb.136.1.177.
Full textAbstract:
Net uptake rates by Glycera dibranchiata Ehlers of 18 amino acids, each present in artificial sea water at an initial concentration of 1 μmol l−1, were estimated using high-performance liquid chromatography (HPLC). Uptake rates for 14C-labelled alanine, arginine, aspartate, glutamate, glycine and serine, presented singly at an initial concentration of lμmol l−1, were estimated by observing disappearance of radioactivity from the ambient solution. Net entry of alanine, arginine, aspartate and serine was estimated by HPLC in parallel samples of the medium. There was no significant difference in the rate of influx of labelled substrate and net entry estimated by HPLC for these amino acids. Ligature of the anterior and posterior ends of the worms did not perceptibly modify rates of uptake. Distribution of radioactivity to the internal and external body wall, coelomocytes, gut and coelomic fluid was observed after 1 h of incubation in lμmol l−1 serine. Rates of exchange of labelled carbon were estimated for all combinations of these internal tissues by taking advantage of morphological features of Glycera. Amino acid pools in each of the tissues of the worms are described, based on HPLC analyses. Internal distribution of radioactivity derived from [14C]serine is compared with total pools based on estimates of tissue volume and the normal serine content of free amino acid pools for each tissue. The distribution of the non-metabolized analogue cycloleucine is also described at the end of 1 h of incubation.
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PÖRTNER, H. O., S. VOGELER, and M. K. GRIESHABER. "Recovery from Anaerobiosis in the Intertidal Worm Sipunculus Nudus: I. Restoration of Aerobic, Steady-State Energy Metabolism." Journal of Experimental Biology 122, no. 1 (1986): 37–50. http://dx.doi.org/10.1242/jeb.122.1.37.
Full textAbstract:
Recovery from 24 h of anaerobiosis was investigated in Sipunculus nudus L. by monitoring changes in the concentrations of anaerobic metabolites in the musculature and in the coelomic plasma. The metabolic events in animals collected during March and October were compared. Anaerobiosis led to an increase of succinate, propionate and acetate in the muscle tissues and the coelomic plasma. Strombine, octopine and alanine (predominantly l- rather than d-alanine) accumulated in the musculature, whereas aspartate and phospho-l-arginine levels decreased. A higher metabolic rate was observed during anaerobiosis in October than in March animals, as indicated by the higher amounts of strombine, octopine and acetate formed. An increase in metabolic rate appears to entail an increase of flux through the Embden-Meyerhof pathway which favours the accumulation of direct derivatives of pyruvate. During recovery, regeneration of phospho-l-arginine occurred during the first 3 h, whereas disposal of succinate, octopine and propionate was observed during the entire 24-h period of recovery. Strombine, alanine and, to a lesser extent, acetate contents remained elevated. The concentration of d-alanine approached that of Lalanine during recovery, indicating the activity of alanine racemase. Malate levels increased transiently, possibly linked to the repletion of the aspartate pool. In October animals, strombine seemed to accumulate transiently during initial recovery, indicating that the energy demand was not met by aerobic metabolism alone. In contrast to the situation in March animals, however, anaerobic glycolysis during recovery obviously becomes important only when the metabolic rate during anaerobiosis was high enough.
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Quintero, María José, Alicia María Muro-Pastor, Antonia Herrero, and Enrique Flores. "Arginine Catabolism in the CyanobacteriumSynechocystis sp. Strain PCC 6803 Involves the Urea Cycle and Arginase Pathway." Journal of Bacteriology 182, no. 4 (2000): 1008–15. http://dx.doi.org/10.1128/jb.182.4.1008-1015.2000.
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ABSTRACT Cells of the unicellular cyanobacterium Synechocystissp. strain PCC 6803 supplemented with micromolar concentrations ofl-[14C]arginine took up, concentrated, and catabolized this amino acid. Metabolism ofl-[14C]arginine generated a set of labeled amino acids that included argininosuccinate, citrulline, glutamate, glutamine, ornithine, and proline. Production of [14C]ornithine preceded that of [14C]citrulline, and the patterns of labeled amino acids were similar in cells incubated withl-[14C]ornithine, suggesting that the reaction of arginase, rendering ornithine and urea, is the main initial step in arginine catabolism. Ornithine followed two metabolic pathways: (i) conversion into citrulline, catalyzed by ornithine carbamoyltransferase, and then, with incorporation of aspartate, conversion into argininosuccinate, in a sort of urea cycle, and (ii) a sort of arginase pathway rendering glutamate (and glutamine) via Δ1pyrroline-5-carboxylate and proline. Consistently with the proposed metabolic scheme (i) an argF (ornithine carbamoyltransferase) insertional mutant was impaired in the production of [14C]citrulline from [14C]arginine; (ii) a proC (Δ1pyrroline-5-carboxylate reductase) insertional mutant was impaired in the production of [14C]proline, [14C]glutamate, and [14C]glutamine from [14C]arginine or [14C]ornithine; and (iii) a putA (proline oxidase) insertional mutant did not produce [14C]glutamate froml-[14C]arginine,l-[14C]ornithine, orl-[14C]proline. Mutation of two open reading frames (sll0228 and sll1077) putatively encoding proteins homologous to arginase indicated, however, that none of these proteins was responsible for the arginase activity detected in this cyanobacterium, and mutation of argD(N-acetylornithine aminotransferase) suggested that this transaminase is not important in the production of Δ1pyrroline-5-carboxylate from ornithine. The metabolic pathways proposed to explain [14C]arginine catabolism also provide a rationale for understanding how nitrogen is made available to the cell after mobilization of cyanophycin [multi-l-arginyl-poly(l-aspartic acid)], a reserve material unique to cyanobacteria.
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Debler, Erik W., Kanishk Jain, Rebeccah A. Warmack, et al. "A glutamate/aspartate switch controls product specificity in a protein arginine methyltransferase." Proceedings of the National Academy of Sciences 113, no. 8 (2016): 2068–73. http://dx.doi.org/10.1073/pnas.1525783113.
Full textAbstract:
Trypanosoma brucei PRMT7 (TbPRMT7) is a protein arginine methyltransferase (PRMT) that strictly monomethylates various substrates, thus classifying it as a type III PRMT. However, the molecular basis of its unique product specificity has remained elusive. Here, we present the structure of TbPRMT7 in complex with its cofactor product S-adenosyl-l-homocysteine (AdoHcy) at 2.8 Å resolution and identify a glutamate residue critical for its monomethylation behavior. TbPRMT7 comprises the conserved methyltransferase and β-barrel domains, an N-terminal extension, and a dimerization arm. The active site at the interface of the N-terminal extension, methyltransferase, and β-barrel domains is stabilized by the dimerization arm of the neighboring protomer, providing a structural basis for dimerization as a prerequisite for catalytic activity. Mutagenesis of active-site residues highlights the importance of Glu181, the second of the two invariant glutamate residues of the double E loop that coordinate the target arginine in substrate peptides/proteins and that increase its nucleophilicity. Strikingly, mutation of Glu181 to aspartate converts TbPRMT7 into a type I PRMT, producing asymmetric dimethylarginine (ADMA). Isothermal titration calorimetry (ITC) using a histone H4 peptide showed that the Glu181Asp mutant has markedly increased affinity for monomethylated peptide with respect to the WT, suggesting that the enlarged active site can favorably accommodate monomethylated peptide and provide sufficient space for ADMA formation. In conclusion, these findings yield valuable insights into the product specificity and the catalytic mechanism of protein arginine methyltransferases and have important implications for the rational (re)design of PRMTs.
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Künstner, Axel, Redouane Aherrahrou, Misa Hirose, et al. "Effect of Differences in the Microbiome of Cyp17a1-Deficient Mice on Atherosclerotic Background." Cells 10, no. 6 (2021): 1292. http://dx.doi.org/10.3390/cells10061292.
Full textAbstract:
CYP17A1 is a cytochrome P450 enzyme that has 17-alpha-hydroxylase and C17,20-lyase activities. Cyp17a11 deficiency is associated with high body mass and visceral fat deposition in atherosclerotic female ApoE knockout (KO, d/d or −/−) mice. In the present study, we aimed to investigate the effects of diet and Cyp17a1 genotype on the gut microbiome. Female Cyp17a1 (d/d) × ApoE (d/d) (DKO) and ApoE (d/d) (controls) were fed either standard chow or a Western-type diet (WTD), and we demonstrated the effects of genetics and diet on the body mass of the mice and composition of their gut microbiome. We found a significantly lower alpha diversity after accounting for the ecological network structure in DKO mice and WTD-fed mice compared with chow-fed ApoE(d/d). Furthermore, we found a strong significant positive association of the Firmicutes vs. Bacteroidota ratio with body mass and the circulating total cholesterol and triglyceride concentrations of the mice when feeding the WTD, independent of the Cyp17a1 genotype. Further pathway enrichment and network analyses revealed a substantial effect of Cyp17a1 genotype on associated cardiovascular and obesity-related pathways involving aspartate and L-arginine. Future studies are required to validate these findings and further investigate the role of aspartate/L-arginine pathways in the obesity and body fat distribution in our mouse model.
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Demchenko, Ivan T., Albert E. Boso, Thomas J. O'Neill, Peter B. Bennett, and Claude A. Piantadosi. "Nitric oxide and cerebral blood flow responses to hyperbaric oxygen." Journal of Applied Physiology 88, no. 4 (2000): 1381–89. http://dx.doi.org/10.1152/jappl.2000.88.4.1381.
Full textAbstract:
We have tested the hypothesis that cerebral nitric oxide (NO) production is involved in hyperbaric O2 (HBO2) neurotoxicity. Regional cerebral blood flow (rCBF) and electroencephalogram (EEG) were measured in anesthetized rats during O2 exposure to 1, 3, 4, and 5 ATA with or without administration of the NO synthase inhibitor ( N ω-nitro-l-arginine methyl ester), l-arginine, NO donors, or the N-methyl-d-aspartate receptor inhibitor MK-801. After 30 min of O2 exposure at 3 and 4 ATA, rCBF decreased by 26–39% and by 37–43%, respectively, and was sustained for 75 min. At 5 ATA, rCBF decreased over 30 min in the substantia nigra by one-third but, thereafter, gradually returned to preexposure levels, preceding the onset of EEG spiking activity. Rats pretreated with N ω-nitro-l-arginine methyl ester and exposed to HBO2 at 5 ATA maintained a low rCBF. MK-801 did not alter the cerebrovascular responses to HBO2at 5 ATA but prevented the EEG spikes. NO donors increased rCBF in control rats but were ineffective during HBO2 exposures. The data provide evidence that relative lack of NO activity contributes to decreased rCBF under HBO2, but, as exposure time is prolonged, NO production increases and augments rCBF in anticipation of neuronal excitation.
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Yu, J. G., T. Ishine, T. Kimura, W. E. O’Brien, and T. J. F. Lee. "l-Citrulline conversion tol-arginine in sphenopalatine ganglia and cerebral perivascular nerves in the pig." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 5 (1997): H2192—H2199. http://dx.doi.org/10.1152/ajpheart.1997.273.5.h2192.
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The presence of nitric oxide synthase (NOS), argininosuccinate synthetase (ASS), and argininosuccinate lyase (ASL) and their coexistence with NADPH-diaphorase (NADPHd), a marker for NOS, in the porcine sphenopalatine ganglia (SPG), pial veins, and the anterior cerebral arteries was examined using immunohistochemical and histochemical staining techniques. NOS-immunoreactive (I), ASS-I, and ASL-I fibers were found in pial veins and the anterior cerebral arteries. NOS, ASS, and ASL immunoreactivities were also found in neuronal cell bodies in the SPG. Almost all neuronal cell bodies in the SPG and nerve fibers in pial veins and the anterior cerebral arteries that were reactive to ASS, ASL, and NOS were also stained positively with NADPHd, suggesting that ASS, ASL, and NOS were colocalized in the same neurons in the SPG and perivascular nerves. With the use of in vitro tissue bath techniques,l-citrulline but notd-citrulline reversed inhibition of neurogenic vasodilation in isolated porcine pial veins produced by NOS inhibitors such as N G-nitro-l-arginine methyl ester. In the presence of l-aspartate,l-arginine was synthesized froml-citrulline in homogenates of SPG and endothelium-denuded cerebral arteries and pial veins. These results provide evidence indicating that perivascular nerves in pial veins like cerebral arteries can convertl-citrulline tol-arginine for synthesizing nitric oxide. The conversion is most likely via an argininosuccinate pathway.
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Khaleel Ali, I., and J. M. Saed Zaed. "Effect of Adding L-Arginine to Broiler Diets on Physiological Performance." IOP Conference Series: Earth and Environmental Science 1262, no. 7 (2023): 072103. http://dx.doi.org/10.1088/1755-1315/1262/7/072103.
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Abstract This research was conducted in the poultry sector of the Department of Animal Production, College of Agriculture, University of Anbar, from October 26, 2022, to December 7, 2022 (42 days). The objective was to compare the effects of incorporating different levels of L-Arginine and vitamin C on the productive and physiological performance of broiler chickens. One hundred and fifty Ross 308 strain broiler chicks, aged one day and of unspecified sex, were utilized in the study. The chicks were individually weighed and randomly assigned to five experimental groups, each consisting of three replicates with ten birds per replicate. The treatments consisted of the following: First treatment Control group (no additives), Second treatment: Addition of arginine at a rate of 1 g/kg of feed, Third treatment: Addition of arginine at a rate of 1.5 g/kg of feed, Fourth treatment: Addition of arginine at a rate of 2 g/kg of feed and Fifth treatment: Addition of vitamin C at a rate of 300 mg/kg of feed The results of the study revealed that utilizing the specified levels of arginine and vitamin C in the diets did not lead to any significant impact on the physiological performance, chemical, and biochemical blood parameters of the broiler chickens. These parameters included Glutathione, Malondialdehyde (MDA), Very Low-Density Lipoprotein (VLDL), Low-Density Lipoprotein (LDL), High-Density Lipoprotein (HDL), Triglycerides, Cholesterol, Creatinine, Uric Acid, AST (Aspartate Aminotransferase), ALT (Alanine Aminotransferase), Ceruloplasmin, Albumin, Protein, Glucose, H/L Ratio (Heterophil to Lymphocyte Ratio), Lymphocytes, and Monocytes. In conclusion, the utilization of the specified levels of arginine and vitamin C in the diets did not result in any significant effects on the studied parameters in the broiler chickens.
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Bondarenko, Volodymyr O., Andriy S. Minukhin, Evgeniy I. Skornyakov, Nadiia M. Kononenko та Maryna O. Ostapets. "DYNAMICS OF FUNCTIONAL CONDITION SEEDMANS AND LIVER IN MEN WITH INFERTILITY UNDER THE INFLUENCE OF ARGININ THERAPY WITH THE COMPLEX OF L-CARNITIN AND BETAINЕ". Wiadomości Lekarskie 73, № 4 (2020): 700–704. http://dx.doi.org/10.36740/wlek202004114.
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The aim of this work was to study the hormonal status androgen-dependent indicators of the ejaculate, spermatogram parameters and liver transaminases in the blood of the infertile males for the treatment of arginine, carnitine and betaine. Materials and methods: The parameters of spermograms, the levels of testosterone, estradiol, alanine aminotransferase and aspartate aminotransferase in the blood, and concentration of fructose in the ejaculate of 31 men with idiopathic pathospermia before and after using the L-Betargin, which contains 1 gram of arginine, 300 mg of L-carnitine and 1 gram of betaine. Results: It is shown that after treatment there is an increase of sperm concentration and their motility, increase the level of fructose in the ejaculate. It is established that the positive effect on spermatogenesis, L-Betargin associated with activation of endocrine function of the testes, improving the androgen-estrogen balance and functional state of the liver in men with infertility. Conclusions: The use of L-Betargin for a month in men with idiopathic pathospermia leads to an increase in the concentration of sperm and increase their motility, while normalizing all parameters of the spermogram.
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Mylostyvyi, R. V., M. O. Lieshchova, P. М. Skliarov, et al. "Cardioprotective effects of L-arginine in a mesatone-induced rat model of chronic heart failure: biochemical and electrocardiographic insights." Ukrainian Journal of Veterinary and Agricultural Sciences 8, no. 1 (2025): 70–76. https://doi.org/10.32718/ujvas8-1.10.
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The management of chronic heart failure (CHF) remains a critical challenge in cardiovascular pathology. This study aimed to investigate the role of L-arginine in a mesatone-induced rat model of CHF. L-arginine exhibits cardioprotective effects. CHF was induced in experimental groups by intramuscular administration of 0.1 mL of a 1 % mesatone solution, followed by daily free swimming until profound fatigue for 21 days. The experiment continued until stable and irreversible myocardial changes developed. One experimental group received L-arginine at a dose of 20 mg/kg intraperitoneally for 10 days. The control group consisted of intact animals. The impact of CHF on the cardiovascular system was assessed through biochemical and electrocardiographic (ECG) parameters. In CHF-induced rats, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels increased by 36.7 % (P ≤ 0.05) and 184.1 % (P ≤ 0.05), respectively, compared to the control group. Additionally, CHF was associated with an increase in creatinine levels by 152.6 % (P ≤ 0.01) and urea levels by 207.0 % (P ≤ 0.05), indicating renal dysfunction. Electrolyte imbalances included elevated sodium, potassium, and chloride levels, reflecting the activation of the renin-angiotensin-aldosterone system (RAAS). CHF also caused significant alterations in ECG parameters, including a 24.8 % (P ≤ 0.05) reduction in heart rate, a 50.2 % (P ≤ 0.05) decrease in R-wave amplitude, and a 192.9 % (P ≤ 0.05) reduction in T-wave amplitude. Additionally, CHF led to a 37.2 % (P ≤ 0.05) prolongation of the QRS complex and a 60.3 % (P ≤ 0.05) increase in QT interval duration, indicating myocardial conduction abnormalities and impaired ventricular repolarization. L-arginine administration demonstrated a cardioprotective effect by reducing AST levels by 27.7 % (P ≤ 0.05) and ALT by 5.8 %, suggesting improved myocardial function. Furthermore, creatinine and urea levels decreased by 46.9 % (P ≤ 0.05) and 60.0 % (P ≤ 0.05), respectively, indicating a beneficial effect on renal function. Electrolyte imbalances were partially corrected, with potassium levels decreasing by 69.9 % (P ≤ 0.05) and chloride levels by 44.1 % (P ≤ 0.05). L-arginine also contributed to the partial normalization of ECG parameters, leading to a 9.0 % (P ≤ 0.05) increase in heart rate, reduction in QT interval prolongation, and improved ventricular conduction. These findings suggest that L-arginine mitigates biochemical and electrophysiological disturbances associated with CHF, supporting its potential as a cardioprotective agent.
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Liebenberg, Nico, Sâmia Joca, and Gregers Wegener. "Nitric oxide involvement in the antidepressant-like effect of ketamine in the Flinders sensitive line rat model of depression." Acta Neuropsychiatrica 27, no. 2 (2014): 90–96. http://dx.doi.org/10.1017/neu.2014.39.
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ObjectiveWe investigated whether the nitric oxide (NO) precursor, l-arginine, can prevent the antidepressant-like action of the fast-acting antidepressant, ketamine, in a genetic rat model of depression, and/or induce changes in the glutamate (Glu)/N-methyl-d-aspartate receptor (NMDAR)/NO/cyclic guanosine monophosphate (cGMP) signalling pathway. Hereby it was evaluated whether the NO signalling system is involved in the antidepressant mechanism of ketamine.MethodsFlinders sensitive line (FSL) rats received single i.p. injections of ketamine (15 mg/kg) with/without pre-treatment (30 min prior) with l-arginine (500 mg/kg). Depression-like behaviour was assessed in the forced swim test (FST) in terms of immobility, and the activation state of the Glu/NMDAR/NO/cGMP pathway was evaluated ex vivo in the frontal cortex and hippocampus regions in terms of total constitutive NOS (cNOS) activity and cGMP concentration.Resultsl-Arginine pre-treatment prevented the antidepressant-like effect of ketamine in the FST, as well as a ketamine-induced increase in cGMP levels in the frontal cortex and hippocampus of FSL rats. Ketamine reduced cNOS activity only in the hippocampus, and this effect was not reversed by l-arginine.ConclusionBoth the behavioural and molecular results from this study indicate an involvement for the NO signalling pathway in the antidepressant action of ketamine. Although not easily interpretable, these findings broaden our knowledge of effects of ketamine on the NO system.
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Yamaguchi, Yusuke, Yushi Hirata, Takeshi Saito, and Hitomi Kumagai. "Combined Effects of Amino Acids in Garlic and Buna-Shimeji (Hypsizygus marmoreus) on Suppression of CCl4-Induced Hepatic Injury in Rats." Foods 10, no. 7 (2021): 1491. http://dx.doi.org/10.3390/foods10071491.
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The combination of the garlic-derived amino acid, S-allyl-l-cysteine sulfoxide (ACSO), and ornithine or arginine on CCl4-induced hepatic injury was examined. After investigating the effectiveness of the mixture of ACSO and ornithine or arginine in preventing hepatic injury in vivo, an extract rich in ACSO and ornithine was prepared by converting arginine in garlic to ornithine by arginase from Hypsizygus marmoreus (buna-shimeji), after screening the productivity of ornithine among 12 kinds of mushrooms. Co-administration of ACSO with ornithine or arginine suppressed the increase in aspartate transaminase, alanine transaminase, and thiobarbituric acid reactive substance, and the decrease in glutathione S-transferase and cytochrome p450 2E1 activities after CCl4 injection more effectively than a single administration of ACSO. All extracts prepared from garlic and buna-shimeji with low and high contents of ACSO and arginine or ornithine significantly suppressed CCl4-induced hepatic injury in rats. Considering that ACSO is tasteless, odourless, and enhances taste, and ornithine has a flat or sweet taste and masks bitterness, the extract rich in ACSO and ornithine from garlic and buna-shimeji could be considered a potential antioxidant food material that can be added to many kinds of food to prevent hepatic injury.
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Coyle, A. J., W. Mitzner, and C. G. Irvin. "Cationic proteins alter smooth muscle function by an epithelium-dependent mechanism." Journal of Applied Physiology 74, no. 4 (1993): 1761–68. http://dx.doi.org/10.1152/jappl.1993.74.4.1761.
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Using a perfused guinea pig tracheal tube preparation, which allows the selective application of agonists to either the serosal or luminal surface, we have investigated whether two synthetic cationic proteins, poly-L-arginine and poly-L-lysine, can modify epithelium-dependent responses. With an intact epithelium, methacholine was approximately 150 times less potent when applied intraluminally than when applied extraluminally. This difference was abolished by chemically removing the epithelium with the detergent CHAPS. Intraluminal application of KCl induced a dose-related relaxation of a precontracted trachea, which was also abolished by epithelium removal. Perfusion of the luminal surface with cationic proteins for 1 h (10 micrograms/ml) increased the potency of intraluminally applied methacholine without modifying the responses to extraluminally applied methacholine. Cationic proteins also attenuated the relaxant effects of intraluminally applied KCl. These effects occurred in the absence of any overt epithelial cell damage. In contrast, when the serosal surface of the trachea was treated with poly-L-arginine, there was no modification of either methacholine-induced contraction or KCl-induced relaxation. The effects of poly-L-arginine were inhibited by coperfusion with the polyanions albumin (10 micrograms/ml) or heparin (100 micrograms/ml). In contrast to cationic proteins, intraluminal perfusion with a polyanion, poly-L-aspartate (10 micrograms/ml), failed to modify either methacholine-induced contraction or KCl-induced relaxation. Our data demonstrate that cationic proteins can modify epithelium-dependent responses in the airways. Although the precise mechanisms are unclear, a role is suggested for a charge-mediated interaction with the respiratory epithelium, resulting in airway smooth muscle dysfunction.
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E, Bon. "Characterization of the Pool of Amino Acids and Their Functional Significance in The Rat Brain." Journal of Clinical Peadiatrics and Care 1, no. 1 (2023): 01–05. http://dx.doi.org/10.58489/2836-8630/006.
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Amino acids (AA) play an important role in the metabolism and functioning of the brain. This is explained not only by their exceptional role as sources of synthesis of a large number of biologically important compounds (proteins, mediators, lipids, biologically active amines). Amino acids and their derivatives are involved in synaptic transmission as neurotransmitters and neuromodulators (glutamate, aspartate, glycine, GABA, taurine), and some AA are involved in the formation of nervous system mediators: methionine – acetylcholine, DOPA, dopamine; tyrosine – catecholamines; serine and cysteine – taurine; tryptophan – serotonin; histidine – histamine; L-arginine – NO; glutamic acid – glutamate.
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E.I, Bon. "Distribution of the Pool of Amino Acids in The Parietal Lobe of Albino Rats." Transplantation Proceedings and Research 2, no. 1 (2023): 01–04. http://dx.doi.org/10.58489/2836-8991/005.
Full textAbstract:
Amino acids (AA) play an important role in the metabolism and functioning of the brain. This is explained not only by their exceptional role as sources of synthesis of a large number of biologically important compounds (proteins, mediators, lipids, biologically active amines). Amino acids and their derivatives are involved in synaptic transmission as neurotransmitters and neuromodulators (glutamate, aspartate, glycine, GABA, taurine), and some AA are involved in the formation of nervous system mediators: methionine – acetylcholine, DOPA, dopamine; tyrosine – catecholamines; serine and cysteine – taurine; tryptophan – serotonin; histidine – histamine; L-arginine – NO; glutamic acid – glutamate.
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Nanatani, Kei, Peter C. Maloney, and Keietsu Abe. "Structural and Functional Importance of Transmembrane Domain 3 (TM3) in the Aspartate:Alanine Antiporter AspT: Topology and Function of the Residues of TM3 and Oligomerization of AspT." Journal of Bacteriology 191, no. 7 (2009): 2122–32. http://dx.doi.org/10.1128/jb.00830-08.
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ABSTRACT AspT, the aspartate:alanine antiporter of Tetragenococcus halophilus, a membrane protein of 543 amino acids with 10 putative transmembrane (TM) helices, is the prototype of the aspartate:alanine exchanger (AAE) family of transporters. Because TM3 (isoleucine 64 to methionine 85) has many amino acid residues that are conserved among members of the AAE family and because TM3 contains two charged residues and four polar residues, it is thought to be located near (or to form part of) the substrate translocation pathway that includes the binding site for the substrates. To elucidate the role of TM3 in the transport process, we carried out cysteine-scanning mutagenesis. The substitutions of tyrosine 75 and serine 84 had the strongest inhibitory effects on transport (initial rates of l-aspartate transport were below 15% of the rate for cysteine-less AspT). Considerable but less-marked effects were observed upon the replacement of methionine 70, phenylalanine 71, glycine 74, arginine 76, serine 83, and methionine 85 (initial rates between 15% and 30% of the rate for cysteine-less AspT). Introduced cysteine residues at the cytoplasmic half of TM3 could be labeled with Oregon green maleimide (OGM), whereas cysteines close to the periplasmic half (residues 64 to 75) were not labeled. These results suggest that TM3 has a hydrophobic core on the periplasmic half and that hydrophilic residues on the cytoplasmic half of TM3 participate in the formation of an aqueous cavity in membranes. Furthermore, the presence of l-aspartate protected the cysteine introduced at glycine 62 against a reaction with OGM. In contrast, l-aspartate stimulated the reactivity of the cysteine introduced at proline 79 with OGM. These results demonstrate that TM3 undergoes l-aspartate-induced conformational alterations. In addition, nonreducing sodium dodecyl sulfate-polyacrylamide gel electrophoresis analyses and a glutaraldehyde cross-linking assay suggest that functional AspT forms homo-oligomers as a functional unit.
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Wu, Guoyao, Fuller W. Bazer, Gregory A. Johnson, M. Carey Satterfield, and Shannon E. Washburn. "Metabolism and Nutrition of L-Glutamate and L-Glutamine in Ruminants." Animals 14, no. 12 (2024): 1788. http://dx.doi.org/10.3390/ani14121788.
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Although both L-glutamate (Glu) and L-glutamine (Gln) have long been considered nutritionally nonessential in ruminants, these two amino acids have enormous nutritional and physiological importance. Results of recent studies revealed that extracellular Gln is extensively degraded by ruminal microbes, but extracellular Glu undergoes little catabolism by these cells due to the near absence of its uptake. Ruminal bacteria hydrolyze Gln to Glu plus ammonia and, intracellularly, use both amino acids for protein synthesis. Microbial proteins and dietary Glu enter the small intestine in ruminants. Both Glu and Gln are the major metabolic fuels and building blocks of proteins, as well as substrates for the syntheses of glutathione and amino acids (alanine, ornithine, citrulline, arginine, proline, and aspartate) in the intestinal mucosa. In addition, Gln and aspartate are essential for purine and pyrimidine syntheses, whereas arginine and proline are necessary for the production of nitric oxide (a major vasodilator) and collagen (the most abundant protein in the body), respectively. Under normal feeding conditions, all diet- and rumen-derived Glu and Gln are extensively utilized by the small intestine and do not enter the portal circulation. Thus, de novo synthesis (e.g., from branched-chain amino acids and α-ketoglutarate) plays a crucial role in the homeostasis of Glu and Gln in the whole body but may be insufficient for maximal growth performance, production (e.g., lactation and pregnancy), and optimal health (particularly intestinal health) in ruminants. This applies to all types of feeding systems used around the world (e.g., rearing on a milk replacer before weaning, pasture-based production, and total mixed rations). Dietary supplementation with the appropriate doses of Glu or Gln [e.g., 0.5 or 1 g/kg body weight (BW)/day, respectively] can safely improve the digestive, endocrine, and reproduction functions of ruminants to enhance their productivity. Both Glu and Gln are truly functional amino acids in the nutrition of ruminants and hold great promise for improving their health and productivity.
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Davydova, Iu V., and A. Yu Lymanska. "Correction of the function of the endothelium is a new goal of prevention and treatment of arterial hypertension in patients with cardiovascular pathology." UKRAINIAN JOURNAL OF PERINATOLOGY AND PEDIATRICS, no. 2(94) (June 28, 2023): 7–12. http://dx.doi.org/10.15574/pp.2023.94.7.
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Purpose - to determine the dynamics of endothelial progenitor cells (EPCs) and asymmetric dimethylarginine (ADMA) in pregnant women with hypertension as markers of the effectiveness of endothelial dysfunction correction on the background of L-arginine therapy (Tivortin, manufactured by Yuria-Pharm). Materials and methods. The study pregnant women were divided into two groups: women with hypertension at 12-15 weeks of gestation (n=29) and women with congenital heart disease at 12-14 weeks of gestation (n=21). The control group consisted of 40 healthy pregnant women. The examination was conducted before the start of oral L-arginine (Tivortin aspartate) and 7-8 weeks after the start of therapy. Tivortin aspartate was administered orally 1 measuring spoon 5 times a day for 6 weeks. The study of the level of EPCs (CD45+/CD34+ phenotype of peripheral blood) was performed by flow cytometry using reagents for the determination of CD34, CD45 differentiation clusters produced by Beckman Coulter Inc. The results are presented in % of ERC from the total number of leukocytes, as well as in absolute values - the number of cells per 1 ml of blood in absolute values. The level of ADMA in plasma was determined by an indirect enzyme-linked immunosorbent assay using the ADMA ELISA test system (manufactured by Immunodiagnostik AG, Germany). The reference values for pregnant women are 0.26-0.60 μmol/l. Results. After treatment with L-arginine (Tivortin), the ADMA index decreased compared to baseline data in the studied groups of pregnant women. Thus, in pregnant women with hypertension, ADMA decreased by almost 15%, which is a marker of improved endothelial function. The same dynamics was observed in the group of women with congenital heart disease. In both study groups of pregnant women, the number of EPCs increased by almost 10% after the addition of L-arginine (Tivortin) to the treatment complex. There was a positive correlation between a decrease in mean systolic blood pressure, an increase in EPCs and a decrease in ADMA after complex treatment. Studies have shown a direct correlation (r=0.75) between blood pressure and the number of ЕРСs and an inverse correlation (r=-0.68) between blood pressure and ADMA. The reduction in blood pressure during treatment was accompanied by an improvement in endothelial function, namely, an increase in the number of ЕРСs, mainly due to the vasodilation potential of the endothelium. There was also a decrease in ADMA against the background of a decrease in systolic blood pressure during treatment. Conclusions. The clinical relevance of asymmetric dimethylarginine as a specific marker in patients with hypertension has been established: a significant increase in its level is observed in patients with cardiovascular disease, in particular, with hypertension, which confirms the role of endothelial dysfunction as a leading pathogenetic factor in the development of hypertension in the absence of anatomical and pathological changes in the vessels. The concept of maintenance therapy in patients with cardiovascular disease aims to restore adequate NO bioavailability by administering exogenous L-arginine. Based on the results of the study of the effect of L-arginine (Tivortin) on the index of ЕРСs, which are actively involved in the repair of damaged endothelium, it can be concluded that this drug has a positive effect on the prognosis of life in patients with hypertension, restoring endothelial function. The research was carried out in accordance with the principles of the Helsinki Declaration. The study protocol was approved by the Local Ethics Committee of all participating institutions. The informed consent of the patient was obtained for conducting the studies. No conflict of interests was declared by the authors.
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Pui Ping, Chung, Muhammad Nadeem Akhtar, Daud Ahmad Israf, Enoch Kumar Perimal, and Mohd Roslan Sulaiman. "Possible Participation of Ionotropic Glutamate Receptors and l-Arginine-Nitric Oxide-Cyclic Guanosine Monophosphate-ATP-Sensitive K+ Channel Pathway in the Antinociceptive Activity of Cardamonin in Acute Pain Animal Models." Molecules 25, no. 22 (2020): 5385. http://dx.doi.org/10.3390/molecules25225385.
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The perception of pain caused by inflammation serves as a warning sign to avoid further injury. The generation and transmission of pain impulses involves various pathways and receptors. Cardamonin isolated from Boesenbergia rotunda (L.) Mansf. has been reported to exert antinociceptive effects in thermal and mechanical pain models; however, the precise mechanism has yet to be examined. The present study investigated the possible mechanisms involved in the antinociceptive activity of cardamonin on protein kinase C, N-methyl-d-aspartate (NMDA) and non-NMDA glutamate receptors, l-arginine/cyclic guanosine monophosphate (cGMP) mechanism, as well as the ATP-sensitive potassium (K+) channel. Cardamonin was administered to the animals intra-peritoneally. Present findings showed that cardamonin significantly inhibited pain elicited by intraplantar injection of phorbol 12-myristate 13-acetate (PMA, a protein kinase C activator) with calculated mean ED50 of 2.0 mg/kg (0.9–4.5 mg/kg). The study presented that pre-treatment with MK-801 (NMDA receptor antagonist) and NBQX (non-NMDA receptor antagonist) significantly modulates the antinociceptive activity of cardamonin at 3 mg/kg when tested with glutamate-induced paw licking test. Pre-treatment with l-arginine (a nitric oxide precursor), ODQ (selective inhibitor of soluble guanylyl cyclase) and glibenclamide (ATP-sensitive K+ channel inhibitor) significantly enhanced the antinociception produced by cardamonin. In conclusion, the present findings showed that the antinociceptive activity of cardamonin might involve the modulation of PKC activity, NMDA and non-NMDA glutamate receptors, l-arginine/nitric oxide/cGMP pathway and ATP-sensitive K+ channel.
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Priya, S. Ranjini, and A. Subhashini. "Characterization and Optimization of Fungal L-Asparaginase Isolated From Soil and Medicinal Plants." Journal of Pure and Applied Microbiology 16, no. 1 (2022): 453–59. http://dx.doi.org/10.22207/jpam.16.1.43.
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L-asparaginase is a therapeutic enzyme that converts L-asparagine into ammonia and L-aspartate. L-asparaginase is used to treat acute lymphoblastic leukaemia. In food manufacturing industries, it is used to inhibit the acrylamide formation. The current investigation has been performed to isolate L-asparaginase producing fungi from different medicinal plants and soil samples, through serial dilution. A total number of 15 fungal isolates were obtained from soil samples and 6 endophytic fungi isolated from medicinal plants. By performing screening of L-asparaginase 67% of positive isolates were obtained from endophytes and soil samples. Optimization of L-asparaginase production was performed for parameters such as pH, temperature, carbon and nitrogen source, and it was found that pH 6, 30˚C, 2 g of glucose, and 1 g of L-arginine is suitable for maximum enzyme production. By performing Sodium dodecyl sulphate polyacrylamide gel electrophoresis the molecular weight of an enzyme was determined to be approximately 11.2 kDa.
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Fabricius, M., N. Akgoren, and M. Lauritzen. "Arginine-nitric oxide pathway and cerebrovascular regulation in cortical spreading depression." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 1 (1995): H23—H29. http://dx.doi.org/10.1152/ajpheart.1995.269.1.h23.
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Nerve cells release nitric oxide (NO) in response to activation of glutamate receptors of the N-methyl-D-aspartate (NMDA) subtype. We explored the hypothesis that NO influences the changes of cerebral blood flow (CBF) during cortical spreading depression (CSD), which is known to be associated with NMDA receptor activation. CBF was monitored in parietal cortex by laser-Doppler flowmetry in halothane-anesthetized rats. Under control conditions, CSD induced regular changes of CBF, which consisted of four phases: a brief hypoperfusion before the direct current (DC) shift; a marked CBF rise during the DC shift; followed by a smaller, but protracted increase of CBF; and a prolonged CBF reduction (the oligemia). NO synthase inhibition by intravenous and/or topical application of NG-nitro-L-arginine enhanced the brief initial hypoperfusion, but the CBF increases and the oligemia were unchanged. L-Arginine prevented the development of the prolonged oligemia after CSD but had no influence on the marked rise of CBF during CSD. Animals treated with L-arginine recovered the reduced vascular reactivity to hypercapnia after CSD much faster than control rats. Functional denervation of cortical and pial arterioles by tetrodotoxin accentuated the pre-CSD hypoperfusion and the oligemia but did not affect the CBF increases. The results suggest that NO is important for the changes of cerebrovascular regulation following CSD. The observations may have clinical importance, since CBF changes during migraine may be triggered by CSD.