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Journal articles on the topic 'Physiological oxidation'

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Published: 4 June 2021

Last updated: 1 August 2024

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1

Miljković, Josip, Ana Shek Vugrovečki, Suzana Milinković Tur, Dražen Đuričić, Sofia Ana Blažević, Siniša Faraguna, and Ivona Žura Žaja. "Oksidacijsko-antioksidacijski procesi i toplinski učinci na oksidativni stres u gmazova." Veterinarska stanica 56, no. 1 (June 19, 2024): 145–59. http://dx.doi.org/10.46419/vs.56.1.1.

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Temperature is the most important abiotic factor and has a direct influence on the physiology of the organism, affecting nearly all other parameters of the living environment of organisms. Ectothermic organisms are highly endangered in the current crisis climate, as they are unable to use metabolic heat to maintain body temperature. Reptiles are ectothermic vertebrates that are also susceptible to temperature fluctuations. Metabolism, muscle and nervous system function and reproduction are closely linked to reptile body temperature. To study the effects of temperature on oxidative stress, it i

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Tardo-Dino, Pierre-Emmanuel, Julianne Touron, Stéphane Baugé, Stéphanie Bourdon, Nathalie Koulmann, and Alexandra Malgoyre. "The effect of a physiological increase in temperature on mitochondrial fatty acid oxidation in rat myofibers." Journal of Applied Physiology 127, no. 2 (August 1, 2019): 312–19. http://dx.doi.org/10.1152/japplphysiol.00652.2018.

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We investigated the effect of temperature increase on mitochondrial fatty acid (FA) and carbohydrate oxidation in the slow-oxidative skeletal muscles (soleus) of rats. We measured mitochondrial respiration at 35°C and 40°C with the physiological substrates pyruvate + 4 mM malate (Pyr) and palmitoyl-CoA (PCoA) + 0.5 mM malate + 2 mM carnitine in permeabilized myofibers under nonphosphorylating ([Formula: see text]) or phosphorylating ([Formula: see text]) conditions. Mitochondrial efficiency was calculated by the respiratory control ratio (RCR = [Formula: see text]/[Formula: see text]). We used

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3

Kelley, D. E., J. P. Reilly, T. Veneman, and L. J. Mandarino. "Effects of insulin on skeletal muscle glucose storage, oxidation, and glycolysis in humans." American Journal of Physiology-Endocrinology and Metabolism 258, no. 6 (June 1, 1990): E923—E929. http://dx.doi.org/10.1152/ajpendo.1990.258.6.e923.

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The effects of physiological hyperinsulinemia (approximately 75 mU/l) on glucose storage, oxidation, and glycolysis in skeletal muscle were assessed with euglycemic clamps performed in seven healthy volunteers, in conjunction with leg balance for glucose, lactate, alanine, O2, and CO2. Infusion of insulin increased leg glucose uptake, storage, and oxidation but did not alter net release of lactate and alanine. The respiratory quotient (RQ) across the leg increased from a basal value of 0.74 +/- 0.02 to 0.99 +/- 0.02 during hyperinsulinemia. Under conditions of insulin stimulation, 49 +/- 5% of

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Ford, Megan M., Amanda L. Smythers, Evan W. McConnell, Sarah C. Lowery, Derrick R. J. Kolling, and Leslie M. Hicks. "Inhibition of TOR in Chlamydomonas reinhardtii Leads to Rapid Cysteine Oxidation Reflecting Sustained Physiological Changes." Cells 8, no. 10 (September 28, 2019): 1171. http://dx.doi.org/10.3390/cells8101171.

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The target of rapamycin (TOR) kinase is a master metabolic regulator with roles in nutritional sensing, protein translation, and autophagy. In Chlamydomonas reinhardtii, a unicellular green alga, TOR has been linked to the regulation of increased triacylglycerol (TAG) accumulation, suggesting that TOR or a downstream target(s) is responsible for the elusive “lipid switch” in control of increasing TAG accumulation under nutrient limitation. However, while TOR has been well characterized in mammalian systems, it is still poorly understood in photosynthetic systems, and little work has been done

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Bonadonna, R. C., S. del Prato, E. Bonora, G. Gulli, A. Solini, and R. A. DeFronzo. "Effects of physiological hyperinsulinemia on the intracellular metabolic partition of plasma glucose." American Journal of Physiology-Endocrinology and Metabolism 265, no. 6 (December 1, 1993): E943—E953. http://dx.doi.org/10.1152/ajpendo.1993.265.6.e943.

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Methodology for assessing the glycolytic and oxidative fluxes from plasma glucose, by measuring 3H2O and 14CO2 rates of production during [3-3H]- and [U-14C]glucose infusion, was tested in healthy subjects. In study 1, during staircase 3H2O infusion in six subjects, calculated rates of 3H2O appearance agreed closely with 3H2O infusion rates. In study 2, when [2-3H]glucose and NaH14CO3 were infused in four subjects in the basal state and during a 4-h euglycemic insulin (approximately 70 microU/ml) clamp, accurate estimates of the rates of [2-3H]glucose detritiation were obtained (94-97% of the

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6

Stadtman, E. R., and C. N. Oliver. "Metal-catalyzed oxidation of proteins. Physiological consequences." Journal of Biological Chemistry 266, no. 4 (February 1991): 2005–8. http://dx.doi.org/10.1016/s0021-9258(18)52199-2.

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7

Thomas, Michael J. "Physiological aspects of low-density lipoprotein oxidation." Current Opinion in Lipidology 11, no. 3 (June 2000): 297–301. http://dx.doi.org/10.1097/00041433-200006000-00011.

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8

Drazic, Adrian, and Jeannette Winter. "The physiological role of reversible methionine oxidation." Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics 1844, no. 8 (August 2014): 1367–82. http://dx.doi.org/10.1016/j.bbapap.2014.01.001.

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9

Harper, M. E., R. M. Dent, V. Bezaire, A. Antoniou, A. Gauthier, S. Monemdjou, and R. McPherson. "UCP3 and its putative function: consistencies and controversies." Biochemical Society Transactions 29, no. 6 (November 1, 2001): 768–73. http://dx.doi.org/10.1042/bst0290768.

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The physiological function of uncoupling protein 3 (UCP3) is as yet unknown. Based on its 57% homology to UCP1 whose physiologic function is uncoupling and thermogenesis, UCP3 was attributed with the function of mitochondrial uncoupling through proton-leak reactions. UCP3 is expressed selectively in muscle, a tissue in which it has been estimated that proton leak accounts for approx. 50% of resting energy metabolism. Genetic linkage, association and variant studies suggest a role for UCP3 in obesity and/or diabetes. Studies of the heterologous expression of UCP3 in yeast provide support for th

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10

Burgoyne, Joseph R., and Philip Eaton. "Contemporary techniques for detecting and identifying proteins susceptible to reversible thiol oxidation." Biochemical Society Transactions 39, no. 5 (September 21, 2011): 1260–67. http://dx.doi.org/10.1042/bst0391260.

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Elevated protein oxidation is a widely reported hallmark of most major diseases. Historically, this ‘oxidative stress’ has been considered causatively detrimental, as the protein oxidation events were interpreted simply as damage. However, recent advances have changed this antiquated view; sensitive methodology for detecting and identifying proteins susceptible to oxidation has revealed a fundamental role for this modification in physiological cell signalling during health. Reversible protein oxidation that is dynamically coupled with cellular reducing systems allows oxidative protein modifica

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Hirota, Yuko, Dongchon Kang, and Tomotake Kanki. "The Physiological Role of Mitophagy: New Insights into Phosphorylation Events." International Journal of Cell Biology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/354914.

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Mitochondria play an essential role in oxidative phosphorylation, fatty acid oxidation, and the regulation of apoptosis. However, this organelle also produces reactive oxygen species (ROS) that continually inflict oxidative damage on mitochondrial DNA, proteins, and lipids, which causes further production of ROS. To oppose this oxidative stress, mitochondria possess quality control systems that include antioxidant enzymes and the repair or degradation of damaged mitochondrial DNA and proteins. If the oxidative stress exceeds the capacity of the mitochondrial quality control system, it seems th

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Bode, Helge B., Axel Zeeck, Kirsten PlÃ¯Â¿Â½ckhahn, and Dieter Jendrossek. "Physiological and Chemical Investigations into Microbial Degradation of Synthetic Poly(cis-1,4-isoprene)." Applied and Environmental Microbiology 66, no. 9 (September 1, 2000): 3680–85. http://dx.doi.org/10.1128/aem.66.9.3680-3685.2000.

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ABSTRACT Streptomyces coelicolor 1A and Pseudomonas citronellolis were able to degrade synthetic high-molecular-weight poly(cis-1,4-isoprene) and vulcanized natural rubber. Growth on the polymers was poor but significantly greater than that of the nondegrading strain Streptomyces lividans 1326 (control). Measurement of the molecular weight distribution of the polymer before and after degradation showed a time-dependent increase in low-molecular-weight polymer molecules forS. coelicolor 1A and P. citronellolis, whereas the molecular weight distribution for the control (S. lividans 1326) remaine

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Zierath, J. R., L. A. Nolte, E. Wahlström, D. Galuska, P. R. Shepherd, B. B. Kahn, and H. Wallberg-Henriksson. "Carrier-mediated fructose uptake significantly contributes to carbohydrate metabolism in human skeletal muscle." Biochemical Journal 311, no. 2 (October 15, 1995): 517–21. http://dx.doi.org/10.1042/bj3110517.

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To determine whether fructose can be utilized as a metabolic substrate for skeletal muscle in man, we investigated its incorporation into glycogen, its oxidation and lactate production in isolated human skeletal muscle. Rates of fructose oxidation and incorporation into glycogen increased in the presence of increasing fructose concentrations (0.1-1.0 mM). Lactate production increased 3-fold when extracellular fructose was increased from 0.1 to 0.5 mM. Cytochalasin B, a competitive inhibitor of hexose transport mediated by the GLUT1 and GLUT4 facilitative glucose transporters, completely inhibi

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Santarelli, Lindsey Ciali, Jianguo Chen, Stefan H. Heinemann та Toshinori Hoshi. "The β1 Subunit Enhances Oxidative Regulation of Large-Conductance Calcium-activated K+ Channels". Journal of General Physiology 124, № 4 (27 вересня 2004): 357–70. http://dx.doi.org/10.1085/jgp.200409144.

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Oxidative stress may alter the functions of many proteins including the Slo1 large conductance calcium-activated potassium channel (BKCa). Previous results demonstrated that in the virtual absence of Ca2+, the oxidant chloramine-T (Ch-T), without the involvement of cysteine oxidation, increases the open probability and slows the deactivation of BKCa channels formed by human Slo1 (hSlo1) α subunits alone. Because native BKCa channel complexes may include the auxiliary subunit β1, we investigated whether β1 influences the oxidative regulation of hSlo1. Oxidation by Ch-T with β1 present shifted t

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15

Poggetti, R. S., E. E. Moore, F. A. Moore, K. Koike, R. Tuder, B. O. Anderson, and A. Banerjee. "Quantifying oxidative injury in the liver." American Journal of Physiology-Gastrointestinal and Liver Physiology 268, no. 3 (March 1, 1995): G471—G479. http://dx.doi.org/10.1152/ajpgi.1995.268.3.g471.

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Oxidative injury is a mechanism common to both ischemia-reperfusion (IR) and leukocyte-mediated injury. Reperfused tissue beds and elaborated mediators can activate a cascade of intercellular and interorgan injuries that often precipitates multiple organ failure. Initiation of lung injury by gut IR is a case in point, but concomitant liver injury may have been overlooked because of the absence of comparably sensitive physiological markers. In this study, we explore the hypothesis that occurrence of portally derived oxidant-induced liver dysfunction may be detected with both sensitivity and spe

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Webster, Keith A., Howard Prentice, and Nanette H. Bishopric. "Oxidation of Zinc Finger Transcription Factors: Physiological Consequences." Antioxidants & Redox Signaling 3, no. 4 (August 2001): 535–48. http://dx.doi.org/10.1089/15230860152542916.

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17

Drevet, Joël R., and Robert John Aitken. "Oxidation of Sperm Nucleus in Mammals: A Physiological Necessity to Some Extent with Adverse Impacts on Oocyte and Offspring." Antioxidants 9, no. 2 (January 23, 2020): 95. http://dx.doi.org/10.3390/antiox9020095.

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Sperm cells have long been known to be good producers of reactive oxygen species, while they are also known to be particularly sensitive to oxidative damage affecting their structures and functions. As with all organic cellular components, sperm nuclear components and, in particular, nucleic acids undergo oxidative alterations that have recently been shown to be commonly encountered in clinical practice. This review will attempt to provide an overview of this situation. After a brief coverage of the biological reasons why the sperm nucleus and associated DNA are sensitive to oxidative damage,

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18

Jonak, Katarzyna, Ida Suppanz, Julian Bender, Agnieszka Chacinska, Bettina Warscheid, and Ulrike Topf. "Ageing-dependent thiol oxidation reveals early oxidation of proteins with core proteostasis functions." Life Science Alliance 7, no. 5 (February 21, 2024): e202302300. http://dx.doi.org/10.26508/lsa.202302300.

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Oxidative post-translational modifications of protein thiols are well recognized as a readily occurring alteration of proteins, which can modify their function and thus control cellular processes. The development of techniques enabling the site-specific assessment of protein thiol oxidation on a proteome-wide scale significantly expanded the number of known oxidation-sensitive protein thiols. However, lacking behind are large-scale data on the redox state of proteins during ageing, a physiological process accompanied by increased levels of endogenous oxidants. Here, we present the landscape of

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Ranea-Robles, Pablo, and Sander M. Houten. "The biochemistry and physiology of long-chain dicarboxylic acid metabolism." Biochemical Journal 480, no. 9 (May 4, 2023): 607–27. http://dx.doi.org/10.1042/bcj20230041.

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Mitochondrial β-oxidation is the most prominent pathway for fatty acid oxidation but alternative oxidative metabolism exists. Fatty acid ω-oxidation is one of these pathways and forms dicarboxylic acids as products. These dicarboxylic acids are metabolized through peroxisomal β-oxidation representing an alternative pathway, which could potentially limit the toxic effects of fatty acid accumulation. Although dicarboxylic acid metabolism is highly active in liver and kidney, its role in physiology has not been explored in depth. In this review, we summarize the biochemical mechanism of the forma

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Allen, Tara J., and Christopher D. Hardin. "Influence of glycogen storage on vascular smooth muscle metabolism." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 6 (June 1, 2000): H1993—H2002. http://dx.doi.org/10.1152/ajpheart.2000.278.6.h1993.

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The role of glycogen as an oxidative substrate for vascular smooth muscle (VSM) remains controversial. To elucidate the importance of glycogen as an oxidative substrate and the influence of glycogen flux on VSM substrate selection, we systematically altered glycogen levels and measured metabolism of glucose, acetate, and glycogen. Hog carotid arteries with glycogen contents ranging from 1 to 11 μmol/g were isometrically contracted in physiological salt solution containing 5 mM [1-13C]glucose and 1 mM [1,2-13C]acetate at 37°C for 6 h. [1-13C]glucose, [1,2-13C]acetate, and glycogen oxidation wer

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Szrok-Jurga, Sylwia, Aleksandra Czumaj, Jacek Turyn, Areta Hebanowska, Julian Swierczynski, Tomasz Sledzinski, and Ewa Stelmanska. "The Physiological and Pathological Role of Acyl-CoA Oxidation." International Journal of Molecular Sciences 24, no. 19 (October 3, 2023): 14857. http://dx.doi.org/10.3390/ijms241914857.

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Fatty acid metabolism, including β-oxidation (βOX), plays an important role in human physiology and pathology. βOX is an essential process in the energy metabolism of most human cells. Moreover, βOX is also the source of acetyl-CoA, the substrate for (a) ketone bodies synthesis, (b) cholesterol synthesis, (c) phase II detoxication, (d) protein acetylation, and (d) the synthesis of many other compounds, including N-acetylglutamate—an important regulator of urea synthesis. This review describes the current knowledge on the importance of the mitochondrial and peroxisomal βOX in various organs, in

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Murray, Andrew J., Hugh E. Montgomery, Martin Feelisch, Michael P. W. Grocott, and Daniel S. Martin. "Metabolic adjustment to high-altitude hypoxia: from genetic signals to physiological implications." Biochemical Society Transactions 46, no. 3 (April 20, 2018): 599–607. http://dx.doi.org/10.1042/bst20170502.

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Ascent to high altitude is associated with physiological responses that counter the stress of hypobaric hypoxia by increasing oxygen delivery and by altering tissue oxygen utilisation via metabolic modulation. At the cellular level, the transcriptional response to hypoxia is mediated by the hypoxia-inducible factor (HIF) pathway and results in promotion of glycolytic capacity and suppression of oxidative metabolism. In Tibetan highlanders, gene variants encoding components of the HIF pathway have undergone selection and are associated with adaptive phenotypic changes, including suppression of

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Fischer, Manuel, Sebastian Horn, Anouar Belkacemi, Kerstin Kojer, Carmelina Petrungaro, Markus Habich, Muna Ali, et al. "Protein import and oxidative folding in the mitochondrial intermembrane space of intact mammalian cells." Molecular Biology of the Cell 24, no. 14 (July 15, 2013): 2160–70. http://dx.doi.org/10.1091/mbc.e12-12-0862.

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Oxidation of cysteine residues to disulfides drives import of many proteins into the intermembrane space of mitochondria. Recent studies in yeast unraveled the basic principles of mitochondrial protein oxidation, but the kinetics under physiological conditions is unknown. We developed assays to follow protein oxidation in living mammalian cells, which reveal that import and oxidative folding of proteins are kinetically and functionally coupled and depend on the oxidoreductase Mia40, the sulfhydryl oxidase augmenter of liver regeneration (ALR), and the intracellular glutathione pool. Kinetics o

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Vatrál, Jaroslav, Roman Boča, and Wolfgang Linert. "Oxidation properties of dopamine at and near physiological conditions." Monatshefte für Chemie - Chemical Monthly 146, no. 11 (September 1, 2015): 1799–805. http://dx.doi.org/10.1007/s00706-015-1560-2.

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25

Stanisz, Jolanta, Burton M. Wice, and David E. Kennell. "Serum factors that stimulate fatty acid oxidation: Physiological specificity." Journal of Cellular Physiology 126, no. 1 (January 1986): 141–46. http://dx.doi.org/10.1002/jcp.1041260119.

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Lee, Tae-Hee, and Tae-Hong Kang. "DNA Oxidation and Excision Repair Pathways." International Journal of Molecular Sciences 20, no. 23 (December 3, 2019): 6092. http://dx.doi.org/10.3390/ijms20236092.

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The physiological impact of the aberrant oxidation products on genomic DNA were demonstrated by embryonic lethality or the cancer susceptibility and/or neurological symptoms of animal impaired in the base excision repair (BER); the major pathway to maintain genomic integrity against non-bulky DNA oxidation. However, growing evidence suggests that other DNA repair pathways or factors that are not primarily associated with the classical BER pathway are also actively involved in the mitigation of oxidative assaults on the genomic DNA, according to the corresponding types of DNA oxidation. Among o

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27

Das, D., P. K. De, and R. K. Banerjee. "Thiocyanate, a plausible physiological electron donor of gastric peroxidase." Biochemical Journal 305, no. 1 (January 1, 1995): 59–64. http://dx.doi.org/10.1042/bj3050059.

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Gastric peroxidase (GPO) was purified to apparent homogeneity to characterize its major physiological electron donor. The enzyme (RZ = 0.7), with a subunit molecular mass of 50 kDa, is a glycoprotein, with a relative abundance of aspartic and glutamic acid over arginine and lysine. It has a Soret maximum at 412 nm, which is shifted to 426 nm by H2O2 due to formation of compound II. Although the physiological electron donors I-, Br- and SCN-, but not Cl-, are oxidized by GPO optimally at acid pH, only I- and SCN- are oxidized appreciably at physiological pH. Considering that the I- concentratio

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28

Pedersen, Line, Caroline Holkmann Olsen, Bente Klarlund Pedersen, and Pernille Hojman. "Muscle-derived expression of the chemokine CXCL1 attenuates diet-induced obesity and improves fatty acid oxidation in the muscle." American Journal of Physiology-Endocrinology and Metabolism 302, no. 7 (April 1, 2012): E831—E840. http://dx.doi.org/10.1152/ajpendo.00339.2011.

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Serum levels and muscle expression of the chemokine CXCL1 increase markedly in response to exercise in mice. Because several studies have established muscle-derived factors as important contributors of metabolic effects of exercise, this study aimed at investigating the effect of increased expression of muscle-derived CXCL1 on systemic and intramuscular metabolic parameters, with focus on fatty acid oxidation and oxidative metabolism in skeletal muscle. By overexpression of CXCL1 in the tibialis cranialis muscle in mice, significant elevations in muscle and serum CXCL1 within a physiological r

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Groop, L. C., R. C. Bonadonna, D. C. Simonson, A. S. Petrides, M. Shank, and R. A. DeFronzo. "Effect of insulin on oxidative and nonoxidative pathways of free fatty acid metabolism in human obesity." American Journal of Physiology-Endocrinology and Metabolism 263, no. 1 (July 1, 1992): E79—E84. http://dx.doi.org/10.1152/ajpendo.1992.263.1.e79.

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The dose-response relationship between the plasma insulin concentration and oxidative and nonoxidative pathways of free fatty acid (FFA) metabolism was examined in 11 obese and 7 lean subjects using a stepwise insulin clamp technique in combination with indirect calorimetry and infusion of [1-14C]palmitate. The fasting plasma FFA concentration was elevated in obese subjects (793 +/- 43 vs. 642 +/- 39 mumol/l; P less than 0.01) and was associated with an increased basal rate of plasma FFA turnover, FFA oxidation, and nonoxidative FFA disposal, i.e., reesterification (all P less than 0.01). Supp

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Zhang, Weiran, Ranwei Zhong, Xiangping Qu, Yang Xiang, and Ming Ji. "Effect of 8-Hydroxyguanine DNA Glycosylase 1 on the Function of Immune Cells." Antioxidants 12, no. 6 (June 19, 2023): 1300. http://dx.doi.org/10.3390/antiox12061300.

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Excess reactive oxygen species (ROS) can cause an imbalance between oxidation and anti-oxidation, leading to the occurrence of oxidative stress in the body. The most common product of ROS-induced base damage is 8-hydroxyguanine (8-oxoG). Failure to promptly remove 8-oxoG often causes mutations during DNA replication. 8-oxoG is cleared from cells by the 8-oxoG DNA glycosylase 1 (OGG1)-mediated oxidative damage base excision repair pathway so as to prevent cells from suffering dysfunction due to oxidative stress. Physiological immune homeostasis and, in particular, immune cell function are vulne

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Hondorp, Elise R., and Rowena G. Matthews. "Oxidation of Cysteine 645 of Cobalamin-Independent Methionine Synthase Causes a Methionine Limitation in Escherichia coli." Journal of Bacteriology 191, no. 10 (March 13, 2009): 3407–10. http://dx.doi.org/10.1128/jb.01722-08.

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ABSTRACT Cobalamin-independent methionine synthase (MetE) catalyzes the final step in Escherichia coli methionine biosynthesis but is inactivated under oxidative conditions, triggering a methionine deficiency. This study demonstrates that the mutation of MetE cysteine 645 to alanine completely eliminates the methionine auxotrophy imposed by diamide treatment, suggesting that modulation of MetE activity via cysteine 645 oxidation has significant physiological consequences for oxidatively stressed cells.

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Kanemura, Shingo, Elza Firdiani Sofia, Naoya Hirai, Masaki Okumura, Hiroshi Kadokura, and Kenji Inaba. "Characterization of the endoplasmic reticulum–resident peroxidases GPx7 and GPx8 shows the higher oxidative activity of GPx7 and its linkage to oxidative protein folding." Journal of Biological Chemistry 295, no. 36 (July 21, 2020): 12772–85. http://dx.doi.org/10.1074/jbc.ra120.013607.

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Oxidative protein folding occurs primarily in the mammalian endoplasmic reticulum, enabled by a diverse network comprising more than 20 members of the protein disulfide isomerase (PDI) family and more than five PDI oxidases. Although the canonical disulfide bond formation pathway involving Ero1α and PDI has been well-studied so far, the physiological roles of the newly identified PDI oxidases, glutathione peroxidase-7 (GPx7) and -8 (GPx8), are only poorly understood. We here demonstrated that human GPx7 has much higher reactivity with H2O2 and hence greater PDI oxidation activity than human GP

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Rasmusson, Allan G., and Sabá V. Wallström. "Involvement of mitochondria in the control of plant cell NAD(P)H reduction levels." Biochemical Society Transactions 38, no. 2 (March 22, 2010): 661–66. http://dx.doi.org/10.1042/bst0380661.

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NADPH and NADH mediate reductant flow between cellular processes, linking central carbon and energy metabolism with intermediary metabolism, stress defence and development. Recent investigations have revealed paths of functional interactions, and have suggested that mitochondrial NADPH oxidation, especially together with the oxidative pentose phosphate pathway, is an important regulator of the cytosolic NADPH reduction level. Furthermore, stress-dependent metabolic pathways substantially affect the NADPH reduction level in particular physiological situations. The mitochondrial impact on the NA

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Timoshnikov, Viktor A., Lilia A. Kichigina, Olga Yu Selyutina, Nikolay E. Polyakov, and George J. Kontoghiorghes. "Antioxidant Activity of Deferasirox and Its Metal Complexes in Model Systems of Oxidative Damage: Comparison with Deferiprone." Molecules 26, no. 16 (August 20, 2021): 5064. http://dx.doi.org/10.3390/molecules26165064.

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Deferasirox is an orally active, lipophilic iron chelating drug used on thousands of patients worldwide for the treatment of transfusional iron overload. The essential transition metals iron and copper are the primary catalysts of reactive oxygen species and oxidative damage in biological systems. The redox effects of deferasirox and its metal complexes with iron, copper and other metals are of pharmacological, toxicological, biological and physiological importance. Several molecular model systems of oxidative damage caused by iron and copper catalysis including the oxidation of ascorbic acid,

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Tretter, Verena, Beatrix Hochreiter, Marie Louise Zach, Katharina Krenn, and Klaus Ulrich Klein. "Understanding Cellular Redox Homeostasis: A Challenge for Precision Medicine." International Journal of Molecular Sciences 23, no. 1 (December 22, 2021): 106. http://dx.doi.org/10.3390/ijms23010106.

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Living organisms use a large repertoire of anabolic and catabolic reactions to maintain their physiological body functions, many of which include oxidation and reduction of substrates. The scientific field of redox biology tries to understand how redox homeostasis is regulated and maintained and which mechanisms are derailed in diverse pathological developments of diseases, where oxidative or reductive stress is an issue. The term “oxidative stress” is defined as an imbalance between the generation of oxidants and the local antioxidative defense. Key mediators of oxidative stress are reactive

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Hernández, José A., Rosa C. López-Sánchez, and Adela Rendón-Ramírez. "Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/1543809.

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The excessive intake of alcohol is a serious public health problem, especially given the severe damage provoked by chronic or prenatal exposure to alcohol that affects many physiological processes, such as memory, motor function, and cognitive abilities. This damage is related to the ethanol oxidation in the brain. The metabolism of ethanol to acetaldehyde and then to acetate is associated with the production of reactive oxygen species that accentuate the oxidative state of cells. This metabolism of ethanol can induce the oxidation of the fatty acids in phospholipids, and the bioactive aldehyd

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Zannini, Flavien, Johannes M. Herrmann, Jérémy Couturier, and Nicolas Rouhier. "Oxidation of Arabidopsis thaliana COX19 Using the Combined Action of ERV1 and Glutathione." Antioxidants 12, no. 11 (November 1, 2023): 1949. http://dx.doi.org/10.3390/antiox12111949.

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Protein import and oxidative folding within the intermembrane space (IMS) of mitochondria relies on the MIA40–ERV1 couple. The MIA40 oxidoreductase usually performs substrate recognition and oxidation and is then regenerated by the FAD-dependent oxidase ERV1. In most eukaryotes, both proteins are essential; however, MIA40 is dispensable in Arabidopsis thaliana. Previous complementation experiments have studied yeast mia40 mutants expressing a redox inactive, but import-competent versions of yeast Mia40 using A. thaliana ERV1 (AtERV1) suggest that AtERV1 catalyzes the oxidation of MIA40 substra

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Takahama, Umeo. "Oxidation of vacuolar and apoplastic phenolic substrates by peroxidase: Physiological significance of the oxidation reactions." Phytochemistry Reviews 3, no. 1-2 (January 2004): 207–19. http://dx.doi.org/10.1023/b:phyt.0000047805.08470.e3.

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Sarkar, Bipul, Arnab Kumar De, and M. K. Adak. "Physiological characterization of SUB1 trait in rice under subsequent submergence and re-aeration with interaction of chemical elicitors." Plant Science Today 4, no. 4 (November 27, 2017): 177–90. http://dx.doi.org/10.14719/pst.2017.4.4.351.

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In the present study, the sensitivity of two chemical elicitors: polyamine (PA) and salicylic (SA) acid were exercised for submergence sensitivity in Swarna Sub1A rice variety. Under 5 days of submergence, the antioxidation responses were more distinguished in plants against control. Along with the anti-oxidation modules, significant changes in biomolecule loss were registered through lipid and protein oxidation by 1.91 and 1.46 -fold respectively. PA and SA treated plants were the reliever to recover the membrane potential. Total carbohydrate and reducing sugars were varied under submergence

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Dulloo, A. G., S. Samec, and J. Seydoux. "Uncoupling protein 3 and fatty acid metabolism." Biochemical Society Transactions 29, no. 6 (November 1, 2001): 785–91. http://dx.doi.org/10.1042/bst0290785.

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A role for uncoupling protein (UCP) 3 in fatty acid metabolism is reviewed within the context of our proposal, first put forward in 1998, that this homologue of UCP1 may be involved in the regulation of lipids as fuel substrate rather than in the mediation of thermogenesis. Since then, the demonstrations of muscle-type differences in UCP3 gene regulation in response to dietary manipulations (starvation, high-fat feeding) or to pharmacological interferences with the flux of lipid substrates between adipose-tissue stores and skeletal-muscle mitochondrial oxidation are all in accord with this pro

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Yeh, Hsien-Wei, Kuan-Hung Lin, Syue-Yi Lyu, Yi-Shan Li, Chun-Man Huang, Yung-Lin Wang, Hao-Wei Shih, Ning-Shian Hsu, Chang-Jer Wu та Tsung-Lin Li. "Biochemical and structural explorations of α-hydroxyacid oxidases reveal a four-electron oxidative decarboxylation reaction". Acta Crystallographica Section D Structural Biology 75, № 8 (30 липня 2019): 733–42. http://dx.doi.org/10.1107/s2059798319009574.

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p-Hydroxymandelate oxidase (Hmo) is a flavin mononucleotide (FMN)-dependent enzyme that oxidizes mandelate to benzoylformate. How the FMN-dependent oxidation is executed by Hmo remains unclear at the molecular level. A continuum of snapshots from crystal structures of Hmo and its mutants in complex with physiological/nonphysiological substrates, products and inhibitors provides a rationale for its substrate enantioselectivity/promiscuity, its active-site geometry/reactivity and its direct hydride-transfer mechanism. A single mutant, Y128F, that extends the two-electron oxidation reaction to a

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Graham, Brian J., Ian W. Windsor, Brian Gold, and Ronald T. Raines. "Boronic acid with high oxidative stability and utility in biological contexts." Proceedings of the National Academy of Sciences 118, no. 10 (March 2, 2021): e2013691118. http://dx.doi.org/10.1073/pnas.2013691118.

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Despite their desirable attributes, boronic acids have had a minimal impact in biological contexts. A significant problem has been their oxidative instability. At physiological pH, phenylboronic acid and its boronate esters are oxidized by reactive oxygen species at rates comparable to those of thiols. After considering the mechanism and kinetics of the oxidation reaction, we reasoned that diminishing electron density on boron could enhance oxidative stability. We found that a boralactone, in which a carboxyl group serves as an intramolecular ligand for the boron, increases stability by 104-fo

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Bjugstad, Kimberly, Paul Gutowski, Jennifer Pekarek, Pamela Bourg, Charles Mains, and David Bar-Or. "Redox Changes in Amateur Race Car Drivers Before and After Racing." Sports Medicine International Open 1, no. 06 (October 2017): E212—E219. http://dx.doi.org/10.1055/s-0043-119065.

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AbstractDespite the unique opportunity race car driving provides to study exercise in extreme conditions, the sport of racing is under-represented. A better understanding of how racing changes physiological measures combined with driver demographics may help reduce driver risks and expand the field of driver science. This study charted the changes in heart rate, body temperature, blood pressure, static oxidation reduction potential (sORP), and antioxidant capacity in drivers before and after racing (n=23). The interaction between racing and driver characteristics on physiological variables wer

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POURCEL, L., J. ROUTABOUL, V. CHEYNIER, L. LEPINIEC, and I. DEBEAUJON. "Flavonoid oxidation in plants: from biochemical properties to physiological functions." Trends in Plant Science 12, no. 1 (January 2007): 29–36. http://dx.doi.org/10.1016/j.tplants.2006.11.006.

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Lian, Di, Ming-Ming Chen, Hanyu Wu, Shoulong Deng, and Xiaoxiang Hu. "The Role of Oxidative Stress in Skeletal Muscle Myogenesis and Muscle Disease." Antioxidants 11, no. 4 (April 11, 2022): 755. http://dx.doi.org/10.3390/antiox11040755.

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The contractile activity, high oxygen consumption and metabolic rate of skeletal muscle cause it to continuously produce moderate levels of oxidant species, such as reactive oxygen species (ROS) and reactive nitrogen species (RNS). Under normal physiological conditions, there is a dynamic balance between the production and elimination of ROS/RNS. However, when the oxidation products exceed the antioxidant defense capacity, the body enters a state of oxidative stress. Myogenesis is an important process to maintain muscle homeostasis and the physiological function of skeletal muscle. Accumulatin

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Elahi, Maqsood M., Yu Xiang Kong, and Bashir M. Matata. "Oxidative Stress as a Mediator of Cardiovascular Disease." Oxidative Medicine and Cellular Longevity 2, no. 5 (2009): 259–69. http://dx.doi.org/10.4161/oxim.2.5.9441.

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During physiological processes molecules undergo chemical changes involving reducing and oxidizing reactions. A molecule with an unpaired electron can combine with a molecule capable of donating an electron. The donation of an electron is termed as oxidation whereas the gaining of an electron is called reduction. Reduction and oxidation can render the reduced molecule unstable and make it free to react with other molecules to cause damage to cellular and sub-cellular components such as membranes, proteins and DNA. In this paper, we have discussed the formation of reactive oxidant species origi

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Bouayed, Jaouad, and Torsten Bohn. "Exogenous Antioxidants—Double-Edged Swords in Cellular Redox State: Health Beneficial Effects at Physiologic Doses versus Deleterious Effects at High Doses." Oxidative Medicine and Cellular Longevity 3, no. 4 (2010): 228–37. http://dx.doi.org/10.4161/oxim.3.4.12858.

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The balance between oxidation and antioxidation is believed to be critical in maintaining healthy biological systems. Under physiological conditions, the human antioxidative defense system including e.g., superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH) and others, allows the elimination of excess reactive oxygen species (ROS) including, among others superoxide anions (O2.-), hydroxyl radicals (OH.), alkoxyl radicals (RO.) and peroxyradicals (ROO.). However, our endogenous antioxidant defense systems are incomplete without exogenous originating reduci

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Alonso-Alvarez, Carlos, Sophie Bertrand, Bruno Faivre, Olivier Chastel, and Gabriele Sorci. "Testosterone and oxidative stress: the oxidation handicap hypothesis." Proceedings of the Royal Society B: Biological Sciences 274, no. 1611 (December 19, 2006): 819–25. http://dx.doi.org/10.1098/rspb.2006.3764.

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Secondary sexual traits (SST) are usually thought to have evolved as honest signals of individual quality during mate choice. Honesty of SST is guaranteed by the cost of producing/maintaining them. In males, the expression of many SST is testosterone-dependent. The immunocompetence handicap hypothesis has been proposed as a possible mechanism ensuring honesty of SST on the basis that testosterone, in addition to its effect on sexual signals, also has an immunosuppressive effect. The immunocompetence handicap hypothesis has received mixed support. However, the cost of testosterone-based signall

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Sun, Yi, Wen-Jia Zhang, Xin Zhao, Ren-Pei Yuan, Hui Jiang, and Xiao-Ping Pu. "PARK7 protein translocating into spermatozoa mitochondria in Chinese asthenozoospermia." REPRODUCTION 148, no. 3 (September 2014): 249–57. http://dx.doi.org/10.1530/rep-14-0222.

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PARK7 (DJ1) is a multifunctional oxidative stress response protein that protects cells against reactive oxygen species (ROS) and mitochondrial damage. PARK7 defects are known to cause various physiological dysfunctions, including infertility. Asthenozoospermia (AS), i.e. low-motile spermatozoa in the ejaculate, is a common cause of human male infertility. In this study, we found that downregulation of PARK7 resulted in increased levels of lipid peroxide and ROS, decreased mitochondrial membrane potential, and reduced mitochondrial complex I enzyme activity in the spermatozoa from AS patients.

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Ando, Chika, and Yasujiro Morimitsu. "A proposed antioxidation mechanism of ergothioneine based on the chemically derived oxidation product hercynine and further decomposition products." Bioscience, Biotechnology, and Biochemistry 85, no. 5 (January 21, 2021): 1175–82. http://dx.doi.org/10.1093/bbb/zbab006.

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ABSTRACT Ergothioneine (ERGO), a thiohistidine betaine, exists in various fungi, plants, and animals. Humans take in ERGO from their diet. ERGO is a strong biological antioxidant, but there are only a limited number of reports about its redox mechanism. The purpose of this study was to clarify the oxidation mechanism of ERGO. Reactions of ERGO with chemical oxidants were performed. The oxidation products of ERGO were analyzed by nuclear magnetic resonance and liquid chromatography-mass spectrometry (LC-MS). The major product of oxidation of ERGO by hydrogen peroxide in physiological conditions

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