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Glutathione peroxidase: the primary agent for the elimination of hydrogen peroxide in erythrocytes.
Gerald Cohen,Paul Hochstein +1 more
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This article is published in Biochemistry.The article was published on 1963-11-01. It has received 658 citations till now. The article focuses on the topics: Glutathione peroxidase & Peroxidase.read more
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Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase
TL;DR: Glutathione peroxidase activity is found to be associated with a relatively stable, nondialyzable, heat-labile, intracellular component which is separable from hemoglobin, by gel filtration and ammonium sulfate precipitation.
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Selenium: Biochemical Role as a Component of Glutathione Peroxidase
TL;DR: When hemolyzates from erythrocytes of selenium-deficient rats were incubated in vitro in the presence of ascorbate or H2O2, added glutathione failed to protect the hemoglobin from oxidative damage.
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Uric acid provides an antioxidant defense in humans against oxidant- and radical-caused aging and cancer: a hypothesis.
TL;DR: It is shown that, at physiological concentrations, urate reduces the oxo-heme oxidant formed by peroxide reaction with hemoglobin, protects erythrocyte ghosts against lipid peroxidation, and protects ERYthrocytes from peroxidative damage leading to lysis.
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Radical-free biology of oxidative stress
TL;DR: Data is summarized supporting a complementary hypothesis for oxidative stress in disease that can occur without free radicals, which is that oxidative stress occurs as a consequence of disruption of thiol redox circuits, which normally function in cell signaling and physiological regulation.
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Induction of manganous superoxide dismutase by tumor necrosis factor: possible protective mechanism.
TL;DR: TNF-alpha induced MnSOD mRNA in all cell lines and normal cells examined in vitro and in various organs of mice in vivo, which may contribute to their reported protective activity against radiation as well as their ability to induce resistance to cell killing induced by the combination of TNF- alpha and cycloheximide.
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The metabolic basis of inherited disease
TL;DR: The metabolic basis of inherited disease, the metabolic basis for inherited disease as mentioned in this paper, The metabolic basis in inherited disease and inherited diseases, and inherited disease diagnosis and management, in the context of inherited diseases
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Microdetermination of oxyhemoglobin, methemoglobin, and sulfhemoglobin in a single sample of blood
TL;DR: The concentration of SHb in a solution containing HbOt, MHb, and SHb is proportional to the residual optical density of the solution after the MHb has been converted into MHbCN by addition of cyanide.
Journal ArticleDOI
Hemoglobin catabolism. I. Glutathione peroxidase, an erythrocyte enzyme which protects hemoglobin from oxidative breakdown.
TL;DR: The most plausible route for the conversion of hemoglobin into biliverdin in vivo is through the oxidation and opening of the tetrapyrrole ring, after which the globin and iron are removed as discussed by the authors.
I. glutathione peroxidase, an erythrocyte enzyme which protects hemoglobin from oxidative breakdown*
TL;DR: Although the exact mechanism of the conversion of hemoglobin into biliverdin in vivo is still in doubt, the most plausible route is through the oxidation and opening of the tetrapyrrole ring, after which the globin and iron are removed.