Role of vitamin E in glutathione-induced oxidant stress: methemoglobin, lipid peroxidation, and hemolysis
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Red blood cells (RBC) from normal and vitamin E-deficient rats were incubated in a hypertonic solution of reduced glutathione adjusted to pH 8. Methemoglobin formation occurred in intact RBC from both normal and vitamin E-deficient rats. Hemolysis was significantly greater in RBC from vitamin E-deficient rats. Experiments with catalase, superoxide dismutase, and methional showed that H(2)O(2) was the primary extracellular source of oxidant stress. Extracellular superoxide and hydroxyl radical were not involved in oxidant stress. Experiments with dimethyl sulfoxide showed that intracellular hydroxyl radical, generated from H(2)O(2), was the hemolytic agent. Neither methemoglobin formation nor lipid peroxidation involved hydroxyl radical. Indeed, lipid peroxidation and hemolysis in RBC from vitamin E-deficient rats were concurrent rather than consecutive events. Phase contrast microscopy showed that rigid, crenated RBC with a precipitate around the interior periphery formed during glutathione-induced oxidant stress. The precipitate dissolved slowly as the crenated RBC were converted to smooth ghosts. It appeared that protein precipitates involving mixed disulfide bonds were reduced and solubilized when extracellular glutathione penetrated the ruptured cell. Comparisons between normal RBC and vitamin E-deficient RBC suggest that vitamin E has little effect on the inward diffusion of extra-cellular H(2)O(2). Vitamin E apparently interacts with different oxidant species derived from intracellular H(2)O(2) in preventing lipid peroxidation and the sulfhydryl group oxidation leading to hemolysis.
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Recycling of α-tocopherol radicals occurs by the oxidation of ascorbate.
“It was demonstrated that recycling of α-tocopherol radicals, next to diffusion of new molecules out of plasma, occurs by the oxidation of ascorbate (24, 121).”
From Red Blood Cell Function and Dysfunction: Redox Regulation, Nitric Oxide Metabolism, Anemia (2017) · cites this paper as [24]
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- Authors
- Brownlee, N. R., Huttner, J. J., Panganamala, R. V., & Cornwell, D. G.
- Affiliations
- The Ohio State University (US)
- Venue
- Journal of Lipid Research
- Publisher
- Elsevier BV
- Published
- 1977-09
- Volume
- 18
- Issue
- 5
- Pages
- 635-644
- ISSN
- 0022-2275 (ISSN-L)
- OpenAlex
- W2125227227
- Cited by
- 99
- References
- 55
- Citations by year
- 2024: 1 · 2023: 3 · 2021: 1 · 2020: 1 · 2019: 1 · 2017: 1 · 2016: 3 · 2013: 2 · 2012: 3
- FWCI
- 10.02
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Lipid Research (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Topics
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Physiology › Erythrocyte Function and Pathophysiology
- Keywords
- vitamin E deficiency, glutathione, oxidative stress, methemoglobin, lipid peroxidation, hemolysis, erythrocytes, hydrogen peroxide, hydroxyl radicals, superoxide, catalase, superoxide dismutase, methionine, sulfhydryl oxidation, cell ghosts
- MeSH terms
- Animals, Catalase, Chromatography, Gas, Dimethyl Sulfoxide, Erythrocytes, Glutathione, Hemolysis, Lipids, Male, Methemoglobin, Microscopy, Phase-Contrast, Oxygen Consumption, Peroxidases, Superoxide Dismutase, Vitamin E Deficiency, Rats
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