Oxidation as a possible mechanism of cellular aging: vitamin E deficiency causes premature aging and IgG binding to erythrocytes.
Open accessAbstract
Senescent-cell antigen is a "neo-antigen" that appears on the surface of senescent cells and initiates IgG binding and cellular removal. As an approach to evaluating oxidation as a possible mechanism for generation of senescent-cell antigen, we studied erythrocytes from vitamin E-deficient rats. Vitamin E is localized primarily in cellular membranes. Its major role is the termination of free-radical chain reactions propagated by the polyunsaturated fatty acids of membrane propagated by the polyunsaturated fatty acids of membrane phospholipids. Results of our studies indicate that erythrocytes of all ages from vitamin E-deficient rats behave like old erythrocytes from normal rats, as determined by their susceptibility to phagocytosis, IgG binding, anion transport ability, and glyceraldehyde-3-phosphate dehydrogenase activity. Increased breakdown products of band 3 were observed with immunoblotting in membranes of erythrocytes from vitamin E-deficient rats. Breakdown products of band 3 are known to increase as cells age in normal individuals. The data suggest that oxidation may be a possible mechanism for erythrocyte aging and generation of senescent-cell antigen in vivo.
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Malfunction of antioxidant defense and/or conditions of increased oxidant production have severe consequences for RBCs on a subcellular level.
“Malfunction of antioxidant defense and/or conditions of increased oxidant production have severe consequences for RBCs on a subcellular level.”
From Red Blood Cell Function and Dysfunction: Redox Regulation, Nitric Oxide Metabolism, Anemia (2017) · cites this paper as [96]
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- Authors
- Kay, M. M., Bosman, G. J., Shapiro, S. S., Bendich, A., & Bassel, P. S.
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1986-04
- Volume
- 83
- Issue
- 8
- Pages
- 2463-2467
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC323318
- OpenAlex
- W2140802223
- Cited by
- 130
- References
- 52
- Citations by year
- 2024: 1 · 2022: 4 · 2021: 3 · 2020: 2 · 2019: 1 · 2017: 1 · 2016: 3 · 2015: 3 · 2012: 3
- FWCI
- 5.58
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- OakTrust (Texas A&M University Libraries) (submittedVersion)
- Topics
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Erythrocyte Function and Pathophysiology
- Keywords
- cellular aging, vitamin E deficiency, erythrocyte aging, IgG binding, oxidative stress, free radicals, membrane phospholipids, phagocytosis, anion transport, glyceraldehyde-3-phosphate dehydrogenase, premature aging
- MeSH terms
- Anemia, Hemolytic, Animals, Anions, Anion Exchange Protein 1, Erythrocyte, Biological Transport, Erythrocyte Aging, Erythrocyte Membrane, Free Radicals, Glyceraldehyde-3-Phosphate Dehydrogenases, Haptoglobins, Lipid Peroxides, Oxidation-Reduction, Phagocytosis, Vitamin E Deficiency, Rats
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