Cited by 130Antioxidant Activity and Oxidative StressGenetics, Aging, and Longevity in Model OrganismsErythrocyte Function and Pathophysiology

Oxidation as a possible mechanism of cellular aging: vitamin E deficiency causes premature aging and IgG binding to erythrocytes.

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Kay, M M, Bosman, G J, Shapiro, S S, Bendich, A, Bassel, P S·1986·Proceedings of the National Academy of Sciences

Abstract

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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  1. [2]Kay, M. M. B. (1975) Proc. Natl. Acad. Sci. USA 72, 3521–3525.
  2. [8]Kay, M. M. B. (1982) in Protides of the Biological Fluids Molecular 29, ed. Peeters, C. (Pergamon, Oxford), pp. 325–328.
  3. [17]Tannert, C. H. (1978) Dissertation (Humbolt University, Berlin).
  4. [20]Khansari, N., Springer, G. F., Merler, E. & Fudenberg, H. H. (1983) Mech. Ageing Dev. 21, 49–58.
  5. [26]Kay, M. M. B., Goodman, S., Whitfield, C., Wong, P., Zaki, L. & Rudloff, V. (1983) Proc. Natl. Acad. Sci. USA 80, 1631–1635.
  6. [27]Kay, M. M. B. (1984) Proc. Natl. Acad. Sci. USA 81, 5753–5757.
  7. [28]Kay, M. M. B., Tracey, C., Goodman, J., Cone, J. C. & Bassel, P. S. (1983) Proc. Natl. Acad. Sci. USA 80, 6882–6886.
  8. [36]Menzel, D. B. (1980) in Vitamin E: A Comprehensive Treatise, ed. Machlin, L. J. (Dekker, New York), pp. 473–494.
  9. [37]Walton, J. R. & Packer, L. (1980) in Vitamin E: A Comprehensive Treatise, ed. Machlin, L. J. (Dekker, New York), pp. 495–518.
  10. [40]Chiu, D., Lubin, B. & Shohet, S. B. (1982) in Free Radicals in Biology, ed. Pryor, W. (Academic, New York), Vol. 5, pp. 115–160.
  11. [46]Oski, F. A. (1983) in Hematology, eds. Williams, W. J., Beutler, E., Erslev, A. J. & Lictman, M. A. (McGraw-Hill, New York), pp. 532–537.
  12. [52]Bendich, A., Gabriel, E. & Machlin, L. J. (1983) Proc. Soc. Exp. Biol. Med. 172, 297–300.
  13. [53]Kay, M. M. B., in Methods in Hematology: Red Cell Membranes, eds. Shohet, S. & Mohandas, N. (Churchill-Livingston, New York), in press.
  14. [55]Towbin, H., Staehelin, T. & Gordon, J. (1979) Proc. Natl. Acad. Sci. USA 76, 4350–4354.

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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
Published
1986-04
Volume
83
Issue
8
Pages
2463-2467
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
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
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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