Improved Erythrocyte Survival with High-Dose Vitamin E in Chronic Hemolyzing G6PD and Glutathione Synthetase Deficiencies
- S. P. SPIELBERG, M.D., Ph.D.;
- L. A. BOXER, M.D.;
- L. M. CORASH, M.D.; and
- J. D. SCHULMAN, M.D.
- National Institute of Child Health and Human Development Bethesda, Maryland Indiana University School of Medicine Indianapolis, Indiana
Excerpt
Glutathione (GSH) and vitamin E both play vital roles in the protection of cells from oxidative stress (1). Decreased reduced erythrocyte GSH resulting from inborn errors of metabolism is associated with hemolytic anemia (2). Hemolysis may be caused by endogenous or drug-induced oxidative damage to erythrocytes. Pharmacologic levels of vitamin E partially protect cells experimentally rendered GSH deficient in tissue culture and in vivo (3, 4). Therefore, we have examined the effects of chronic administration of high doses of vitamin E on erythrocyte survival in two patients with inherited disorders of GSH metabolism. Both patients have chronic hemolytic anemia, one
This 100-word excerpt has been provided in the absence of an abstract.
Acknowledgments
The authors thank Anthony Adams for technical assistance.
Article and Author Information
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This work was supported in part by U.S. Public Health Service Grants AI 13586 and AI 10894. Dr. L. A. Boxer is an Established Investigator of the American Heart Association.
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