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Blood, 1 September 2000, Vol. 96, No. 5, pp. 1985-1988

RED CELLS

Red cells from glutathione peroxidase-1-deficient mice have nearly normal defenses against exogenous peroxides

Robert M. Johnson, Gerard Goyette Jr, Yaddanapudi Ravindranath, and Ye-Shih Ho

From the Department of Biochemistry and Molecular Biology, the Department of Pediatrics, and the Institute of Chemical Toxicology, Wayne State Medical School, Detroit, MI.

The role of glutathione peroxidase in red cell anti-oxidant defense was examined using erythrocytes from mice with a genetically engineered disruption of the glutathione peroxidase-1 (GSHPx-1) gene. Because GSHPx-1 is the sole glutathione peroxidase in the erythrocyte, all red cell GSH peroxidase activity was eliminated. Oxidation of hemoglobin and membrane lipids, using the cis-parinaric acid assay, was determined during oxidant challenge from cumene hydroperoxide and H2O2. No difference was detected between wild-type red cells and GSHPx-1-deficient cells, even at high H2O2 exposures. Thus, GSHPx-1 appears to play little or no role in the defense of the erythrocyte against exposure to peroxide. Simultaneous exposure to an H2O2 flux and the catalase inhibitor 3-amino-1,2,4-triazole supported this conclusion. Hemoglobin oxidation occurred only when catalase was depleted. Circulating erythrocytes from the GSHPx-1-deficient mice exhibited a slight reduction in membrane thiols, indicating that high exposure to peroxides might occur naturally in the circulation.

© 2000 by The American Society of Hematology.
 

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