| First Author | Johnson RM | Year | 2000 |
| Journal | Blood | Volume | 96 |
| Issue | 5 | Pages | 1985-8 |
| PubMed ID | 10961904 | Mgi Jnum | J:64216 |
| Mgi Id | MGI:1888868 | Doi | 10.1182/blood.v96.5.1985.h8001985_1985_1988 |
| Citation | Johnson RM, et al. (2000) Red cells from glutathione peroxidase-1-deficient mice have nearly normal defenses against exogenous peroxides. Blood 96(5):1985-8 |
| abstractText | 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 H(2)O(2). No difference was detected between wild-type red cells and GSHPx-1-deficient cells, even at high H(2)O(2) 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 H(2)O(2) 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. (Blood. 2000;96:1985-1988) |
