| Abstract: | Selenium deficiency causes a fall in rat cardiac glutathione peroxidase activity. As a consequence, isolated perfused selenium-deficient heart does not release increased amounts of GSSG when hydroperoxide is infused. However, the total amount of glutathione measured as intracellular GSH, intracellular GSSG and GSSG released from the heart when hydroperoxide is infused does not equal the total glutathione measured in these pools in untreated hearts (Xia, Y., Hill, K.E. and Burk, R.F. (1985) J. Nutr. 115, 733-742). GSSG can react with protein sulfhydryl groups to form glutathione-protein mixed disulfides (PrS-SG). PrS-SG were measured in perfused selenium-deficient and control hearts infused with t-butylhydroperoxide and were found to account for the previously unmeasured glutathione. The ability of the selenium-deficient heart to transport GSSG was also examined. GSSG was produced non-enzymatically by infusing diamide. The diamide-treated selenium-deficient heart formed GSSG and released it at the same rate as similarly-treated control heart. Thus although selenium deficiency decreases GSSG formation by glutathione peroxidase, it does not affect cardiac GSSG transport. |
