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[Rotruck first established the selenium dependence of the GSH-peroxidase that relied on glucose-6-phosphate dehydrogenase-GSH-reductasedriven recycling of GSH to protect erythrocytes from oxidation (311, 312): in erythrocytes from selenium-deficient rats, glucose-mediated reduction of GSH had no protective effect against oxidation.] In fact, in studies of hydrogen peroxide metabolism in cultured cells from GPx-1-deficient and wild-type mice, exposure to hydrogen peroxide led to a transient increase in oxidized GSH in wild-type cells, whereas GSSG did not fluctuate in GPx-1-deficient cells (229)