Studies were undertaken to determine whether or not dietary selenium (Se), as sodium selenite, at suboptimal (unsupplemented torula yeast diets, 0.02 ppm Se) or supplemented up to dietary excess, but nontoxic, levels (5.0 ppm Se) could selectively modify hepatic and renal reduced glutathione (GSH) levels and the enzymes involved in GSH metabolism. Male rats were provided torula yeast semipurified diets containing approximately 0.02 ppm Se in the basal diet and supplements of 0.1, 2.0, or 5.0 ppm Se for 3 or 6 weeks. Hepatic GSH increased in a nonlinear manner, with increasing dietary Se at both time points. Renal GSH was not similarly influenced. Neither hepatic nor renal gamma-glutamylcysteine synthetase or gamma-glutamyl transpeptidase activities are altered by supplements of Se. This suggests that synthetic and degradation enzyme activities are not influenced by Se. The capacity for the maintenance of GSH in the reduced state by glutathione reductase activity increased with increasing levels of dietary Se in the liver but not in the kidney. In both tissues greater Se supplements yielded greater tissue burdens of Se. These results suggest that GSH metabolism in hepatic and renal systems is differentially mediated, and the basis for these differences could be influenced by the relative levels in glutathione metabolizing enzymes.