A study was designed to assess the effects of a high-protein diet on the activities of several enzymes involved in the cellular antioxidative defence mechanism. Two strains of mice, a senescence-prone series (SAM-P/1) and a senescence-resistant series (SAM-R/1), were each divided into two groups, and fed either a control (20% casein) or a high-protein (40% casein) diet, respectively, for 11 months from the age of 2 months. Blood and liver were assayed for specific activities of catalase, superoxide dismutase (SOD), and glutathione peroxidase, and the levels of oxidized protein. Ingestion of the high-protein diet decreased the specific activity of catalase in the erythrocytes from both strains of mice, and decreased that of SOD in liver from both strains of mice; however the activity of SOD in erythrocytes from SAM-R/1 was increased. In accordance with these changes, ingestion of the high-protein diet produced an increase in the level of oxidized protein, compared with ingestion the control diet, in erythrocytes from SAM-R/1, and a much more significant increase in erythrocytes from SAM-P/1. There was also an increase in the level of oxidized protein in plasma from SAM-P/1. These results are largely, if not completely, consistent with the notion that high-protein ingestion accelerates the cellular aging process by augmenting the level of oxidized protein in erythrocytes.
The effects of selenium deficiency on the antioxidative status of erythrocytes from male SAM-R/1 mice were studied. The erythrocytes were obtained from mice fed Torula yeast-based, Se-deficient and Se-adequate diets for one year. The erythrocytes obtained were separated into 4 fractions of different cell density by densitygradient centrifugation, and the respective fractions were compared for activities of glutathione peroxidase (GSHPx), superoxide dismutase and catalase and for the levels of oxidized protein. Se deficiency depressed GSHPx activities significantly (about 90%) in all 4 density fractions, but depressed superoxide dismutase and catalase activities non-significantly in the respective density fractions and also in the whole erythrocyte fraction. The levels of oxidized protein were significantIy higher in the 3 low-density fractions from Se-deficient mice than in the corresponding fractions from Se-adequate mice. These results indicate that Se deficiency impairs cellular antioxidative status, inflicts oxidative damage on erythrocytes, and accelerates their aging.