When hemolyzates from erythrocytes of selenium-deficient rats were incubated in vitro in the presence of ascorbate or H(2)O(2), added glutathione failed to protect the hemoglobin from oxidative damage. This occurred because the erythrocytes were practically devoid of glutathione-peroxidase activity. Extensively purified preparations of glutathione peroxidase contained a large part of the (75)Se of erythrocytes labeled in vivo. Many of the nutritional effects of selenium can be explained by its role in glutathione peroxidase.

Experiments were conducted with male rats to quantitate the relation ship between dietary selenium (Se) intake and the amount of the enzyme glutathione peroxidase (GSH-Px) in erythrocytes and liver. Weanling male rats were fed torula yeast-based diets with 0, 0.05, 0.1, 0.5, 1.0, or 5.0 ppm Se supplemented as sodium selenite. Liver GSH-Px fell to undetectable levels (<1% of that found in the weanling rats) within 24 days in the O ppm Se group; feeding 0.1 ppm Se, or greater, caused liver GSH-Px to increase above that found in the weanling rats. The erythrocyte GSH-Px response to lack of dietary Se was somewhat smaller in magnitude and more gradual; however, only 21% of initial erythrocyte GSH-Px activity remained in the unsupplemented group after 66 days. Increased dietary Se resulted in corresponding increases of erythrocyte GSH-Px activity. Resupplementing with 0.1, 0.5, or 5.0 ppm Se elevated the depressed erythrocyte GSH-Px levels of the deficient rats. Increased dietary Se provided for both faster elevation, and higher maximal GSH-Px activity which in all cases was achieved 60 to 90 days after resupplementation. The results suggest that tissue GSH-Px can be used as an indicator of animal Se status, but other factors such as age, sex, and dietary vitamin E may have to be considered. Lack of GSH-Px in livers of Se-deficient rats may explain the liver necrosis observed when the diet is also deficient in vitamin E and sulfur-containing amino acids.

Japanese quail given 20 parts per million of mercury as methylmercury in diets containing 17 percent (by weight) tuna survived longer than quail given this concentration of methylmercury in a corn-soya diet. Tuna has a relatively high content of selenium and tends to accumulate additional selenium when mercury is present. A content of selenium in the diet comparable to that supplied by tuna decreased methylmercury toxicity in rats. Selenium in tuna, far from being a hazard in itself, may lessen the danger to man of mercury in tuna.

SUMMARY Age‐associated changes in the chemical composition of bovine biceps femoris muscle were studied. Veal muscle had significantly lower Kjeldahl nitrogen and higher moisture contents than muscle from the three older age groups studied. Muscle from veal and from the oldest group (cows, 10 years) possessed less fat than muscle from the two intermediate groups (steers, 1–2 years, and cows, 5 years). A modified procedure for determination of hydroxyproline and its use directly on mean hydrolysates are described. Use of this technique failed to reveal any significant differences in the hydroxyproline content, and presumably the connective‐tissue content, of muscle from the four groups. Warner‐Bratzler shear‐force values of cores from biceps femoris steaks from the three oldest groups indicated that tenderness decreased with age. A method is given for isolation of large quantities of connective tissue from biceps femoris. Chemical analyses of these connective‐tissue residues are presented, and the possibility is discussed that the veal connective tissue contains large amounts of reticulin.

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