Toy P, Hatfield S, Bull R, Couri D
Res Commun Chem Pathol Pharmacol. 1978 Jul;21(1):115-31.
Studies were conducted in an attempt to define a biochemical index of selenium toxicity rather than weight loss, liver disease and death. Rats, maintained on selenium deficient diets, received in drinking water various levels of selenium as Na2SeO3(0.1, 1.0, 1.5, 2.0 ppm). Changes in selenium dependent glutathione peroxidase (GSH-Px) activities and specific activities (nCi75Se/ug Se) were determined in liver, kidney and plasma at baseline and two and ten weeks after repletion. In intial selenium deficient rats, GSH-Px activities were markedly depressed and specific activities elevated as compared to 0.1 ppm controls. After two weeks, liver and plasma GSH-Px activiities increased, and plasma, liver and kidney specific activities decreased in a concentration dependent manner. In kidney, there were no differences in enzyme activity at either two or ten weeks. At ten weeks, liver GSH-Px activities continued to increase in the 1.0 ppm group, but were depressed at both the 1.5 and 2.0 ppm levels. Specific activities were also depressed in liver and excretion was not increased at these levels. This suggests a biochemical toxicity in liver at levels above 1.0 ppm after ten weeks, prior to the onset of gross pathological changes.
开展了多项研究，旨在确定硒中毒的生化指标，而非体重减轻、肝病和死亡情况。给维持在缺硒饮食状态下的大鼠饮用含不同水平硒（以亚硒酸钠形式，0.1、1.0、1.5、2.0 ppm）的水。在补充硒之前、补充后两周和十周时，测定肝脏、肾脏和血浆中硒依赖性谷胱甘肽过氧化物酶（GSH-Px）的活性及比活性（nCi75Se/μg硒）。在初始缺硒的大鼠中，与0.1 ppm对照组相比，GSH-Px活性显著降低，比活性升高。两周后，肝脏和血浆中的GSH-Px活性增加，血浆、肝脏和肾脏的比活性呈浓度依赖性降低。在肾脏中，两周和十周时酶活性均无差异。十周时，1.0 ppm组肝脏中的GSH-Px活性持续增加，但在1.5和2.0 ppm水平时降低。肝脏中的比活性也降低，且在这些水平时排泄并未增加。这表明十周后，在明显病理变化出现之前，硒水平高于1.0 ppm时肝脏存在生化毒性。
