Ontogenic changes in the nephrotoxicity of chromate correlate with the glutathione oxidoreduction system.

D Appenroth
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Abstract

The role of GSH concentration and GSSG reductase activity in age differences in chromate nephrotoxicity was investigated. Young and adult rats were injected with 2 and 1 mg sodium chromate/100 g body weight (BW), respectively, which led to equal Cr concentrations in renal tissue. Cr nephrotoxicity was lower in young than in adult rats. It was shown that from 30 minutes after the chromate injection GSSG reductase activity in renal tissue was increased in adult but decreased in young rats by the chromate. GSSG reductase activity was increased in young rats by pretreatment with phenobarbital. The consequence was an enhancement of chromate nephrotoxicity as shown by proteinuria. Renal GSH concentration is lower in young rats and limiting for chromate reduction in vitro in these animals. Therefore, GSH concentration was increased by pretreatment with N-acetylcysteine, which enhanced chromate nephrotoxicity significantly. These results reflect the important role of the GSH oxidoreduction system in chromate nephrotoxicity and its relationship to age differences.

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铬酸盐肾毒性的个体变化与谷胱甘肽氧化还原系统有关。
研究了GSH浓度和GSSG还原酶活性在铬酸盐肾毒性年龄差异中的作用。幼龄大鼠和成年大鼠分别注射2 mg /100 g体重的铬酸钠和1 mg /100 g体重的铬酸钠,使肾组织中铬浓度相等。幼鼠肾毒性低于成年大鼠。结果表明,注射铬酸盐30分钟后,成年大鼠肾组织GSSG还原酶活性升高,而幼鼠肾组织GSSG还原酶活性降低。苯巴比妥预处理能提高幼龄大鼠GSSG还原酶活性。结果是铬酸盐肾毒性的增强,如蛋白尿所示。幼龄大鼠肾GSH浓度较低,限制了这些动物体外铬酸盐还原。因此,n -乙酰半胱氨酸预处理使GSH浓度升高,显著增强了铬酸盐的肾毒性。这些结果反映了谷胱甘肽氧化还原系统在铬酸盐肾毒性中的重要作用及其与年龄差异的关系。
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