铬酸盐肾毒性的个体发生变化与谷胱甘肽氧化还原系统相关。

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

作者信息

Appenroth D

机构信息

Institute of Pharmacology and Toxicology, Friedrich Schiller University, Jena, Fed. Rep. of Germany.

出版信息

J Trace Elem Electrolytes Health Dis. 1994 Mar;8(1):33-6.

PMID:7804027

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.

摘要

研究了谷胱甘肽（GSH）浓度和谷胱甘肽二硫化物（GSSG）还原酶活性在铬酸盐肾毒性年龄差异中的作用。分别给幼年和成年大鼠注射2和1mg铬酸钠/100g体重，这使得肾组织中的铬浓度相等。幼年大鼠的铬肾毒性低于成年大鼠。结果表明，铬酸盐注射30分钟后，成年大鼠肾组织中的GSSG还原酶活性增加，而幼年大鼠则降低。苯巴比妥预处理可使幼年大鼠的GSSG还原酶活性增加。结果是蛋白尿显示铬酸盐肾毒性增强。幼年大鼠的肾GSH浓度较低，限制了这些动物体外铬酸盐的还原。因此，N-乙酰半胱氨酸预处理可增加GSH浓度，显著增强铬酸盐肾毒性。这些结果反映了GSH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。