Gstraunthaler G, Pfaller W, Kotanko P
Biochem Pharmacol. 1983 Oct 1;32(19):2969-72. doi: 10.1016/0006-2952(83)90404-5.
Nephrotoxic acute renal failure was experimentally induced in male rats by s.c. application of mercuric chloride and i.p. administration of maleate, respectively. Mercuric chloride and maleate are known to enhance the formation of free radicals and peroxides, which presumably overload the cell's natural elimination mechanisms for these highly reactive intermediates. In addition, a reduction in activities of superoxide dismutase, catalase and glutathione-peroxidase, enzymes responsible for the protection of cells against peroxidative action of superoxide anions and hyperperoxides was found. In both models of acute renal failure, enhanced lipid peroxidation in kidney homogenates in vitro, monitored as malondialdehyde production, was observed. Furthermore, HgCl2 and maleate may react with free SH-groups and thus lead to a depletion of glutathione in tubular cells. Indeed, renal cortical contents of reduced and oxidized glutathione were drastically diminished. These results suggest that alterations in membrane integrity, possibly caused by peroxidative processes, can be considered the cause underlying the well-known disturbances in renal function commonly observed during the initiation phase of HgCl2 and maleate induced acute renal failure.
通过分别皮下注射氯化汞和腹腔注射马来酸盐，在雄性大鼠中实验性诱导肾毒性急性肾衰竭。已知氯化汞和马来酸盐会增强自由基和过氧化物的形成，这可能会使细胞对这些高反应性中间体的天然清除机制不堪重负。此外，还发现超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶的活性降低，这些酶负责保护细胞免受超氧阴离子和过氧化物的过氧化作用。在两种急性肾衰竭模型中，均观察到体外肾匀浆中脂质过氧化增强，以丙二醛生成量来监测。此外，HgCl2和马来酸盐可能与游离的巯基反应，从而导致肾小管细胞中谷胱甘肽的消耗。实际上，还原型和氧化型谷胱甘肽的肾皮质含量大幅减少。这些结果表明，可能由过氧化过程引起的膜完整性改变可被视为在HgCl2和马来酸盐诱导的急性肾衰竭起始阶段常见的众所周知的肾功能障碍的潜在原因。
