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Free radical scavengers in mercuric chloride-induced acute renal failure in the rat

Authors
Journal
Journal of Laboratory and Clinical Medicine
0022-2143
Publisher
Elsevier
Publication Date

Abstract

Abstract Oxygen free radicals have recently been found to mediate cell injury after ischemia in the kidney. We sought to determine whether oxygen free radicals mediate damage in mercuric chloride (HgCl 2)-induced acute renal failure, a toxic model of acute renal failure. Neither superoxide dismutase nor allopurinol, which scavenges or inhibits production of superoxide radical, respectively, provided protection against renal dysfunction after HgCl 2. Similarly, the hydroxyl radical scavengers tryptophan, N-acetyl-tryptophan, and ascorbic acid were unable to protect against HgCl 2. However, dimethylthiourea and dimethyl sulfoxide, both hydroxyl radical scavengers, were beneficial. Dimethylthiourea completely prevented the rise in plasma creatinine concentration after HgCl 2. In control rats plasma creatinine concentration rose from 0.4 mg/dl to 3.2 ± 0.8, 5.1 ± 1.0, and 6.1 ± 1.6 mg/dl at 24, 48, and 72 hours after HgCl 2. Dimethylthiourea-treated rats had plasma creatinine concentration <0.5 mg/dl at all times. Furthermore, a mixture of HgCl 2 and equimolar amounts of dimethylthiouria was less toxic than HgCl 2 alone. Dimethyl sulfoxide attenuated the HgCl 2-induced rise in creatinine concentration: 1.3 ± 0.2, 3.2 ± 0.3, and 3.1 ± 0.2 mg/dl at 24, 48, and 72 hours after HgCl 2. Measurement of kidney malondialdehyde content after HgCl 2 provided no evidence for oxygen free radical-mediated lipid peroxidation. We conclude that there is no convincing role for oxygen free radicals in the pathogenesis of HgCl 2-induced acute renal failure. The ability of dimethylthiourea and dimethyl sulfoxide to protect against HgCl 2-induced renal dysfunction may be related to their ability to form complexes with Hg 2+.

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