Journal
HUMAN & EXPERIMENTAL TOXICOLOGY
Volume 28, Issue 4, Pages 221-229Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/0960327109102365
Keywords
antioxidants; cadmium; kidney; N-acetylcysteine; oxidative stress; rats
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Funding
- National Nature Science Foundation of China [30440050, 30571364]
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In the present study, female Sprague-Dawley rats received CdCl2 (50 mg/L through drinking water) and/or N-acetylcysteine (NAC, 120 mg/kg/day, orally) to investigate the protective effect of NAC on Cd-induced renal damage. Renal toxicity was evaluated by measuring the contents of total protein, beta(2)-microglobulin, and beta(1)-microglobulin in the urine and urinary enzyme markers of tubular necrosis, as well as levels of serum urea nitrogen and serum creatinine. Activities of antioxidant enzymes and contents of glutathione, malondialdehyde, and trace elements in the kidney were also measured. Animals that received both Cd and NAC showed a better renal function than those receiving Cd alone. In addition, NAC significantly reduced the levels of lipid peroxidation (LPO) in the kidney of cadmium-treated rats. The enzymic and nonenzymatic antioxidants levels are not restored, but their further decrease is prevented by NAC. Also NAC administration does not modify the urinary excretion of cadmium or contents of cadmium in the serum and kidney. In conclusion, NAC exerts its protective effect by decreased LPO and improving antioxidants status to prevent renal tubular damage induced by chronic Cd administration, most probably through its antioxidant properties.
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