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Protective Effect of Naringenin Against Lead-Induced Oxidative Stress in Rats

Wang, Jicang, Yang, Zijun, Lin, Lin, Zhao, Zhanqin, Liu, Zongping, Liu, Xuezhong
Biological trace element research 2012 v.146 no.3 pp. 354-359
alanine transaminase, antioxidant activity, aspartate transaminase, biomarkers, catalase, creatinine, glutathione, glutathione peroxidase, hepatoprotective effect, hepatotoxicity, kidneys, lead, lead acetate, liver, naringenin, oral administration, oxidative stress, rats, superoxide dismutase, urea, uric acid
Oxidative stress is thought to be involved in lead-induced toxicity. The aim of this study was to investigate the possible protective role of naringenin on lead-induced oxidative stress in the liver and kidney of rats. In the present investigation, lead acetate (500 mg Pb/L) was administered orally for 8 weeks to induce hepatotoxicity and nephrotoxicity. The levels of hepatic and renal markers such as alanine aminotransferase, aspartate aminotransferase, urea, uric acid, and creatinine were significantly (P < 0.05) increased following lead acetate administration. Lead-induced oxidative stress in liver and kidney tissue was indicated by a significant (P < 0.05) increase in the level of maleic dialdehyde and decreased levels of reduced glutathione, superoxide dismutase, catalase, and glutathione peroxidase. Naringenin markedly attenuated lead-induced biochemical alterations in serum, liver, and kidney tissues (P < 0.05). The present study suggests that naringenin shows antioxidant activity and plays a protective role against lead-induced oxidative damage in the liver and kidney of rats.