Ameliorative Action of Curcumin in Cisplatin-mediated Hepatotoxicity: An In Vivo Study in Wistar Rats

Background and Aims tin (CP) is regarded as a major anticancer drug against a wide spectrum of leukemia and other malignancies. The mode of action of CP on cancer cells is attributed to its property of releasing free radicals which, at the same time, has the potential to damage liver and kidney cells. The tissue-specific toxicity of CP to the kidneys is well documented. However, there is a paucity of literature on systemic toxicity and also the amelioration of such effect. The aim of the present study was to evaluate the damage caused by CP and its modulation by using the antioxidant capacity of curcumin (CMN, a natural polyphenolic compound) in Wistar rats. s luated the ameliorative effect of CMN (200 mg/kg body weight, b.w.) on the toxicity of CP in rat liver. Oxidative stress biomarkers, enzymatic and nonenzymatic antioxidants were evaluated for assessing the mitigatory potential of CMN against CP-induced toxicity. s le dose of CP (7 mg/kg b.w.) caused marked hepatic damage. CP caused a significant increase in lipid peroxidation (LPO) level and protein carbonyl (PC) content. Pretreatment of rat with CMN significantly restored the LPO levels and PC content. It also replenished the CP-induced modulatory effects on altered enzymatic and nonenzymatic antioxidants in liver. sion sults clearly demonstrated that the role of oxidative stress is detrimental in systemic toxicity induced by CP and suggest a mitigatory effect of CMN on CP-induced hepatotoxicity in rat.