Abstract
Nickel, a major environmental pollutant, is known for its clastogenic, toxic, and carcinogenic potential. In this article, we report the effect of Acorus calamus on nickel chloride (NiCl^sub 2^)-induced renal oxidative stress, toxicity, and cell proliferation response in male Wistar rats. NiCl^sub 2^ (250 μmol/kg body weight/mL) enhanced reduced renal glutathione content (GSH) glutathione-S-transferase (GST), glutathione reductase (GR), lipid peroxidation (LPO), H^sub 2^O^sub 2^ generation, blood urea nitrogen (BUN), and serum creatinine with a concomitant decrease in the activity of glutathione peroxidase (GPx) (p<0.001). NiCl^sub 2^ administration also dose-dependently induced the renal ornithine decarboxylase (ODC) activity several-fold as compared to salinetreated control rats. Similarly, renal DNA synthesis, which is measured in terms of [^sup 3^H] thymidine incorporation in DNA, was elevated following NiCl^sub 2^ treatment. Prophylactic treatment of rats with A. calamus (100 and 200 mg/kg body weight po) daily for 1 wk resulted in the diminution of NiCl^sub 2^-mediated damage, as evident from the downregulation of glutathione content, GST, GR, LPO, H^sub 2^O^sub 2^ generation, BUN, serum creatinine, DNA synthesis (p<0.001), and ODC activity (p<0.01) with concomitant restoration of GPx activity. These results clearly demonstrate the role of oxidative stress and its relation to renal disfunctioning and suggest a protective effect of A. calamus on NiCl^sub 2^-induced nephrotoxicity in a rat experimental model.[PUBLICATION ABSTRACT]