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 (NiCl2)-induced renal oxidative stress, toxicity, and cell proliferation response in male Wistar rats. NiCl2 (250 micromol/kg
body weight/mL) enhanced reduced renal
glutathione content (GSH),
glutathione- S-transferase (GST),
glutathione reductase (GR), lipid peroxidation (LPO), H2O2 generation, blood
urea nitrogen (BUN), and serum
creatinine with a concomitant decrease in the activity of
glutathione peroxidase (GPx) (p < 0.001). NiCl2 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 [3H]
thymidine incorporation in
DNA, was elevated following NiCl2 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 NiCl2- mediated damage, as evident from the downregulation of
glutathione content, GST, GR, LPO, H2O2 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 NiCl2-induced nephrotoxicity in a rat experimental model.