Nickel, a major
environmental pollutant is a known potent nephrotoxic agent. In this communication we report the chemopreventive effect of Terminalia chebula on
nickel chloride (NiCl(2)) induced renal oxidative stress, toxicity and cell proliferation response in male Wistar rats. Administration of NiCl(2) (250micromoL Ni/kg
body weight) to male Wistar rats resulted in an increase in the reduced renal
glutathione content (GSH),
glutathione-S-transferase (GST),
glutathione reductase (GR), lipid peroxidation (LPO), H(2)O(2) generation, blood
urea nitrogen (BUN) and serum
creatinine with a concomitant decrease in the activity of
glutathione peroxidase (p<0.001).
Nickel chloride (NiCl(2)) treatment also induced
tumor promotion markers, viz.,
ornithine decarboxylase (ODC) activity and
thymidine [(3)H] incorporation into renal
DNA (p<0.001). Prophylactic treatment of rats with T. chebula (25mg/kg
body weight and 50mg/kg
body weight) daily for one week resulted in the diminution of NiCl(2) mediated damage as evident from the down regulation of
glutathione content, GST, GR, LPO, H(2)O(2) generation, BUN, serum
creatinine,
DNA synthesis (p<0.001) and ODC activity (p<0.01) with concomitant restoration of GPx activity. Thus, the present investigation suggests that T. chebula extract could be used as therapeutic agent for
cancer prevention as evident from this study where it blocks or suppresses the events associated with chemical
carcinogenesis.