Ellagic acid ameliorates nickel induced biochemical alterations: diminution of oxidative stress

Nickel, a major environmental pollutant is known for its clastogenic, toxic and carcinogenic potentials. The present investigation shows that ellagic acid proves to be exceptional in the amelioration of the nickel-induced bio chemical alterations in serum, liver and kidney. Administration of nickel ( 250 mu mol Ni/kg body wt) to female Wistar rats, resulted in increase in th e reduced glutathione (GSH) content [kidney (*P<0.05) and liver (**P<0.001) ] and Glutathione-S-transferase (GST) and glutathione reductase (GR) activi ties [kidney and liver, (**P<0.001)]. Ellagic acid treatment to the intoxic ated rats leads to the formation of soluble ellagic acid-metal complex whic h facilitates excretion of nickel from the cell or tissue, thus amelioratin g nickel-induced toxicity, as evident from the down regulation of GSH conte nt, GST and GR activities with concomitant restoration of glutathione perox idase (GPx) activity in liver and kidney. Our data shows that ellagic acid maintains cell membrane integrity through sequestration of metal ions from the extracellular fluid, as evident from the alleviated levels of serum glu tamate oxaloacetate transaminase, (SGOT), serum glutamate pyruvate transami nase (SGPT) and lactate dehydrogenase (LDH) when compared to nickel treated group. Similarly, the enhanced blood urea nitrogen (BUN) and serum creatin ine levels that are indicative of renal injury showed a reduction of about 45 and 40%, respectively. The data also show that treatment of ellagic acid after 30 min of nickel administration exhibits maximum inhibition in a dos e-dependent manner. In summary, our data suggests that ellagic acid act as an effective chelating agent in suppressing nickel-induced renal and hepati c biochemical alterations.