Zn induced molecular responses associated with oxidative stress, DNA damage and histopathological lesions in liver and kidney of the fish, Channa punctatus (Bloch, 1793).

Zn is essential for normal physiological functioning of all organisms in small quantities, but when its concentration enhances in surrounding environment it acts as a toxicant to organisms. Common sources of Zn pollution are electroplating, alloying, mining, and allied industrial operations. The present study aims to assess the biochemical, histopathological and genotoxicological implications under Zn intoxication along with its accumulation patterns in prime biotransformation sites-liver and kidney, of a bottom feeder fish, Channa punctatus. Fish were chronically exposed to two different concentrations of Zni.e., 5mg/L (permissible limit, T1) and 10mg/L (twice the permissible limit, T2). Simultaneous control was maintained. A significant (p<0.05) increment in Zn bioaccumulation, antioxidant enzymes activities of SOD, CAT and GR and induction in micronuclei frequencies along with the significant (p<0.05) decrement in total protein and GSH were observed in all the exposed groups after 28 d. Altered biochemical parameters coupled with enhanced induction in micronuclei and accumulation of Zn in liver and kidney of fish can be regarded as sensitive biomarkers of Zn induced toxicological manifestations and thus, they may be effectively utilized for reliable ecotoxicological biomonitoring of aquatic regimes polluted with Zn.