Zn2+ induced molecular responses associated with oxidative stress, DNA damage and histopathological lesions in liver and kidney of the fish, Channa punctatus (Bloch, 1793).

Zn2+ 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 Zn2+ pollution are electroplating, alloying, mining, and allied industrial operations. The present study aims to assess the biochemical, histopathological and genotoxicological implications under Zn2+ 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 Zn2+i.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 Zn2+ 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 Zn2+ in liver and kidney of fish can be regarded as sensitive biomarkers of Zn2+ induced toxicological manifestations and thus, they may be effectively utilized for reliable ecotoxicological biomonitoring of aquatic regimes polluted with Zn2+.