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., 5 mg/L (permissible limit, T1) and 10 mg/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⁺.

少量的Zn ²⁺对于所有生物的正常生理功能都是必不可少的，但是当其在周围环境中的浓度增加时，它将对生物起到毒害作用。Zn ²⁺污染的常见来源是电镀，合金化，采矿和相关的工业生产。本研究旨在评估底层给食鱼长鳍金枪鱼（Channa punctatus）在Zn ²⁺中毒下的生化，组织病理学和遗传毒理学意义，以及其在主要生物转化位点-肝脏和肾脏中的积累模式。鱼长期暴露于两种不同浓度的Zn ^2+，即 5 mg / L（允许极限，T1）和10 mg / L（两倍，允许极限，T2）。维持同时控制。在所有暴露组中，均观察到锌²⁺生物累积显着（p <0.05）增加，SOD，CAT和GR的抗氧化酶活性以及微核频率的诱导以及总蛋白质和谷胱甘肽的显着（p <0.05）减少。 28 d后。改变的生化参数，加上增强的微核诱导和鱼肝和肾中Zn ^2+的积累，可以被视为Zn ²⁺诱导的毒理学表现的敏感生物标志物，因此，它们可以有效地用于对污染水生环境进行可靠的生态毒理生物监测与Zn ²⁺。