Abstract
Chronic arsenicosis has threatened the survival of aquatic animals with molecular mechanisms yet clear. In the present study, liver damage was evident by fluctuated activities of transaminases and declined ATPases in common carp under arsenic (As) exposure for 30 days. Mechanically, As significantly decreased cytochrome P-1A (CYP1A) activity and increased reactive oxygen species (ROS) content, which corroborated mitochondrial dysfunction in the hepatocytes. This hypothesis was further suggested by Caspase-3-executed apoptosis by death receptor pathway (Fas, TNF-α and Caspase-8) and mitochondrial pathway (Bax, Bcl-2 and Caspase-9). The above results indicated that As-elicited oxidative damage lead to apoptotic hepatic injury in carp. On the contrary, zinc (Zn) exerted an ROS scavenger and an antidote to As in the present model evidenced by alleviated liver injury and restored liver function index. Moreover, Zn and As co-administration displayed partially recovered CYPs enzyme system and quenched apoptotic positive cells compared As treated alone. These outcomes could be applied to develop counter practices based on Zn preparations to decrease the biotoxicity of As.