Waterborne exposure to
arsenic trioxide (
As2O3) is inevitable due to its widespread industrial and agricultural applications. Oxidative stress and cascaded programmed cell death is now hypothesized to be the dominant mechanisms of arseniasis evidenced in vivo and in vitro. This study aimed to explore the interaction of divalent
zinc ion (Zn2+), an efficient
reactive oxygen species (ROS) scavenger with
arsenite in the heart of common carp, and extensively investigated the exact signaling molecules involved. Significant induction of
cardiotoxicity including oxidative stress, apoptosis and autophagy was evident in heart tissues following
arsenite exposure (P < 0.05). The dissipation of
antioxidant enzymes (SOD and CAT) was induced by ROS burst, leading to oxidative damage and lipid peroxidation (MDA).
Arsenite induced classic apoptotic hallmarks, characterized by
chromatin degradation and subsequent formation of clumps adjacent, and elevated expression of Bax/Bcl-2 and
Caspase family, and also increased autophagic flux evidenced by accelerated formation (LC3) and degradation (p62) of autophagosomes. PI3K/Akt/mTOR pathway was phosphorylated inhibited, while MAPK signaling (p38, ERK and JNK) displayed elevated phosphorylation levels in
arsenite-exposed heart tissues. In contrast, above phenomena were effectively inhibited by Zn2+, which supplement attenuated
arsenite-induced myocardial toxicity through inhibition of apoptosis and autophagy via PI3K/Akt/mTOR pathway, as well as suppressing intracellular ROS cluster via activating antioxidative system via MAPK pathway. Our results provided experimental explanation and evidences for
cardiotoxicity of
arsenite. Furthermore, our findings hint that the application of
zinc preparations may provide a candidate for the prevention and treatment for
arsenic poisoning.