The cardiotoxicity of the common carp (Cyprinus carpio) exposed to environmentally relevant concentrations of arsenic and subsequently relieved by zinc supplementation. (October 2019)

• Record Type: Journal Article
• Authors: Zhao, Hongjing; Wang, Yu; Liu, Juanjuan; Guo, Menghao; Fei, Dongxue; Yu, Hongxian; Xing, Mingwei
• Is Part Of: Environmental pollution. Volume 253(2019)
• Page Start: 741
• Page End: 748
• Publication Date: 2019-10
• Subjects: Environmental pollution -- Antagonist -- Aquatic animal -- Apoptosis -- Autophagy; Pollution -- Periodicals; Pollution -- Environmental aspects -- Periodicals; Environmental Pollution -- Periodicals; Pollution -- Périodiques; Pollution -- Aspect de l'environnement -- Périodiques; Pollution -- Effets physiologiques -- Périodiques; Pollution; Pollution -- Environmental aspects; Periodicals; Electronic journals; 363.73
• DOI: 10.1016/j.envpol.2019.07.065
• Languages: English
• ISSNs: 0269-7491

Abstract

Abstract: Waterborne exposure to arsenic trioxide (As2 O3 ) 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 (Zn 2+ ), 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 Zn 2+, 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. Graphical abstract: Image 1 Highlights: Arsenic cardiac accumulation induces ROS burst and collapse of antioxidant system. Apoptosis and autophagy are induced under arsenic stress. Zinc antagonizes cardiotoxicity of arsenic via MAPK and PI3K/Akt/mTOR pathways.