The protective effect of Zn2+ on As3+ toxicity in common carp: Resistance to oxidative stress, inhibition of endoplasmic reticulum stress, apoptosis and autophagy

Abstract

Carp has a wide range of edible value. As a vital organ that plays a crucial role in the innate immunity and respiratory system, gill may cause pollutants to enter fish during gas exchange. The negative effects of arsenic (As) pollution in the aquaculture industry cannot be ignored. Zinc (Zn) has the potential to replace endogenous antioxidants. This study aimed to investigate the comprehensive effects of As2O3 and ZnCl2 on carp gills. The obtained results found that: 1) As3+ can cause significant gill damage; fortunately, Zn co-administration significantly recovered the histopathological damage, antioxidant function and barrier function of carp gill tissue (Occludin, Claudins and Zonula Occludens (ZOs)); 2) from the perspective of mRNA and protein levels, after the Zn2+ pretreatment, heat shock response (HSPs), endoplasmic reticulum stress (glucose regulatory protein 78 (GRP78), phosphorylated PKR-like ER Kinase (p-PERK), phosphorylated eukaryotic initiation factor 2 α (p -eIF2α)), apoptosis (cysteyl aspartate specific protease 3/9 (Cas 3/9), B cells Lymphoma-2 (Bcl-2), BCL2-related X (Bax)) and autophagy (microtubule-associated protein 1 light chain 3 (LC3) and sequestosome 1 (P62) caused by As3+) have decreased. In conclusion, this study preliminarily showed that As3+ and Zn2+ have antagonistic effects on carp gill tissues. These informations emphasized the importance of assessing the injury and recovery ability of organisms after the input of heavy metal and elements, and enhanced the understanding of the potential impact of As3+ and Zn2+ to freshwater ecosystems and aquaculture.