Zinc Alleviates Arsenic-Induced Inflammation and Apoptosis in the Head Kidney of Common Carp by Inhibiting Oxidative Stress and Endoplasmic Reticulum Stress.

Abstract

Arsenic (As) pollution is ubiquitous in water, which shows immunotoxicity to aquatic organisms. As an indispensable regulator of gene transcription and enzymatic modification, zinc (Zn) may play a preventive and therapeutic effect on As toxicity. The purpose of this study was to investigate the interactions of As and Zn on the head kidney of common carp Cyprinus carpio. Herein the carp were treated alone or in combination with waterborne As3+ (2.83mg/L) and/or Zn2+ (1mg/L). Results suggested a head kidney-toxic effect of As exposure, which was manifested by the histopathological damage of the head kidney, elevation of nuclear translocation of pro-inflammatory nuclear factor-kappa light chain enhancer of B cells (NF-κB), and blockage of the anti-oxidative nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. The global activation of three endoplasmic reticulum (ER) stress pathways led to the execution of programmed cell death, including ER apoptosis mediated by C/EBP-homologous protein (CHOP), death receptor-mediated exogenous cell apoptosis, and the endogenous apoptosis executed by Caspases9. The combined application of Zn can significantly improve the histopathological damage of the head kidney, the imbalance of the antioxidant system, and the apoptosis outcomes due to ER stress. In conclusion, this study indicates that Zn has an antagonistic effect on the head kidney injury of common carp induced by sub-chronic As exposure. The results of this study provide basic data for the risk assessment of As accumulation in an aquatic environment and a reference for the use of Zn preparation in aquaculture.