Zinc antagonizes common carp (Cyprinus carpio) intestinal arsenic poisoning through PI3K/AKT/mTOR signaling cascade and MAPK pathway

蛋白激酶B PI3K/AKT/mTOR通路 砷毒性 激酶 细胞生物学 MAPK/ERK通路 生物 信号转导 生物化学 化学 有机化学
作者
Menghao Guo,Yu Wang,Hongjing Zhao,Dongxu Wang,Kai Yin,Yachen Liu,Baoying Li,Mingwei Xing
出处
期刊:Aquatic Toxicology [Elsevier BV]
卷期号:240: 105986-105986 被引量:34
标识
DOI:10.1016/j.aquatox.2021.105986
摘要

Arsenic (As) pollution is a serious and longstanding problem, which has obvious threaten to aquatic organisms. The study aimed to explore the mitigation effect of natural antioxidant zinc (Zn) on As toxicity in the foregut and midgut of common carp (Cyprinus carpio L.), and in-depth disclose related signal cascade. Carps were treated with Zn2+ (1 mg/L) and/or As3+ (2.83 mg/L) for a period of 30 days. Under As exposure, the foregut and midgut showed obvious burst of reactive oxygen species (ROS) and breakdown of antioxidant system. What followed is the activation of the endogenous and exogenous apoptotic pathways, and the rise of autophagy level prompted by the increase in LC3 II and the down-regulation of p62. Mitochondrial swelling, cristae fragmentation and autophagosomes were observed under the electron microscope, which also means the occurrence of apoptosis and autophagy. In addition, As induced the activation of p38 mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK) and the inhibition of extracellular signal-related kinase (ERK) in MAPK signaling, and up-regulated the level of autophagy through the inhibition of the phosphatidylinositol 3 kinase (PI3K)/AKT/ mammalian target of rapamycin (mTOR) signaling cascade. However, Zn supplementation has clearly reversed the above phenomenon, and it basically has no effect on foregut and midgut. In conclusion, this study shows that Zn can alleviate the damage caused by subchronic As exposure, which provides a reference for the use of Zn preparations in aquaculture.
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