Combined exposure of emamectin benzoate and microplastics induces tight junction disorder, immune disorder and inflammation in carp midgut via lysosome/ROS/ferroptosis pathway

Xu Shi; Tong Xu; Meichen Gao; Yanju Bi; Jiaqi Wang; Yilin Yin; Shiwen Xu

doi:10.1016/j.watres.2024.121660

Combined exposure of emamectin benzoate and microplastics induces tight junction disorder, immune disorder and inflammation in carp midgut via lysosome/ROS/ferroptosis pathway

Water Res. 2024 Apr 22:257:121660. doi: 10.1016/j.watres.2024.121660. Online ahead of print.

Authors

Xu Shi¹, Tong Xu¹, Meichen Gao¹, Yanju Bi¹, Jiaqi Wang¹, Yilin Yin¹, Shiwen Xu²

Affiliations

¹ College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China.
² College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China; Laboratory of Embryo Biotechnology, College of Life Science, Northeast Agricultural University, Harbin, 150030, PR China. Electronic address: shiwenxu@neau.edu.cn.

PMID: 38688190
DOI: 10.1016/j.watres.2024.121660

Abstract

Pesticides and plastics bring convenience to agriculture and life, but also bring residual pollution in the environment. Emamectin benzoate (EMB) is the most popular pesticide at present. The harm of microplastics (MPs) to water and aquatic organisms is gradually increasing, and the possibility that it appears synchronously with various pesticides increases. However, the damage of EMB and MPs to the carp midgut and its mechanism have not been clarified. Therefore, based on the EMB or/and MPs exposure models, this study explored the mechanism of midgut injury through transcriptomics, immunofluorescence, western blot methods, and so on. Studies in vivo and in vitro showed that EMB or MPs exposure caused cilia shortening, lysosome damage, and ROS overproduction, which led to Fe²⁺ content increase, GSH/GSSG system disorder, lipid peroxidation, and ferroptosis. This process further led to the down-regulation of Cx43, Occludin, Claudin, and ZO-1, which further caused barrier damage, immune-related genes (immunoglobulin, IFN-γ) decrease and inflammation-related genes (TNF-α, IL-1β) increase. Combined exposure was more significant than that of single exposure, and the addition of EN6 and NAC proved that lysosome/ROS/ferroptosis regulated these midgut damages. In conclusion, EMB or/and MPs exposure induce tight junction disorder, immune disorder and inflammation in carp midgut through the lysosome/ROS/ferroptosis pathway.

Keywords: Carp midgut; EMB; Ferroptosis; Lysosome/ROS; MPs.