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Emamectin benzoate exposure induced carp kidney injury by triggering mitochondrial oxidative stress to accelerate ferroptosis and autophagy

文献类型： 外文期刊

作者： Li, Lu 1 ; Li, Wan 2 ; Liu, Yufeng 3 ; Han, Bing 1 ; Yu, Yanbo 1 ; Lin, Hongjin 1 ;

作者机构： 1.Northeast Agr Univ, Harbin 150030, Peoples R China

2.Heilongjiang Acad Agr Sci, Inst Crop Cultivat & Tillage, Harbin 150086, Peoples R China

3.Heilongjiang Acad Agr Sci, Inst Anim Husb Res, Harbin 150086, Peoples R China

4.Northeast Agr Univ, Coll Vet Med, Dept Heilongjiang Common Anim Dis Prevent & Treatm, Key Lab Prov Educ, Harbin 150030, Peoples R China

关键词： EMB; Oxidative stress; Mitochondrial damage; Ferroptosis; Autophagy; Carp kidney

期刊名称：PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY （ 影响因子：4.2； 五年影响因子：4.6 ）

ISSN： 0048-3575

年卷期： 2024 年 203 卷

页码：

收录情况： SCI

摘要： Emamectin benzoate (EMB), commonly used as an insecticide in fishery production, inevitably leaves residual chemicals in aquatic environments. High-level EMB exposure can cause severe damage to multiple systems of marine animals, potentially through mechanisms involving severe mitochondrial damage and oxidative stress. However, it is not clear yet how EMB exposure at a certain level can cause damage to fish kidney tissue. In this study, we exposed carps to an aquatic environment containing 2.4 mu g/L of EMB and cultured carp kidney cells in vitro, established a cell model exposed to EMB. Our findings revealed that EMB exposure resulted in severe kidney tissue damage in carp and compromised the viability of grass carp kidney cells (CIK cells). By RNA-seq analysis, EMB exposure led to significant differences in mitochondrial homeostasis, response to ROS, ferroptosis, and autophagy signals in carp kidney tissue. Mechanistically, EMB exposure induced mitochondrial oxidative stress by promoting the generation of mitochondrial superoxide and reducing the activity of antioxidant enzymes. Additionally, EMB exposure triggered loss of mitochondrial membrane potential, an imbalance in mitochondrial fusion/division homeostasis, and dysfunction in oxidative phosphorylation, ultimately impairing ATP synthesis. Notably, EMB exposure also accelerated excessive autophagy and ferroptosis of cells by contributing to the formation of lipid peroxides and autophagosomes, and the deposition of Fe2+. However, Nacetyl-L-cysteine (NAC) treatment alleviated the damage and death of CIK cells by inhibiting oxidative stress. Overall, our study demonstrated that EMB exposure induced mitochondrial oxidative stress, impaired mitochondrial homeostasis, and function, promoted autophagy and ferroptosis of kidney cells, and ultimately led to kidney tissue damage in carp. Our research enhanced the toxicological understanding on EMB exposure and provides a model reference for comparative medicine.

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