Emamectin benzoate and nanoplastics induce PANoptosis of common carp (Cyprinus carpio) gill through MAPK pathway

• Published in: Pesticide biochemistry and physiology 2024-12, Vol.206, p.106202, Article 106202
• Main Authors: Ju, Zhangyi, Bi, Yanju, Gao, Meichen, Yin, Yilin, Xu, Tong, Xu, Shiwen
• Format: Article
• Language: English
• Subjects: acetylcysteine; Animals; aquatic environment; carp; Carps - metabolism; caspase-3; caspase-8; class; Cyprinus carpio; Emamectin benzoate; exposure models; Fish epidermal cells; fluorescence; fluorescent antibody technique; Gills - drug effects; Gills - metabolism; Ivermectin - analogs & derivatives; Ivermectin - toxicity; MAP Kinase Signaling System - drug effects; Microplastics - toxicity; Nanoparticles - toxicity; Nanoplastics; oxidative stress; Oxidative Stress - drug effects; PANoptosis; PANoptosomes; pesticides; protein synthesis; Reactive Oxygen Species - metabolism; Water Pollutants, Chemical - toxicity; Western blotting
• ISSN: 0048-3575; 1095-9939; 1095-9939
• DOI: 10.1016/j.pestbp.2024.106202

Emamectin benzoate (EMB) is a pesticide that is frequently used. Nanoplastics (NPs) are a recently identified class of pollutants that are ubiquitous in the environment. In the aquatic environment, NPs can appear together with EMB, which may exacerbates the damage to water and aquatic organisms. However, the damage and mechanism of EMB and NPs to the gill tissue of common carp (Cyprinus carpio) remain unclear. Therefore, an EMB or/NPs exposure model was constructed to explore the mechanism of EMB or/NPs exposure on carp gill damage. This study was done by immunofluorescence, RT-qPCR, Western blot and other methods. Both in vitro and in vivo data indicated that EMB or NPs exposure could lead to gill tissue destruction, oxidative stress with the increased of ROS fluorescence intensity, MDA and H2O2 content, and the decreased CAT and GSH-PX activity, and the activation of MAPK pathway. Subsequently, PANoptosomes were activated with the up-regulated mRNA and protein expression of RIPK-1, Caspase-1,NLRP3, ACS, RIPK-3, Caspase-8, resulting in PANoptosis including the increased GSDMD, Caspase-3, MLKL expression. Notably, the results following combined exposure were more pronounced than those observed following exposure alone. The addition of N-acetylcysteine (NAC) and 3-methylindole (3-MI) further evidenced that EMB or/and NPs exposure can induce gill damage via the ROS/MAPK/PANoptosis pathway. Therefore, the present study reveals that EMB or/NPs exposure induces PANoptosis in carp gill by activating ROS/p38/MAPK signaling. [Display omitted] •EMB or NPs cause PANoptosis through ROS/MAPK pathway.•Inhibiting oxidative stress can alleviate the damage caused by EMB or NPs.•EMB or NPs can induce PANoptosis by activating PANoptosomes.•The toxicity of EMB and NPs combined exposure was more significant than that of single exposure.