Emamectin Benzoate and Microplastics Led to Skeletal Muscle Atrophy in Common Carp via Induced Oxidative Stress, Mitochondrial Dysfunction, and Protein Synthesis and Degradation Imbalance.

Pesticides and plastics have brought convenience to agricultural production and daily life, but they have also led to environmental pollution through residual chemicals. Emamectin benzoate (EMB) is among the most widely used insecticides, which can cause environmental pollution and harm the health of organisms. Additionally, microplastics (MPs), a relatively new type of pollutant, not only are increasing in residual amounts within water bodies and aquatic organisms but also exacerbate pollution by adsorbing other pollutants, leading to a mixed pollution scenario. Nevertheless, the toxicity and mechanism of EMB and MPs on common carp skeletal muscle have not been elucidated. Therefore, we established exposure models for EMB and MPs, and methods such as hematoxylin and eosin staining, immunofluorescence staining, JC-1 staining, and western blotting were employed to investigate the underlying mechanisms of skeletal muscle damage. The results of in vivo and in vitro experiments indicated that exposure to EMB or MPs led to oxidative stress, which in turn caused mitochondrial fusion/fission imbalance (with decreased Mfn1, Mfn2, and OPA1 and increased DRP1), reduced mitochondrial membrane potential, decreased ATP content, reduced protein synthesis, and increased degradation, ultimately resulting in skeletal muscle atrophy. Joint exposure caused more severe damage than single exposure, and the addition of NAC can effectively alleviate skeletal muscle atrophy. In summary, exposure to EMB and/or MPs induced excessive reactive oxygen species (ROS) production, giving rise to mitochondrial dysfunction and an imbalance in skeletal muscle protein synthesis and degradation, ultimately resulting in skeletal muscle atrophy in common carp.