Mitochondrial dysfunction and lipometabolic disturbance induced by the co-effect of polystyrene nanoplastics and copper impede early life stage development of zebrafish (Danio rerio)

Knowledge about the co-effect of nanoplastics (NPs) and copper (Cu) on early life stage energy metabolism and development of fish is still limited. In this study, zebrafish embryos were exposed to environmentally-relevant concentrations of polystyrene NPs, Cu and their mixture from 2 h to 98 h post-fertilization (hpf), respectively. The co-exposure to NPs and Cu induced the overproduction of reactive oxygen species (ROS), thereby causing mitochondria damage (the reduction of mitochondrial membrane potential and mtDNA copy number). Also, the co-exposure to NPs and Cu caused mitochondrial dysfunction, which led to the reduction of the mitochondrial complex enzyme activity, resulting in ATP synthesis ability reduction. Besides, the co-exposure to NPs and Cu increased fat synthesis and reduced fat hydrolysis and fatty acid oxidation, resulting in inhibition of the utilization of lipids from the yolk sac. Hence, mitochondrial dysfunction and blocked lipid utilization cause insufficient energy supply, which has an adverse impact on the development and survival of zebrafish in the early life stage. This study will provide a basis for assessing the risk of the biological toxicity of contamination of NPs and Cu to early life stage energy metabolism and development of fish and even other animals.