Amino modifications exacerbate the developmental abnormalities of polystyrene microplastics via mitochondria-mediated apoptosis pathway in zebrafish larvae.

Microplastics (MPs) are ubiquitous in the environment and have been identified as a potential threat to ecosystems. However, the mechanisms of toxicity of modified MPs remain unknown. This study investigated the developmental toxicity of amino-modified polystyrene microplastics (PS-NH) with environmentally relevant concentrations ranging from 0.1 to 100 μg/L in the early developmental stages of zebrafish. Adding amino functional groups resulted in significant alterations in the surface morphology and zeta potential of traditional polystyrene microplastics (PS-MPs). Zebrafish larvae exposed to PS-NH exhibited increased developmental toxicity compared to PS-MPs, as indicated by reduced body length, heart rate, and spontaneous movement. The expression of cat1, sod1, gstr1, nrf2a, nrf2b, and HO-1, as well as alterations in ROS, SOD, CAT, and MDA levels, all demonstrated oxidative damage caused by PS-NH exposure. Mitochondrial dysfunction was also induced, as evidenced by changes in the expression of cox4i1, ndufs1, and uqcrc1, as well as changes in the levels of ATP, cytochrome c, NAD, and NADH. Furthermore, PS-NH exposure disrupted apoptosis regulation, increasing apoptotic cells and caspase activity, along with changes in caspase-3 and bcl-2 expression. Molecular docking showed that PS-NH interacts with bcl-2 with high binding energy. This study contributes to understanding the toxic effects and mechanisms of charge-modified MPs in zebrafish.