Nanoplastic Exposure Mediates Neurodevelopmental Toxicity by Activating the Oxidative Stress Response in Zebrafish (<i>Danio rerio</i>)

The global accumulation and adverse effects of nanoplastics (NPs) are a growing concern for the environment and human health. In recent years, more and more studies have begun to focus on the toxicity of plastic particles for early animal development. Different particle sizes of plastic particles have different toxicities to biological development. Nevertheless, the potential toxicological effects of 20 nm NPs, especially on neurodevelopment, have not been well investigated. In this paper, we used fluorescence microscopy to determine neurotoxicity in zebrafish at different concentrations of NPs. Moreover, the behavioral analysis demonstrated that NPs induced abnormal behavior of zebrafish. The results revealed developmental defects in zebrafish embryos after exposure to different concentrations (0, 0.3, 3, and 9 mg/L) of NPs. The morphological deformities, including abnormal body length and the rates of heart, survival, and hatching, were induced after NP exposure in zebrafish embryos. In addition, the development of primary motor neurons was observed the inhibitory effects of NPs on the length, occurrence, and development of primary motor neurons in <i>Tg(hb9:GFP)</i>. Quantitative polymerase chain reaction analysis suggested that exposure to NPs significantly affects the expression of the genes involved in the occurrence and differentiation of primary motor neurons in zebrafish. Furthermore, the indicators associated with oxidative stress and apoptosis were found to be modified in zebrafish embryos at 24 and 48 h following exposure to NPs. Our findings demonstrated that NPs could cause toxicity in primary motor neurons by activating the oxidative stress response and inducing apoptosis, consequently impairing motor performance.