Developmental cardiovascular disruption triggered by polystyrene nanoplastics in zebrafish mediated through oxidative stress.

The rising prevalence of polystyrene nanoplastics (PSNPs) in aquatic ecosystems poses not only ecological threats but also growing concerns for human health, particularly through their potential to interfere with cardiovascular development and function. This study investigated the cardiotoxic effects of PSNPs (25 nm) exposure on zebrafish embryos, a well-established vertebrate model in toxicology. PSNPs were exposed on Tg(fli1: EGFP) zebrafish embryos at concentrations of 0.01, 0.1, 1, and 10 μg/mL for 96 h post-fertilization (hpf). Cardiovascular function and morphology were evaluated during early development. The exposure disrupted cardiovascular development, leading to abnormalities such as altered heart rate, pericardial edema, impaired blood vessel formation, reduced red blood cell velocity, and decreased aortic diameter and ventricular volume between 48 and 96 hpf. Increased reactive oxygen species and apoptosis suggest oxidative stress is a key mechanism of toxicity. Gene expression analysis showed that PSNP exposure disrupted genes related to cardiovascular development, apoptotic signaling, as well as antioxidant defense mechanisms. Co-exposure of glutathione (GSH) at 50 μM, a powerful antioxidant, significantly mitigated the harmful effects of PSNPs, suggesting that oxidative stress is crucial to PSNP-induced cardiovascular toxicity. The results demonstrate the urgency of addressing nanoplastic pollution and highlight potential antioxidant-based strategies for mitigating its health impacts.