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Vitamin E (VitE), a potent antioxidant, has demonstrated significant potential in mitigating oxidative stress and cellular damage, making it a valuable agent for countering environmental toxicities, including those caused by polystyrene nanoplastics (PSNPs). This study examined the effects of PSNPs on the zebrafish visual system and evaluated the protective role of VitE. Zebrafish embryos were exposed to PSNPs (0.01, 0.1, 1, and 10 μg/mL) with or without 20 μM VitE co-treatment from fertilization to 6 days post-fertilization (dpf). Visual function, morphology, and molecular responses were assessed at 4 or 6 dpf. Exposure to PSNPs at concentrations of 0.1 to 10 μg/mL significantly increased bioaccumulation in the zebrafish eye in a concentration-dependent manner and disrupted the visual system. These disruptions caused a reduction in the eye-to-body length ratio and decreased optomotor response positivity and swimming distance, indicating impaired visual function and behavior. Furthermore, PSNPs elevated reactive oxygen species (ROS) levels, induced retinal apoptosis, and disrupted gene expression related to visual development (six6, pax2, pax6a, and pax6b), apoptosis (tp53, casp3, bax, and bcl2a), and antioxidant defense (sod1, cat, and gpx1a). VitE co-treatment significantly mitigated these adverse effects, reducing oxidative damage, restoring antioxidant defenses, and preserving retinal function. This study highlights the potential of VitE as a protective agent against PSNP-induced visual dysfunction and underlines the urgent need to address nanoplastic pollution to protect aquatic ecosystems.
Saputra et al. (Thu,) studied this question.