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Polystyrene nanoplastics cause developmental abnormalities, oxidative damage and immune toxicity in early zebrafish development

Comparative Biochemistry and Physiology Part C Toxicology & Pharmacology 2025 11 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 68 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Febriyansyah Saputra, Agoes Soegianto, Azzah Dyah Pramata, Shao‐Yang Hu

Summary

Zebrafish embryos exposed to polystyrene nanoplastics showed dose-dependent developmental problems including delayed hatching, reduced survival, smaller body size, and the nanoplastics accumulated in critical organs like the eyes, heart, liver, and brain. The particles triggered oxidative stress that damaged cells and activated inflammatory immune responses, demonstrating how nanoplastic contamination in water can cause widespread harm to developing organisms.

Aquatic organisms are increasingly affected by polystyrene nanoplastics (PSNPs), which have the potential to disrupt development, induce oxidative stress, and impair immune function. This study examined the effects of PSNPs on zebrafish (Danio rerio) embryos exposed to 0.01, 0.1, 1, and 10 μg/mL from 2 to 120 h post-fertilization (hpf). The findings indicated that developmental abnormalities occurred in a dose-dependent manner, including delayed hatching, decreased survival rates, reduced body length, smaller eye diameter, and enlarged yolk sac area. PSNPs accumulated in the chorion and yolk sac as early as 6 hpf and were detected in vital tissues, such as the eyes, heart, yolk sac, liver, pancreas, intestine, neuromasts, and tail, immediately after hatching. By 120 hpf, PSNPs significantly reduced swimming distance and velocity. Exposure to PSNPs induced oxidative damage evidenced by altered expression of antioxidant-related genes (CAT1, GPX1A, SOD1, NRF2, KEAP1, HSP70, MT), disrupting cellular homeostasis and causing structural and organ defects. Immune toxicity was marked by dysregulated expression of immune-related genes (IL-1β, IL-6, NF-κB, TNF-α, C3B, TLR-1, TLR-3, TLR-4), indicating inflammation and innate immune activation triggered by oxidative damage. This study highlights the interconnected impacts of developmental abnormalities, oxidative damage, and immune toxicity caused by PSNPs exposure, highlighting the systemic impacts of nanoplastics contamination in aquatic environments.

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