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The synergistic effects of UV-328 and polystyrene microplastics on zebrafish embryos: developmental toxicity, oxidative stress, and neurotoxicity

Aquatic Toxicology 2026 Score: 50 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Xinlu Yang, Xinyi Liao, Lixiang Zhong, Mingfu Lin, Menghuan Zhang, Menghuan Zhang, Jun Wang, Jun Wang, Yumei Huang

Summary

Researchers investigated the combined toxicity of polystyrene microplastics and the UV stabilizer UV-328 on zebrafish embryos and found that the two pollutants acted synergistically to cause developmental abnormalities. The combination induced greater oxidative stress and neurotoxic effects than either substance alone, disrupting embryo hatching rates and development. The findings suggest that microplastics and UV stabilizers together may pose amplified risks to aquatic organisms compared to individual exposures.

Polymers
Body Systems

Microplastics (MPs) and ultraviolet stabilizer-328 (UV-328) are prevalent emerging pollutants in aquatic environments, yet their combined toxicity remains poorly understood. This study investigated the individual and joint toxicity of polystyrene microplastics (PS-MPs, 1000 µg/L) and UV-328 (1, 10, and 100 µg/L) on the early development of zebrafish (Danio rerio), revealing novel insights into their synergistic interactions. It was found that PS-MPs and UV-328 acted synergistically to induce developmental toxicity in zebrafish larvae and triggered oxidative stress responses. Transcriptome analysis and qRT-PCR validation showed co-activation of the peroxisome pathway and FoxO signaling pathway as compensatory antioxidant responses after co-exposure. However, this response was insufficient to counteract oxidative damage, and it still led to an exacerbation of cellular oxidative stress. The neurotoxicity caused by co-exposure to UV-328 and PS-MPs in zebrafish larvae was primarily attributed to disruption of the cholinergic signaling pathway. Notably, the neurotoxic effects were partially attenuated at higher concentrations of UV-328. The mechanism might involve upregulation of the Gap43 gene and activation of the mTOR signaling pathway. This study had revealed a new mechanism for the combined toxicity of microplastics and coexisting pollutants on aquatic organisms, emphasizing the need to consider the synergistic effects of pollutants in environmental risk assessment and management. These findings provided a scientific basis for formulating more comprehensive ecological protection strategies.

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