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Aged nanoplastics reprogram the ER stress-autophagy crosstalk: A mechanistic gateway to skeletal malformations in zebrafish

Aquatic Toxicology 2025 2 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 58 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.

Wanjing Liu, Sharon R. Long, Wanjing Liu, Chunhua Zhan Wanjing Liu, Wanjing Liu, Wanjing Liu, Chunhua Zhan Chunhua Zhan Chunhua Zhan Xingqiao Wen, Xingqiao Wen, Wanjing Liu, Mingqiu Dai, Chunhua Zhan Xingqiao Wen, Yufan Pan, Wanjing Liu, Sharon R. Long, Yufan Pan, Wanjing Liu, Wanjing Liu, Wanjing Liu, Yufan Pan, Yufan Pan, Wanjing Liu, Wanjing Liu, Yufan Pan, Wanjing Liu, Chunhua Zhan Yufan Pan, Yufan Pan, Chunhua Zhan Chunhua Zhan Wanjing Liu, Wanjing Liu, Chunhua Zhan

Summary

Researchers exposed zebrafish embryos to both new and UV-aged nanoplastics and found that the aged particles caused significantly worse skeletal deformities, higher mortality, and lower hatching rates. The aged nanoplastics disrupted cellular stress responses and a self-cleaning process called autophagy in developing bone and cartilage cells. The study suggests that weathered nanoplastics in the environment may pose greater developmental risks than freshly produced particles.

Polymers

Body Systems

Musculoskeletal Reproductive

Models

Zebrafish

Micro(nano)plastics (MNPs) are pervasive in aquatic environments, with aged MNPs being the predominant form due to environmental weathering. However, their developmental toxicity, particularly regarding skeletal formation, remains poorly understood. In this study, aged polystyrene nanoplastics (PSNPs) were prepared via 48-hour UV irradiation and compared with pristine PSNPs in zebrafish embryo exposures starting within 4 h post-fertilization (hpf) and lasting for 7 days. Both pristine and aged PSNPs induced skeletal malformations, but aged PSNPs caused more severe effects, including decreased hatching rates, increased mortality, and altered larval body length. Histopathological analysis revealed disrupted muscle fiber organization and lipid accumulation in the yolk sac. Elevated reactive oxygen species (ROS) and calcium ion levels were observed in both treatment groups. Aged PSNPs significantly upregulated GRP78 and RAB7 protein expression, increased transcription of the Endoplasmic Reticulum stress (ER stress) marker eif2α, and downregulated key genes involved in bone development (bmp2b, bmp4) and autophagy (atg13, atg5). These findings indicate that aged PSNPs exacerbate oxidative stress, activate ER stress pathways, inhibit autophagy, and impair skeletal development. This study highlights the heightened developmental toxicity of environmentally aged MNPs and underscores the necessity of including aged plastic particles in ecological risk assessments.

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