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The silent saboteurs: How ultraviolet (UV)-aged polystyrene nanoplastics disrupt the regenerative capacity of goldfish (Carassius auratus) caudal fins

Comparative Biochemistry and Physiology Part C Toxicology & Pharmacology 2026
Deshan Chen, Deshan Chen, Tian Wang, Tian Wang, Lei Han, Lei Han, Hongwei Wang, Hongwei Wang, Ommati MM, Ping Sun, Ping Sun

Summary

Researchers exposed goldfish to UV-aged polystyrene nanoplastics and found that the particles significantly impaired the fish's ability to regenerate their tail fins in a dose- and time-dependent manner. At higher concentrations, the aged nanoplastics disrupted oxidative stress responses, immune function, and key regeneration gene pathways. The study suggests that environmentally weathered nanoplastics may pose sublethal but meaningful threats to aquatic organisms' recovery from injury.

Polymers
Body Systems

Nanoplastics (NPs) are emerging as significant environmental hazards, especially in aquatic ecosystems, where they predominantly exist in aged forms due to weathering processes. Fish, known for their remarkable ability to regenerate injured caudal fins through intricate biological mechanisms, serve as an ideal model for studying sublethal effects of environmental pollutants. This study investigates the toxic impacts of aged polystyrene nanoplastics (PS-NPs) on caudal fin regeneration in goldfish, focusing on molecular, cellular, and physiological responses. Goldfish were exposed to UV-aged PS-NPs (50 nm) at concentrations of 0, 10, 100, and 1000 μg/L, and regeneration was monitored at 7-, 14-, and 35 days post-amputation (dpa). Results demonstrated that caudal fin regeneration was significantly impaired in a concentration- and time-dependent manner. Under exposure to a low concentration (10 μg/L) of aged PS-NPs, goldfish showed an adaptive antioxidant response. Exposure to medium-high concentrations (100-1000 μg/L) led to abnormal ROS activity, disordered apoptosis, and abnormal transcription of core genes in oxidative stress (gpx, sod), immune-inflammation (mpeg1, il-1β, tnf-α), and regeneration pathways (fgf20a, runx2a). This ultimately led to a significant inhibition of caudal fin regeneration at 35 dpa. This study indicates that UV-aged PS-NPs can inhibit the regeneration of goldfish tail fins by disrupting the coordinated function of the oxidative stress-immune-apoptosis-regeneration pathway. The study highlights the risks posed by aged NPs in aquatic environments, emphasizing their potential to impair critical tissue regeneration processes in fish, with broader implications for ecosystem health and resilience.

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