Membrane-targeted molecular binding and redox collapse underlie UV-328 toxicity in Chlorella pyrenoidosa

Benzotriazole ultraviolet stabilizer UV-328 has attracted increasing attention due to its environmental persistence, bioaccumulative potential, and inclusion in the Stockholm Convention. However, its toxicological effects on aquatic primary producers remain insufficiently understood. In this study, we systematically examined the multi-faceted responses of Chlorella pyrenoidosa to UV-328 exposure. Growth inhibition assays revealed time- and concentration-dependent toxicity, with IC₅₀ values varying between 86.8 and 137.9 mg L^-1 over 96 h. A strong linear internal dose-response relationship was established for photosynthetic impairment and oxidative stress within the physiologically valid range (0-250 mg L^-1), whereas lethal exposures led to a collapse in the bioconcentration factor (BCF) and loss of membrane integrity. Transcriptomic profiling (at 48 h, under 100 and 300 mg L^-1 exposure) identified 194 responsive genes enriched in membrane lipid metabolism, antioxidant defense, and protein processing. Docking analysis further predicted 11 potential protein targets, six of which were membrane-localized and linked to redox and metabolic regulation. They were implicated in oxidative stress response and metabolic maintenance. The results underscored the multifactorial toxicity of UV-328, characterized by membrane-associated disruption and oxidative overload. This work provides molecular insight into UV-328's toxicity mechanisms and informs ecological risk assessment specific industrial applications where UV-328 remains in use.