Combined oxybenzone and UVB exposure induces metabolic and neural dysregulation in Mugilogobius chulae embryos and larvae.

The widespread use of sunscreens has contaminated aquatic environments with UV filters like oxybenzone (BP-3), which act as endocrine disruptors in aquatic organisms and exhibit enhanced toxicity under UV radiation. This study employed a multi-omics approach integrating responses from genes to whole organisms to investigate UVB-potentiated toxicity of BP-3 in embryos of the marine fish Mugilogobius chulae. Results demonstrated that UVB significantly amplified BP-3 toxicity, reducing LC from 5674 μg L⁻¹ to 3653 μg L⁻¹ and impairing key developmental endpoints: spontaneous movement, heart rate, and body length. Notably, BP-3 exhibited moderate binding affinity to ERs of M. chulae, and disrupted estrogen signaling, concurrently driving energy dysregulation via the PI3K/Akt-TOR-FoxO signaling axis under combined exposure. Specifically, PI3K/Akt downregulation reduced energy supply, triggering lipid accumulation; indeed, TOR upregulation exacerbated metabolic burden through abnormal reprogramming. The suppression of autophagy genes hindered the clearance of lipid droplets and organelles, fueling metabolic dysfunction and oxidative stress. ROS accumulation, along with neural disruptions like elevated AChE activity, compromised neural function, ultimately exhibited a decrease in swimming distance, speed, and activity duration. These findings established that UVB and BP-3 co-exposure drove metabolic dysregulation, oxidative damage, and neurotoxicity-highlighting the growing ecotoxicological risks of UV filters in aquatic ecosystems under climate-driven UV intensification.