Samreen, Xinda Zhang, Jun Wang
Prometryn, a typical thiomethyl-triazine herbicide, has been frequently detected in global coastal waters, and its long-term ecological risks to marine organisms have raised urgent concerns. This study investigated tissue-specific bioaccumulation, depuration, and toxicological effects in female marine medaka (Oryzias melastigma) exposed to environmentally relevant 10 and higher sublethal 100 μg/L prometryn for 42 days, followed by an 18-day depuration period. Prometryn exhibited dose- and time-dependent bioaccumulation, and the concentrations of prometryn in the liver, intestine, and ovary peaked at 7.5, 7.1, and 6.9 μg/g after the exposure. Prometryn exposure elevated mortality, inhibited growth, suppressed hepatosomatic and gonadosomatic indices (HSI/GSI), and induced severe histopathological alterations across multiple tissues. Moreover, exposure to 10 μg/L prometryn resulted in 5,578 differentially expressed genes (DEGs), which were significantly enriched for components of the peroxisome proliferator-activated receptor (PPAR) pathway. Molecular docking confirmed the stable binding of prometryn to the PPARα, PPARβ, and PPARγ isoforms, suggesting a potential interaction with the PPAR signaling pathway. Although over 80% of prometryn was eliminated within the first four days and became nearly undetectable after 18 days of depuration, body weight normalized only in the low-exposure group; HSI/GSI remained significantly suppressed in both pre-exposure groups, and key metabolic regulators showed incomplete transcriptional normalization (DEGs decreased to only 2,438 post-depuration). Thus, prometryn exposure induced lasting adverse effects that persisted even after its environmental presence had ceased. These findings strongly advocate integrating molecular and physiological recovery indicators into the ecological risk assessment of chemical pollution.