Investigating the physiological mechanisms of juvenile flounder in response to waterborne exposure of methylmercury

Numerous studies have highlighted the deleterious effects of methylmercury (MeHg) on fish. However, the mechanisms underlying the physiological responses across different tissues during the early life stages (ELSs) in marine fish remain insufficiently understood. In this context, the present study utilised juvenile flounder (Paralichthys olivaceus) to conduct a 15-day exposure experiment at concentrations of 0, 0.1, and 10.0 μg L⁻¹ of MeHg. After exposure, we assessed growth parameters, MeHg accumulation, and biomarkers reflecting a range of physiological responses. The results revealed a significant dose-dependent and tissue-specific trend in MeHg accumulation in the liver, intestines, and kidneys. Specifically, MeHg accumulation increased with the exposure concentration, with the liver showing the highest levels. Notably, MeHg exposure did not significantly affect fish growth. Furthermore, MeHg induced substantial oxidative damage in all the three tissues. Physiological responses related to antioxidant capacity, immune response, detoxification, and metabolism were significantly activated in response to MeHg, as indicated by the elevated activity of relevant biomarkers. Principal component analyses (PCA) confirmed the dose-dependence and tissue specificity of these physiological responses. It revealed that oxidative damage and toxicity to antioxidant and immune functions in the liver were more pronounced than those in other tissues. Star plots of the biomarker deviation index (BDI) and integrated biomarker response (IBR) illustrated the dynamic adaptive strategies employed by different physiological responses under low and high MeHg exposure, with the intestine demonstrating the most complex response. This study provides valuable insights into the mechanistic responses of marine fish to MeHg exposure during the ELS.