The role of Nrf2/Keap1 signaling in inorganic mercury induced oxidative stress in the liver of large yellow croaker Pseudosciaena crocea

• Antioxidant system were involved in defending against oxidative damage of Hg exposure.
• Positive correlations were observed between activities and expression levels of antioxidant enzymes.
• Nrf2 is required for the protracted induction these antioxidant enzyme genes.

The aim of the present study was to evaluate the effects of acute inorganic Hg exposure (0, 32 and 64 μg Hg L−1) on lipid peroxidation, activities and gene expression of antioxidant enzymes (Cu/Zn-SOD, CAT, GPx, GR and GST), and mRNA levels of the Keap1-Nrf2 signaling molecules at different exposure times (6 h, 12 h, 24 h, 48 h, and 96 h) in the liver of large yellow croaker Pseudosciaena crocea. The results showed that lipid peroxidation was sharply reduced by 32 μg Hg L−1 during 6–12 h before returning to control levels. Similarly, lipid peroxidation was significantly reduced during 6–12 h followed by a sharp increase towards the end of the exposure in the 64 μg Hg L−1 group. There was a negative relationship between lipid peroxidation and antioxidant enzyme activities, and positive relationship between activities and gene expression of antioxidant enzymes, suggesting that the changes at a molecular level may underlie enzymatic level and accordingly affect hepatic lipid peroxidation. Obtained results also showed a coordinated transcriptional regulation of antioxidant genes, suggesting that Nrf2 is required for the protracted induction of these genes. Furthermore, a negative relationship between the mRNA levels of Nrf2 and Keap1 indicated that Keap1 may play an important role in switching off the Nrf2 response. In conclusion, this is the first study to elucidate effects of waterborne Hg on antioxidant system in large yellow croaker through the Keap1-Nrf2 pathway, which will aid our understanding of the molecular mechanisms of waterborne heavy metal on antioxidant responses in fish.