Zinc acclimation mitigated high zinc induced oxidative stress by enhancing antioxidant defenses in large yellow croaker Pseudosciaena crocea

• High Zn induced oxidative stress in fish.
• Low Zn pre-exposure protected fish against oxidative stress under high Zn stress.
• This protection depended on the regulation at enzymatic and transcriptional levels.
• Transcription factor Nrf2 played a central role in antioxidant defenses.

The hypothesis tested in the present study was that Zn acclimation will alleviate high Zn induced oxidative stress in large yellow croaker Pseudosciaena crocea. To the end, fish were pre-exposed to 0 and 2 mg Zn L−1 for 48 h and then exposed to 0 and 10 mg Zn L−1 for 48 h. Lipid peroxidation, activities and mRNA levels of antioxidant enzyme genes (Cu/Zn-SOD, CAT, GPx and GR), and gene expressions of Nrf2–Keap1 signaling molecules at different exposure time (12 h, 24 h and 48 h) were determined in the liver and spleen of large yellow croaker. 10 mg Zn L−1 exposure alone enhanced lipid peroxidation in the liver during 12–48 h and in the spleen during 24–48 h. Although 2 mg Zn L−1 pre-exposure did not affect lipid peroxidation, 2 mg Zn L−1 pre-exposure mitigated high Zn induced oxidative stress. The positive effect of Zn acclimation could be attributed to the up-regulated expression and activities of antioxidant enzyme genes under high Zn stress. Obtained results also showed a coordinated transcriptional regulation of antioxidant genes, suggesting that Nrf2 is required for the protracted induction of these genes. Besides, the sharp increase in Keap1 expression levels would support its role in switching off Nrf2 response. In conclusion, Zn acclimation mitigated high Zn-induced oxidative stress in large yellow croker, emphasizing a central role of transcription factor Nrf2 in the process.