17α-methyltestosterone induced hepatocyte apoptosis through endoplasmic reticulum stress in Takifugu fasciatus

17α-methyltestosterone (17α-MT) is an emerging pollutant, which is harmful to the endocrine system and reproduction of fish. We investigated the effects of different concentrations of 17α-MT (0, 5, 30, 60, and 100 mg/kg) on endoplasmic reticulum stress (ERS) and apoptosis in the liver of Takifugu fasciatus. Results show that: (1) with the increase of 17α-MT treatment concentration, liver transaminases (alanine aminotransferase; aspartate aminotransferase) and the mRNA expression of ERS marker genes (glucose-regulated protein 78; calreticulin) of T. fasciatus were significantly increased compared with the control group (P<0.05); (2) the activity of succinate dehydrogenase (SDH), Caspase3 and Caspase9 in the liver of T. fasciatus increased with the increase of 17α-MT concentration compared with the control group (P<0.05); (3) by using 4-phenylbutyricacid (4-PBA) inhibitors to stimulate ERS through in vitro experiments, the expression of ERS and apoptosis-related genes significantly decreased (P<0.05), and the apoptosis rate of T. fasciatus hepatocytes was significantly inhibited (P<0.05) under 17α-MT treatment. This study confirmed that ERS played an important role in the induction of apoptosis in the hepatocytes of T. fasciatus, which enriched the ecotoxicological information of environmental androgens.