SeMet attenuates TBBPA-induced hepatocyte injury via inhibiting endoplasmic reticulum stress.

Tetrabromobisphenol A (TBBPA) is the most widely used brominated flame retardant in the world. Due to its abuse and emission, TBBPA, as a persistent organic pollutant, can produce strong teratogenic and other toxic effects on environmental organisms. Selenomethionine (SeMet) is organic selenium with potent antioxidant and detoxification functions that could be used to alleviate adverse effects of several environmental contaminants, such as fish, but their protection of TBBPA is not clear. This study explored the toxic mechanism of TBBPA and the detoxification effect of SeMet on common carp and grass carp hepatocytes (L8824 cells). Our findings showed exposure to TBBPA at a concentration of 0.35 mg/L for 30 days caused reactive oxygen species over-production, endoplasmic reticulum (ER) stress and depolarization of mitochondrial membrane potential, which led to autophagy and apoptosis. Fortunately, these abnormal alterations caused by TBBPA could be significantly reversed by 1.0 mg/kg SeMet pre-treatment through alleviating ER stress. This study not only illustrates the potential molecular mechanism of SeMet antagonizing TBBPA-induced hepatotoxicity, but also provides new clues for organic selenium antagonizing biological and ecological safety issues caused by industrial additive pollution.