The role of BNIP3 and blocked autophagy flux in arsenic induced oxidative stress induced liver injury in rats

Abstract Arsenic is a widely distributed environmental toxic substance in nature. Chronic arsenic exposure can cause permanent damage to the liver of humans and animals, resulting to the death of poisoned patients. However, the mechanism of liver damage caused by arsenic poisoning is yet unclear. Here, four different concentrations of sodium arsenite (NaAsO2) [control group (0 mg/L), low dose (25 mg/L), medium dose (50 mg/L), and high dose group (100 mg/L)]were established to induce liver injury in rats. Took into account this, the relationship and potential mechanisms of oxidative stress, Bcl-2/adenovirus E1B-19-kDa interacting protein 3 (BNIP3), and inhibition of autophagy flux in liver injury caused by arsenic poisoning were studied. The results indicated that long-term exposure to NaAsO2 could induce oxidative stress, leading to high expression of BNIP3 and impaired autophagy flux, resulting in liver damage. This research provides an important basis for future research on liver damage caused by chronic arsenic exposure and prevention and treatment with BNIP3 as the target.