HS exposure-induced oxidative stress promotes LPS-mediated hepatocyte autophagy through the PI3K/AKT/TOR pathway.

Hydrogen sulfide (HS), a common air pollutant and toxic gas, is detrimental to organisms and the environment. Exposure to highly concentrated HS can induce oxidative stress and autophagy. However, the mechanism underlying the liver damage caused by HS has not been identified. Lipopolysaccharide (LPS), the key component of endotoxin, can induce oxidative stress and autophagy. For this experiment, we used one-day-old chickens as model organisms to evaluate the effects of HS combined with LPS on oxidative stress and autophagy. The four groups (control group, LPS group, HS group and HS-LPS group) were observed by electron microscopy, detected by oxidative stress kit, analyzed by quantitative real-time quantitative PCR, and analyzed by Western blot. We found that the activities of antioxidant enzymes (superoxide dismutase, antioxidant glutathione, catalase, and glutathione peroxidase) decreased in the HS group compared to those in the control group; however, malondialdehyde levels in the HS group increased. Molecular-level studies showed that the expression of genes associated with the PI3K/ AKT/ TOR pathways in the HS group decreased, whereas the expression of other autophagy-related genes (Beclin1, ATG5 and the ratio of LC3-II/ LC3-I) increased compared to that in the control group. These findings suggest that HS caused oxidative stress and induced autophagy through the PI3K/ AKT/ TOR pathway in chicken liver cells. Additionally, exposure to HS aggravated LPS-induced oxidative stress and autophagy injury. Capsule: Aerial exposure to HS can cause oxidative stress in chicken livers and induce autophagy through the PI3K/AKT/TOR pathway, and can aggravate LPS-induced oxidative stress and autophagy.