H₂S exposure-induced oxidative stress promotes LPS-mediated hepatocyte autophagy through the PI3K/AKT/TOR pathway

Hydrogen sulfide (H₂S), a common air pollutant and toxic gas, is detrimental to organisms and the environment. Exposure to highly concentrated H₂S can induce oxidative stress and autophagy. However, the mechanism underlying the liver damage caused by H₂S 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 H₂S combined with LPS on oxidative stress and autophagy. The four groups (control group, LPS group, H₂S group and H₂S-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 H₂S group compared to those in the control group; however, malondialdehyde levels in the H₂S group increased. Molecular-level studies showed that the expression of genes associated with the PI3K/ AKT/ TOR pathways in the H₂S 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 H₂S caused oxidative stress and induced autophagy through the PI3K/ AKT/ TOR pathway in chicken liver cells. Additionally, exposure to H₂S aggravated LPS-induced oxidative stress and autophagy injury. Capsule: Aerial exposure to H₂S 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.