H2S inhalation-induced energy metabolism disturbance is involved in LPS mediated hepatocyte apoptosis through mitochondrial pathway

Abstract Hydrogen sulfide (H 2 S) is a toxic gas and one of the air pollutants of great concern. High-concentrated H 2 S can induce energy metabolism disturbance and apoptosis. However, the mechanism of H 2 S-induced liver injuries is unknown. Lipopolysaccharide (LPS), the main component of endotoxin, can cause fulminant hepatitis. Here, we evaluated the effects of H 2 S combined with LPS on the energy metabolism and apoptosis pathway in the liver using a one-day-old chicken as a model. Our results showed that the expression levels of energy metabolism-related genes (AMP-activated protein kinase (AMPK), Hypoxia-inducible factor-1 (HIF-1), aconitase 2 (ACO2), hexokinase1 (HK1), hexokinase 2 (HK2), lactate dehydrogenase A (LDHA), lactate dehydrogenase B (LDHB), phosphofructokinase (PFK), pyruvate kinase (PK) and succinate dehydrogenase B (SDHB)) tended to decrease, that the status of apoptosis increased, and that the expression levels of apoptosis-related genes (caspase3, BCL2, and bax) increased in H 2 S group, suggesting that H 2 S exposure disturbed the energy metabolism in the liver and induced hepatocyte apoptosis through the mitochondrial pathway. In addition, H 2 S combined with the LPS aggravated the level of energy metabolism disorders and apoptosis, indicating that H 2 S inhalation-induced energy metabolism disturbance is involved in LPS-mediated hepatocyte apoptosis through the mitochondrial pathway.