Ameliorative Effect of Selenomethionine on Cadmium-Induced Hepatocyte Apoptosis via Regulating PI3K/AKT Pathway in Chickens.

Selenium (Se) is a trace element for human and animal health. Cadmium (Cd) is a known human carcinogen. The effects of Cd on the environment and humans are well known. Because chickens are at the top of the food chain, it is a good experimental animal model for assessing heavy metal toxicity and its potential threat to humans. Selenomethionine (Se-met) is a suitable form for nutritional Se supplementation. Therefore, the toxicity of Cd to the chicken liver and the antagonistic effects of Se-met on Cd were examined at the molecular level in the present study. The results showed that oxidative stress indicators (apoptosis-related genes, P13K/AKT pathway-related genes, and heat shock proteins (HSPs)-related genes) in the Cd group have changed significantly, indicating Cd induced hepatocyte stress and apoptosis. Interestingly, the changes in oxidative stress indicators (apoptosis-related genes, P13K/AKT pathway-related genes, and HSPs-related genes) in the Cd-Se-met group were mitigated compared with the control group. Our results indicated that Cd can induce hepatocyte apoptosis and stress in the chickens. Se-met has an ameliorative effect on Cd-induced apoptosis of chicken hepatocyte by regulating PI3K/AKT pathway. Our findings will provide a new insight for better understanding of the detoxification function of Se-met to heavy metals.