Ameliorative Effect of Selenomethionine on Cadmium-Induced Hepatocyte Apoptosis via Regulating PI3K/AKT Pathway in Chickens
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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.
KeywordsSelenomethionine Cadmium Oxidative stress Apoptosis P13K/AKT pathway HSPs
The study was financially supported by the Project Fund of Academic Cadre of Northeast Agricultural University (Project No. 700-507001).
Compliance with Ethical Standards
All experiments were approved by the Institutional Animal Care and Use Committee of Northeast Agricultural University.
Conflict of Interest
The authors declare that they have no conflict of interest.
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