Selenium protects against cadmium-induced kidney apoptosis in chickens by activating the PI3K/AKT/Bcl-2 signaling pathway.

Cadmium (Cd) is a toxic heavy metal that can induce apoptosis. Selenium (Se) is a necessary trace element and can antagonize the toxicity of many heavy metals, including Cd. PI3K/AKT/Bcl-2 is a key survival signaling pathway that regulates cellular defense system against oxidative injury as well as cell proliferation, survival, and apoptosis. The antagonistic effects of Se on Cd-induced toxicity have been reported. However, little is known about the effect of Se on Cd-induced apoptosis in chicken kidneys via the PI3K/AKT/Bcl-2 signaling pathway. In the present study, we fed chickens with Se, Cd, or both Se and Cd supplements, and after 90 days of treatment, we detected the related index. The results showed that the activity of inducible nitric oxide synthase (iNOS) and concentration of nitric oxide (NO) were increased; activities of the mitochondrial respiratory chain complexes (complexes I, II, and V) and ATPases (the Na-K-ATPase, the Mg-ATPase, and the Ca-ATPase) were decreased; expression of PI3K, AKT, and Bcl-2 were decreased; and expression of Bax, Bak, P53, Caspase-3, Caspase-9, and cytochrome c (Cyt c) were increased. Additionally, the results of the TUNEL assay showed that the number of apoptotic cells was increased in the Cd group. By contrast, there was a significant improvement of the correlation indicators and occurrence of apoptosis in the Se + Cd group compared to the Cd group. In conclusion, our results confirmed that Se had a positive effect on ameliorating Cd-induced apoptosis in chicken kidney tissue by activating the PI3K/AKT/Bcl-2 signaling pathway.