Selenium alleviates cadmium-induced oxidative stress, endoplasmic reticulum stress and programmed necrosis in chicken testes.

Cadmium (Cd) is a common heavy metal pollutant, and one of the important target organs of its toxicity is the testis. Selenium (Se) has the ability to antagonize the toxicity of Cd. However, the mechanism of the alleviating effects of Se on Cd in chicken testis injury through oxidative stress, endoplasmic reticulum stress (ERS), and programmed necrosis remained unclear. To explore this, 80 7-day-old chickens were divided into the Control group, the Se group (1.00 mg/kg Se), the Cd group (150.00 mg/kg Cd), and the CdSe group. On the 30th and 60th days, serum and chicken testis tissue samples were collected for testing. The results showed that Cd exposure resulted in swelling and deformation of seminiferous tubules, and thinning of the seminiferous epithelium. The ROS and MDA increased, and the SOD, CAT, GSH, GSH-Px decreased. The expression of GRP78, PERK, IRE1, ATF6, CHOP, and JNK in the Cd group increased. The expression of TNF-α, TNFR1, RIP1, RIP3, MLKL, and PARP1 increased, while the expression of Caspase-8 decreased. Histopathological changes, oxidative stress, ERS, and programmed necrosis were improved after CdSe treatment. In conclusion, Se antagonized the toxicity of Cd, and Se could alleviate Cd-induced oxidative stress, ERS, and programmed necrosis in chicken testis.