Antagonistic effect of selenium on programmed necrosis of testicular Leydig cells caused by cadmium through endoplasmic reticulum stress in chicken.

Cadmium (Cd) is a widely distributed environmental contaminant that is highly toxic to animals and humans. However, detailed reports on Cd-induced programmed necrosis have not been seen in chicken testicular Leydig cells. Selenium (Se) is a trace element in the human body that has cytoprotective effects in a variety of pathological damages caused by heavy metals.

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.

Selenium-Alleviated Testicular Toxicity by Modulating Inflammation, Heat Shock Response, and Autophagy Under Oxidative Stress in Lead-Treated Chickens.

Lead (Pb), a toxic pollutant, is toxic to the testis. However, biological events during testicular Pb poisoning were not well understood. Selenium (Se) has the ability to antagonize Pb toxicity.