Selenium Deficiency Induces Apoptosis, Mitochondrial Dynamic Imbalance, and Inflammatory Responses in Calf Liver

Selenium (Se) deficiency significantly impacts the cow breeding industry by reducing the milk quality of dairy cows and affecting the health of calves. The molecular mechanism of Se deficiency-induced damage to calves, however, remains unclear. The present study investigated whether Se deficiency induces oxidative stress, apoptosis, and inflammation in calf liver tissues. We collected the liver tissues of calves with Se deficiency. Experimental results showed that Se deficiency weakened the activity of antioxidant enzymes and increased the accumulation of oxidation products in the liver. Se deficiency also led to excessive fission of the mitochondria and downregulated the expression of the Mfn2 and Opa1 genes in the calf liver. Mitochondrial damage-induced apoptosis by increasing the expression of pro-apoptotic genes such as CytC, Cas3, Cas9, fas, and Cas8, leading to a decrease in energy metabolism. Se deficiency also triggered the expression of inflammatory-related factors such as IL-1β, IL-6, TNF-α, and NF-κB. Taken together, the results suggest that Se deficiency causes oxidative stress, triggers an inflammatory response, disrupts mitochondrial dynamic balance, and then induces apoptosis, eventually leading to calf liver damage. These findings might provide valuable clues for elucidating the mechanism of Se deficiency-induced injury in domestic animals.