Selenium Deficiency-Induced Oxidative Stress Causes Myocardial Injury in Calves by Activating Inflammation, Apoptosis, and Necroptosis

Abstract

Selenium (Se) is essential for human and animal health, but there have been few studies on the mechanisms of injury in dairy cows with Se deficiency. This study aimed to evaluate the effects of Se deficiency on myocardial injury in weaned calves. The Se-D group had significantly lower myocardial Se concentrations than the Se-C group. Histological analysis indicated that Se deficiency induced a large area of necrosis in the myocardium, accompanied by inflammatory changes. Se deficiency significantly decreased the expression of 10 of the 21 selenoprotein genes and increased the expression of SEPHS2. Furthermore, we found that oxidative stress occurred in the Se-D group by detection of redox-related indicators. Additionally, TUNEL staining showed that Se deficiency causes severe apoptosis in the myocardium, which was characterized by activating the exogenous apoptotic pathway and the mitochondrial apoptotic pathway. Se deficiency also induced necroptosis in the myocardium by upregulating MLKL, RIPK1, and RIPK3. Moreover, Se-deficient calves have severe inflammation in the myocardium. Se deficiency significantly reduced anti-inflammatory factor levels while increasing pro-inflammatory factor levels. We also found that the NF-κB pathway and MAPK pathway were activated in Se-deficient conditions. Our findings suggest that Se deficiency causes myocardial injury in weaned calves by regulating oxidative stress, inflammation, apoptosis, and necroptosis.