Selenium deficiency causes oxidative stress and activates inflammation, apoptosis, and necroptosis in the intestine of weaned calves

Abstract

Selenium performs a variety of biological functions in organisms, including antioxidant and anti-inflammatory effects. This study investigated how selenium deficiency affects weaned calves' intestines. According to ICP-MS analysis of intestinal selenium concentrations in calves, the Se-D group had a significantly lower concentration of selenium. Hematoxylin-eosin staining showed that the intestinal epithelial cells were detached, the goblet cells were lost, and the intestinal villi were fragmented and loosely arranged in the Se-D group, along with hyperemia and inflammatory infiltration. Nine of the 22 selenoprotein genes were down-regulated in response to selenium deficiency in RT-PCR, whereas six genes were up-regulated. In the Se-D group, oxidative stress was detected by measuring redox levels in the intestines. Furthermore, TUNEL staining, RT-PCR, and WB results indicated that both intrinsic and extrinsic apoptosis pathways are activated in the intestine during selenium deficiency. Selenium deficiency also induced necroptosis in the intestine through upregulation of MLKL, RIPK1, and RIPK3 mRNA levels. In addition, according to hematoxylin-eosin staining and ELISA, selenium-deficient calves had severe inflammation in their intestines. As a result of RT-PCR and WB analyses, we found that selenium deficiency was associated with NF-κB and MAPK pathways. Our study suggested that weaned calves' intestines are affected by selenium deficiency, which causes oxidative stress, inflammation, apoptosis, and necroptosis.

Extracellular Vesicles Derived from Selenium-Deficient MAC-T Cells Aggravated Inflammation and Apoptosis by Triggering the Endoplasmic Reticulum (ER) Stress/PI3K-AKT-mTOR Pathway in Bovine Mammary Epithelial Cells

“…Se deficiency destroys the body's REDOX homeostasis, and ROS accumulation promotes the occurrence of oxidative stress in mastitis [37]. Previous studies have confirmed that Se deficiency causes inflammatory damage through oxidative stress in chickens [38], mice [39], carps [40], and cattle [41]. The present study established the Se-deficient MAC-T cell model in vitro by continuous delivery culture using FBS with very low Se concentrations.…”