Selenoproteins synergistically protect porcine skeletal muscle from oxidative damage via relieving mitochondrial dysfunction and endoplasmic reticulum stress

Jinzhong Jing; Ying He; Yan Liu; Jiayong Tang; Longqiong Wang; Gang Jia; Guangmang Liu; Xiaoling Chen; Gang Tian; Jingyi Cai; Lianqiang Che; Bo Kang; Hua Zhao

doi:10.1186/s40104-023-00877-6

Selenoproteins synergistically protect porcine skeletal muscle from oxidative damage via relieving mitochondrial dysfunction and endoplasmic reticulum stress

J Anim Sci Biotechnol. 2023 Jun 4;14(1):79. doi: 10.1186/s40104-023-00877-6.

Authors

Jinzhong Jing^#¹, Ying He^#¹, Yan Liu¹, Jiayong Tang¹, Longqiong Wang¹, Gang Jia¹, Guangmang Liu¹, Xiaoling Chen¹, Gang Tian¹, Jingyi Cai¹, Lianqiang Che¹, Bo Kang², Hua Zhao³

Affiliations

¹ Key Laboratory for Animal Disease-Resistance Nutrition of Ministry of Education, of China Ministry of Agriculture and Rural Affairs, of Sichuan Province, Animal Nutrition Institute, Sichuan Agricultural University, Chengdu, 611130, Sichuan, China.
² College of Animal Science and Technology, Sichuan Agricultural University, Chengdu, 611130, Sichuan, China.
³ Key Laboratory for Animal Disease-Resistance Nutrition of Ministry of Education, of China Ministry of Agriculture and Rural Affairs, of Sichuan Province, Animal Nutrition Institute, Sichuan Agricultural University, Chengdu, 611130, Sichuan, China. zhua666@126.com.

^# Contributed equally.

Abstract

Background: The skeletal muscle of pigs is vulnerable to oxidative damage, resulting in growth retardation. Selenoproteins are important components of antioxidant systems for animals, which are generally regulated by dietary selenium (Se) level. Here, we developed the dietary oxidative stress (DOS)-inducing pig model to investigate the protective effects of selenoproteins on DOS-induced skeletal muscle growth retardation.

Results: Dietary oxidative stress caused porcine skeletal muscle oxidative damage and growth retardation, which is accompanied by mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and protein and lipid metabolism disorders. Supplementation with Se (0.3, 0.6 or 0.9 mg Se/kg) in form of hydroxy selenomethionine (OH-SeMet) linearly increased muscular Se deposition and exhibited protective effects via regulating the expression of selenotranscriptome and key selenoproteins, which was mainly reflected in lower ROS levels and higher antioxidant capacity in skeletal muscle, and the mitigation of mitochondrial dysfunction and ER stress. What's more, selenoproteins inhibited DOS induced protein and lipid degradation and improved protein and lipid biosynthesis via regulating AKT/mTOR/S6K1 and AMPK/SREBP-1 signalling pathways in skeletal muscle. However, several parameters such as the activity of GSH-Px and T-SOD, the protein abundance of JNK2, CLPP, SELENOS and SELENOF did not show dose-dependent changes. Notably, several key selenoproteins such as MSRB1, SELENOW, SELENOM, SELENON and SELENOS play the unique roles during this protection.

Conclusions: Increased expression of selenoproteins by dietary OH-SeMet could synergistically alleviate mitochondrial dysfunction and ER stress, recover protein and lipid biosynthesis, thus alleviate skeletal muscle growth retardation. Our study provides preventive measure for OS-dependent skeletal muscle retardation in livestock husbandry.

Keywords: Dietary oxidative stress; Endoplasmic reticulum stress; Growth retardation; Mitochondrial dysfunction; Selenoproteins; Skeletal muscle.

Abstract

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