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

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.

Selenomethionine alleviates chronic heat stress-induced breast muscle injury and poor meat quality in broilers via relieving mitochondrial dysfunction and endoplasmic reticulum stress

In the present study,the chronic heat stress(CHS)broiler model was developed to investigate the potential protection mechanism of organic selenium(selenomethionine,SeMet)on CHS-induced skeletal muscle growth retardation and poor meat quality.Four hundred Arbor Acres male broilers(680±70 g,21 d old)were grouped into 5 treatments with 8 replicates of 10 broilers per replicate.Broilers in the control group were raised in a thermoneutral environment(22±2°C)and fed with a basal diet.The other four treatments were exposed to hyperthermic conditions(33±2°C,24 h in each day)and fed on the basal diet supplied with SeMet at 0.0,0.2,0.4,and 0.6 mg Se/kg,respectively,for 21 d.Results showed that CHS reduced(P<0.05)the growth performance,decreased(P<0.05)the breast muscle weight and impaired the meat quality of breast muscle in broilers.CHS induced protein metabolic disorder in breast muscle,which increased(P<0.05)the expression of caspase 3,caspase 8,caspase 9 and ubiquitin proteasome system related genes,while decreased the protein expression of P-4EBP1.CHS also decreased the antioxidant capacity and induced mitochondrial stress and endoplasmic reticulum(ER)stress in breast muscle,which increased(P<0.05)the ROS levels,decreased the concentration of ATP,increased the protein expression of HSP60 and CLPX,and increased(P<0.05)the expression of ER stress biomarkers.Dietary SeMet supplementation linearly increased(P<0.05)breast muscle Se concentration and exhibited protective effects via up-regulating the expression of the selenotranscriptome and several key selenoproteins,which increased(P<0.05)body weight,improved meat quality,enhanced antioxidant capacity and mitigated mitochondrial stress and ER stress.What's more,SeMet suppressed protein degradation and improved protein biosynthesis though inhibiting the caspase and ubiquitin proteasome system and promoting the mTOR-4EBP1 pathway.In conclusion,dietary SeMet supplementation increases the expression of several key selenoproteins,alleviates mitochondrial dysfunction and ER stress,improves protein biosynthesis,suppresses protein degradation,thus increases the body weight and improves meat quality of broilers exposed to CHS.