title: Gene expression of endoplasmic reticulum resident selenoproteins correlates with apoptosis in various muscles of se-deficient chicks.
abstract: Dietary selenium (Se) deficiency causes muscular dystrophy in various species, but the molecular mechanism remains unclear. Our objectives were to investigate: 1) if dietary Se deficiency induced different amounts of oxidative stress, lipid peroxidation, and cell apoptosis in 3 skeletal muscles; and 2) if the distribution and expression of 4 endoplasmic reticulum (ER) resident selenoprotein genes (Sepn1, Selk, Sels, and Selt) were related to oxidative damages in these muscles. Two groups of day-old layer chicks (n = 60/group) were fed a corn-soy basal diet (33 μg Se/kg; produced in the Se-deficient area of Heilongjiang, China) or the diet supplemented with Se (as sodium selenite) at 0.15 mg/kg for 55 d. Dietary Se deficiency resulted in accelerated (P < 0.05) cell apoptosis that was associated with decreased glutathione peroxidase activity and elevated lipid peroxidation in these muscles. All these responses were stronger in the pectoral muscle than in the thigh and wing muscles (P < 0.05). Relative distribution of the 4 ER resident selenoprotein gene mRNA amounts and their responses to dietary Se deficiency were consistent with the resultant oxidative stress and cell apoptosis in the 3 muscles. Expression of Sepn1, Sels, and Selt in these muscles was correlated with (r > 0.72; P < 0.05) that of Sepsecs encoding a key enzyme for biosynthesis of selenocysteine (selenocysteinyl-tRNA synthase). In conclusion, the pectoral muscle demonstrated unique expression patterns of the ER resident selenoprotein genes and GPx activity, along with elevated susceptibility to oxidative cell death, compared with the other skeletal muscles. These features might help explain why it is a primary target of Se deficiency diseases in chicks.
authors.affiliation: Department of Veterinary Medicine, Northeast Agricultural University, Harbin, Heilongjiang, China.
authors.forename: Hai-Dong
authors.initials: HD
authors.lastname: Yao
authors.forename: Qiong
authors.initials: Q
authors.lastname: Wu
authors.forename: Zi-Wei
authors.initials: ZW
authors.lastname: Zhang
authors.forename: Jiu-Li
authors.initials: JL
authors.lastname: Zhang
authors.forename: Shu
authors.initials: S
authors.lastname: Li
authors.forename: Jia-Qiang
authors.initials: JQ
authors.lastname: Huang
authors.forename: Fa-Zheng
authors.initials: FZ
authors.lastname: Ren
authors.forename: Shi-Wen
authors.initials: SW
authors.lastname: Xu
authors.forename: Xiao-Long
authors.initials: XL
authors.lastname: Wang
authors.forename: Xin Gen
authors.initials: XG
authors.lastname: Lei
mesh_terms: D000604:Amino Acyl-tRNA Synthetases / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D002645:Chickens; D003677:Deficiency Diseases / Q000378:metabolism*; D019587:Dietary Supplements; D004195:Disease Models, Animal; D004721:Endoplasmic Reticulum / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression; D005979:Glutathione Peroxidase / Q000378:metabolism; D015227:Lipid Peroxidation; D009124:Muscle Proteins / Q000235:genetics / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000378:metabolism*; D018384:Oxidative Stress; D012333:RNA, Messenger / Q000378:metabolism; D012346:RNA, Transfer, Amino Acyl / Q000378:metabolism; D012643:Selenium / Q000172:deficiency* / Q000378:metabolism / Q000494:pharmacology; D017279:Selenocysteine / Q000096:biosynthesis; D051140:Selenoproteins / Q000235:genetics / Q000378:metabolism*; D014131:Trace Elements / Q000172:deficiency / Q000378:metabolism / Q000494:pharmacology
chemical_list: D009124:Muscle Proteins; D012333:RNA, Messenger; D012346:RNA, Transfer, Amino Acyl; C435489:SELENON protein, human; D051140:Selenoproteins; D014131:Trace Elements; C112705:selenocysteinyl-tRNA; D017279:Selenocysteine; D005979:Glutathione Peroxidase; D000604:Amino Acyl-tRNA Synthetases; D012643:Selenium