title: The selenium deficiency disease exudative diathesis in chicks is associated with downregulation of seven common selenoprotein genes in liver and muscle.
abstract: Fast-growing broiler chicks are susceptible to Se deficiency diseases including exudative diathesis (ED). Our objective was to determine if ED could be induced by feeding a current, practical diet and if the incidence was related to selenogenome expression in liver and muscle of chicks. Four groups of day-old broiler chicks (n = 60/group) were fed a corn-soy basal diet (BD; 14 μg Se/kg; produced in the Se-deficient area of Sichuan, China and not supplemented with Se or vitamin E), the BD and all-rac-α-tocopheryl acetate at 50 mg/kg and Se (as sodium selenite) at 0.3 mg/kg, or both of these nutrients for 6 wk. A high incidence of ED and mortality of chicks were induced by the BD. The incidences and mortality were completely prevented by supplemental dietary Se but were only partially decreased by supplemental α-tocopherol acetate. Dietary Se deficiency decreased (P < 0.05) mRNA levels of 7 common selenoprotein genes (Gpx1, Gpx4, Sepw1, Sepn1, Sepp1, Selo, and Selk) in muscle and liver. Whereas supplementing α-tocopherol acetate enhanced (P < 0.05) only the muscle Sepx1 mRNA level, it actually decreased (P < 0.05) hepatic Gpx1, Seli, Txnrd1, and Txnrd2 mRNA levels. In conclusion, dietary Se protected chicks from the Se deficiency disease ED, probably by upregulating selenoprotein genes coding for oxidation- and/or lesion-protective proteins. The protection by vitamin E might be mediated via selenoproteins not assayed in this study and/or Se-independent mechanisms. The inverse relationship between hepatic expression of 4 redox-related selenoprotein genes and vitamin E status revealed a novel interaction between Se and vitamin E in vivo.
authors.affiliation: International Center of Future Agriculture for Human Health, Sichuan Agricultural University, Chengdu, Sichuan, China.
authors.forename: Jia-Qiang
authors.initials: JQ
authors.lastname: Huang
authors.forename: Dai-Lin
authors.initials: DL
authors.lastname: Li
authors.forename: Hua
authors.initials: H
authors.lastname: Zhao
authors.forename: Lv-Hui
authors.initials: LH
authors.lastname: Sun
authors.forename: Xin-Jie
authors.initials: XJ
authors.lastname: Xia
authors.forename: Kang-Ning
authors.initials: KN
authors.lastname: Wang
authors.forename: Xugang
authors.initials: X
authors.lastname: Luo
authors.forename: Xin Gen
authors.initials: XG
authors.lastname: Lei
mesh_terms: D000821:Animal Feed / Q000032:analysis; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D002645:Chickens; D003677:Deficiency Diseases / Q000378:metabolism / Q000662:veterinary*; D004032:Diet / Q000662:veterinary; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation / Q000187:drug effects*; D008099:Liver / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism; D011201:Poultry Diseases / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012643:Selenium / Q000172:deficiency*; D051140:Selenoproteins / Q000235:genetics / Q000378:metabolism*; D018038:Sodium Selenite / Q000008:administration & dosage / Q000494:pharmacology; D014810:Vitamin E / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D012333:RNA, Messenger; D051140:Selenoproteins; D014810:Vitamin E; D012643:Selenium; D018038:Sodium Selenite