The Effect Of Dietary Selenium And Vitamin E Deficiency On The Selenoprotein Genes Expression In Liver And Muscle Of Broiler

Selenium (Se), an essential trace element, and vitamin E, a lipid soluble antioxidant. arc important mediators for protection against oxidative stress. Recent work has demonstrated that deficiencies in either Se or vitamin E result in increased viral pathogenicity and altered immune responses. Furthermore, Se deficiency in poultry, especially together with vitamin E deficiency, causes Se-deficiency diseases including exudative diathesis, pancreatic dystrophy and nutritional muscular dystrophy. This study was designed to use selenium and/or vitamin E diet fed broiler chickens, build the chicks Se-VE deficiency model. Then, The selenoprotein genes expression in liver and muscle were detected. Provide the basis for the study of selenium and vitamin E in chicks in vivo biological mechanism.A feeding experiment was carried out to compare the effects of supplementing a poultry meal-based diet with selenium(as sodium selenite) or Vitamin E (as a-tocopherol)on broiler chickens. The aim of this experiment is to investigate the selenoprotein expression is or not associated with selenium deficiency disease.In this experiment, A total of255day-old male broiler poults were selected. While15chicks were killed on the day1for baseline analyses, the rest of240animals were all oiled into four dietary treatment groups (n=60). Four groups (n=6G/group) of One-day-old male broiler chickens (mean weight42.3±0.6g) were fed a corn-soy basal diet (BD. Se deficient,0.014ppm), The experimental grower diets were supplemented with Se at0.3mg/kg or/and VE at50mg/kg of feed, as follows:T-(-Se-VE)=BD, T2(-Se+VE)=BD+50VE, T3(+Se-VE)=BD+0.3Se and T4(+Se+VE)=BD+50VE+0.3Se.The development of deficiency signs were followed grossly, biochemically and histochemically. Gross signs of selenium and VE deficiency included growth retardation marked by particularly poor growth of muscle, liver and pancreas and Exudative Quality(ED). In the third week of trial1, one-third of the chicken appeared ED,appearing as though they were going to die, In the fourth week of trial1one-half of the chickens appeared ED,and one-eighth of trial2appeared ED.Dietary Se deficiency decreased (P<0.05) mRNA levels of7common selenoprotein genes(Gpx1, Gpx4, Sepw1, Sepn1, Sepp1, Selo, and Selk) in muscle and liver. While supplementing a-tocopherol acetate enhanced (P<0.05) only muscle Sepx1mRNA level, it actually decreased (P<0.05) hepatic Gpxl, Sell, Txnrd1, and Txnrd2mRNA levels. In conclusion, dietary Se protected chicks from the Se-deficiency diseases probably by up-regulating selenoprotein genes coding for oxidation-and(or)lesion-protective proteins. The protection of vitamin E might be mediated via selenoproteins un-assayed in this study and (or) Se-independent mechanisms. The inverse relationship between hepatic expression of4redox-related selenoprotein genes and vitamin E status revealed a novel interaction between Se and vitamin E in vivo.