Effect of vitamin E and selenium on resistance to oxidative stress in chicken superficial pectoralis muscle.
One-day-old chicks were reared using diets that differed in their vitamin E and/or selenium content. In chicks depleted of both selenium and vitamin E, signs of exudative diathesis on the superficial pectoralis muscle were observed. The purpose of this research was to determine the defective points of the antioxidant defense system, which made this tissue highly susceptible to nutritionally-induced oxidative stress. Vitamin E, and selenium in lower magnitude, were the factors that strikingly affected the course of mitochondrial lipid peroxidation. Animals fed diets deficient in vitamin E and selenium displayed the lowest reduced glutathione level and glutathione peroxidase activity. The decreased levels of reduced glutathione were not due to a defective activity of glutathione reductase, which was increased in both mitochondria and cytosol. The absence of vitamin E was linked to lowering of mitochondrial thiol levels. The Glutathione peroxidase/Cu,Zn-superoxide dismutase ratio was 2.8 in animals fed selenium and vitamin E, and decreased to 0.13 in animals deficient in both nutrients. This change was indicative of oxidant-induced damage mediated by hydrogen peroxide. Catalase activity increased in an attempt to counteract the decrease in glutathione peroxidase activity. The results obtained showed that alpha-tocopherol and Se deficiencies caused multiple alterations in the antioxidant system and adversely affected the redox state of chicken superficial pectoralis muscle.
Avanzo
J L
JL
Departamento de Ciências Básicas, Faculdade de Zootecnia e Engenharia de Alimentos, Universidade de São Paulo, Av. Duque de Caxias Norte, 225, 13635-900, P.O. Box 23, Pirassununga/SP, Brazil.
de Mendonça
C X
CX
Pugine
S M
SM
de Cerqueira Cesar
M
M
D000818:Animals; D002374:Catalase / Q000032:analysis* / Q000187:drug effects; D002645:Chickens; D004032:Diet; D019587:Dietary Supplements; D005978:Glutathione / Q000032:analysis* / Q000502:physiology; D005979:Glutathione Peroxidase / Q000097:blood; D066298:In Vitro Techniques; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D010544:Peroxidases / Q000032:analysis* / Q000187:drug effects; D012643:Selenium / Q000008:administration & dosage / Q000172:deficiency / Q000378:metabolism / Q000494:pharmacology*; D013438:Sulfhydryl Compounds / Q000378:metabolism; D013482:Superoxide Dismutase / Q000032:analysis* / Q000187:drug effects; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D014811:Vitamin E Deficiency / Q000097:blood / Q000378:metabolism
D013438:Sulfhydryl Compounds; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D010544:Peroxidases; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D012643:Selenium