The effects of dietary selenium and vitamin E on avian white muscle disease as measured by both chemical and physical parameters.
Commercial chicken broilers were fed a semipurified diet deficient in vitamin E and selenium from day 1 to day 13 ex ova and subsequently fed varying levels of dietary selenium and vitamin E. All birds were sacrificed on the 28th day, stored for 36 hr at 2 C to allow the onset and resolution of rigor, and frozen at -32 C until needed. Total cathepsin content of the Pectoralis major depended upon dietary vitamin E for birds receiving 0 to 12 IU/kg, whereas selenium administered at .05 to .16 ppm in the diet showed no statistically significant effect. Similarly, total protein content of P. major increased with increasing level of dietary vitamin E, but the level of dietary selenium had no effect. Muscle break strength was significantly affected by dietary selenium and vitamin E (P = .0092) interacting together. Catheptic activity and muscle protein explained 6.36% and 3.58% of the viriability in muscle break strength. Birds with more advanced avian white muscle disease showed higher break strength values. Ultrastructural deterioration of the myipathic muscle included disintegration of blood vessel walls, transverse tubules, and mitochondrial membranes as well as the obvious disruption of the myofibrillar components. Myelin figures were present in diseased, but not in normal, muscle. Accumulation of adipocytes both extracellularly and intracellularly occurred in selenium and vitamin E-deficient birds.
D000818:Animals; D002645:Chickens; D009132:Muscles / Q000648:ultrastructure; D009137:Muscular Dystrophy, Animal / Q000188:drug therapy*; D011201:Poultry Diseases / Q000188:drug therapy*; D012643:Selenium / Q000627:therapeutic use*; D014810:Vitamin E / Q000627:therapeutic use*; D014912:White Muscle Disease / Q000188:drug therapy*
D014810:Vitamin E; D012643:Selenium