4-hydroxy-2-nonenal and Swine-Diseases

4-hydroxy-2-nonenal has been researched along with Swine-Diseases* in 1 studies

Other Studies

1 other study(ies) available for 4-hydroxy-2-nonenal and Swine-Diseases

ArticleYear
Feeding corn oil to vitamin E-deficient pigs increases lipid peroxidation and decreases tissue glutathione concentrations.
    International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vitaminologie et de nutrition, 1995, Volume: 65, Issue:3

    Dietetic microangiopathy ("mulberry heart disease") is a common disease of weaned pigs in several countries. It is characterised by sudden death and has been associated with vitamin E deficiency. We investigated whether it could be induced by depleting pigs of vitamin E with or without a mild peroxidative challenge. In a 2 x 2 experiment, the effect on pigs of depletion of alpha-tocopherol and supplementation with alpha-tocopherol-stripped corn oil were investigated. Although dietetic microangiopathy was not induced, there was evidence of lipid peroxidation, as judged by increased concentrations of Fe++(-)induced 4-hydroxynonenal (4-HNE) and decreased amounts of linolenic acid (C18:3, omega-3) in tissue. Reduced glutathione (GSH) can conjugate to 4-HNE in an attempt to detoxify this highly toxic compound. GSH concentrations were decreased in skeletal muscle, but not in heart, of pigs that were depleted of alpha-tocopherol with or without supplementation with corn oil. The activity of glucose-6-phosphate dehydrogenase (G6PDH) was higher in heart than in skeletal muscles. It is postulated that sufficient NADPH may be produced in heart to maintain GSH concentrations at a level sufficient to conjugate the excess 4-HNE produced by alpha-tocopherol deficiency and/or oil supplementation.

    Topics: Aldehydes; Animals; Corn Oil; Dietary Fats, Unsaturated; Glucosephosphate Dehydrogenase; Glutathione; Lipid Peroxidation; Muscle, Skeletal; Myocardium; NADP; Swine; Swine Diseases; Vitamin E Deficiency

1995