Altered acyl-CoA metabolism in riboflavin deficiency.

Veitch, Keith;Draye, J P;Vamecq, J.;Causey, A. G.;Van Hoof, François;et.al.
(1989) Biochimica et Biophysica Acta : international journal of biochemistry and biophysics — Vol. 1006, n° 3, p. 335-343 (1989)

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  • Veitch, KeithUCLouvain
    Author
  • Draye, J PUCLouvain
    Author
  • Vamecq, J.UCLouvain
    Author
  • Causey, A. G.Department of Child Health & Clinical Biochemistry, The Medical School, The University, Newcastle upon Tyne, U.K.
    Author
  • Van Hoof, FrançoisUCLouvain
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Abstract
We have recently described the effects of riboflavin deficiency on the metabolism of dicarboxylic acids (Draye et al. (1988) Eur. J. Biochem. 178, 183-189). As both mitochondria and peroxisomes are thought to be involved, we have examined the activities of various enzymes in these organelles in the livers of riboflavin-deficient rats. Mitochondrial beta-oxidation of fatty acids was severely depressed due to loss of activity of the three fatty acyl-CoA dehydrogenases, whereas there was an enhancement of peroxisomal beta-oxidation due to an increased activity of the FAD-dependent fatty acyl-CoA oxidase, although the activities of other peroxisomal flavoproteins, D-amino acid oxidase and glycolate oxidase, were lowered. Hepatocyte morphometry revealed an increase in the numbers of peroxisomes, indicating a proliferation induced by the deficiency. The mitochondrial acyl-CoA dehydrogenases involved in branched-chain amino acid metabolism were also severely decreased leading to characteristic organic acidurias. There was some loss of activity of the flavin-dependent sections of the electron transport chain (complexes I and II), but these were probably not sufficient to affect normal function in vivo. The specificity of these effects allows the use of the riboflavin-deficient rat as a model for the study of dicarboxylate metabolism.
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Veitch, K., Draye, J. P., Vamecq, J., Causey, A. G., Bartlett, K., Sherratt, H. S., & Van Hoof, F. (1989). Altered acyl-CoA metabolism in riboflavin deficiency. Biochimica et Biophysica Acta : international journal of biochemistry and biophysics, 1006(3), 335-343. https://hdl.handle.net/2078.5/30809 (Original work published 1989)