Riboflavin deficiency and beta-oxidation systems in rat liver.
Weanling rats were fed a riboflavin-deficient diet. The mitochondrial fatty acid oxidation in liver was depressed in riboflavin deficiency but restored after supplementation of riboflavin. Among the enzymes involved in this system, only the acyl-CoA dehydrogenase (EC 1.3.99.2 and 1.3.99.3) activities varied with the change in fatty acid oxidation. An accumulation of the apoforms of acyl-CoA dehydrogenases was found in riboflavin deficiency. The levels of electron transfer flavoprotein and other enzymes involved in the beta-oxidation system remained unchanged. The peroxisomal fatty acid oxidation and levels of individual enzymes of this system remained constant. No accumulation of the apoform of acyl-CoA oxidase was observed under simple, riboflavin-deficient conditions. However, accumulation of a large amount of apo-acyl-CoA oxidase was observed when the peroxisomal system was induced by administration of a peroxisome proliferator, di(2-ethylhexyl)phthalate, under riboflavin-deficient conditions.
D042962:Acyl-CoA Oxidase; D000818:Animals; D004051:Diethylhexyl Phthalate / Q000494:pharmacology; D004790:Enzyme Induction; D005227:Fatty Acids / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D008297:Male; D008830:Microbodies / Q000201:enzymology; D008930:Mitochondria, Liver / Q000201:enzymology; D010084:Oxidation-Reduction; D010088:Oxidoreductases / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012257:Riboflavin Deficiency / Q000378:metabolism*
D005227:Fatty Acids; D004051:Diethylhexyl Phthalate; D010088:Oxidoreductases; D042962:Acyl-CoA Oxidase