Riboflavin deficiency and beta-oxidation systems in rat liver.

Abstract

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.

• Authors: T Sakurai, S Miyazawa, S Furuta, T Hashimoto
• Journal: Lipids (Lipids) Vol. 17 Issue 9 Pg. 598-604 (Sep 1982) ISSN: 0024-4201 [Print] United States
• PMID: 7144448 (Publication Type: Journal Article)

Chemical References

• Fatty Acids
• Diethylhexyl Phthalate
• Oxidoreductases
• Acyl-CoA Oxidase

Topics

• Acyl-CoA Oxidase
• Animals
• Diethylhexyl Phthalate (pharmacology)
• Enzyme Induction
• Fatty Acids (metabolism)
• Liver (metabolism)
• Male
• Microbodies (enzymology)
• Mitochondria, Liver (enzymology)
• Oxidation-Reduction
• Oxidoreductases (metabolism)
• Rats
• Rats, Inbred Strains
• Riboflavin Deficiency (metabolism)