Sakurai T, Miyazawa S, Furuta S, Hashimoto T
Lipids. 1982 Sep;17(9):598-604. doi: 10.1007/BF02535365.
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.
给断乳大鼠喂食缺乏核黄素的饮食。核黄素缺乏时,肝脏中的线粒体脂肪酸氧化受到抑制,但补充核黄素后恢复。在该系统涉及的酶中,只有酰基辅酶A脱氢酶(EC 1.3.99.2和1.3.99.3)的活性随脂肪酸氧化的变化而变化。在核黄素缺乏时发现酰基辅酶A脱氢酶的脱辅基形式积累。电子传递黄素蛋白和β-氧化系统中涉及的其他酶的水平保持不变。过氧化物酶体脂肪酸氧化及该系统中各酶的水平保持恒定。在单纯核黄素缺乏的条件下,未观察到酰基辅酶A氧化酶脱辅基形式的积累。然而,在核黄素缺乏的条件下,当通过给予过氧化物酶体增殖剂邻苯二甲酸二(2-乙基己基)酯诱导过氧化物酶体系统时,观察到大量脱辅基酰基辅酶A氧化酶的积累。