Brady P S, Hoppel C L
Biochem J. 1985 Aug 1;229(3):717-21. doi: 10.1042/bj2290717.
The effects of riboflavin deficiency on hepatic peroxisomal and mitochondrial palmitoyl-CoA oxidation were examined in weanling Wistar-strain male rats. The specific activities of peroxisomal catalase and palmitoyl-CoA-dependent NAD+ reduction were not affected by up to 10 weeks of riboflavin deficiency. In contrast, the specific activity of mitochondrial carnitine-dependent palmitoyl-CoA oxidation was depressed by 75% at 10 weeks of deficiency. The amount of peroxisomal protein per g of liver was not affected by riboflavin deficiency, whereas, expressed per liver, both riboflavin-deficient and pair-fed controls showed decreased peroxisomal protein compared with controls fed ad libitum. Hepatic mitochondria, but not peroxisomes, were sensitive to riboflavin deficiency.
在断乳的Wistar品系雄性大鼠中,研究了核黄素缺乏对肝脏过氧化物酶体和线粒体棕榈酰辅酶A氧化的影响。长达10周的核黄素缺乏并未影响过氧化物酶体过氧化氢酶的比活性以及棕榈酰辅酶A依赖性NAD⁺还原。相反,缺乏10周时,线粒体肉碱依赖性棕榈酰辅酶A氧化的比活性降低了75%。每克肝脏的过氧化物酶体蛋白量不受核黄素缺乏的影响,然而,以每个肝脏表示时,与自由采食的对照组相比,核黄素缺乏组和配对喂养对照组的过氧化物酶体蛋白均减少。肝脏线粒体而非过氧化物酶体对核黄素缺乏敏感。