Frenkel E P, Kitchens R L, Savage H E, Seibert R A, Lane M
Am J Clin Nutr. 1979 Jan;32(1):10-5. doi: 10.1093/ajcn/32.1.10.
The neurological sequelae of riboflavin deficiency posed the possibility that this tissue injury was mediated by defective vitamin B12 function due to the requirement for riboflavin-dependent oxidoreductase systems in B12 coenzyme synthesis and function. Studies of the B12-dependent enzymatic reactions (5-methyltetrahydrofolic-homocysteine methyltransferase and methylmalonyl coenzyme A mutase) in a fiboflavin-deficient rat model documented normal B12 activity in liver and neural tissue. In addition, examination of neural lipids and separation and analysis of neural fatty acids failed to reveal the increased odd chain fatty acids characteristically seen in the B12-deficient state. Thus, the neural tissue sequelae of riboflavin deficiency do not appear to relate to B12 coenzyme function.
核黄素缺乏的神经后遗症引发了一种可能性，即这种组织损伤是由维生素B12功能缺陷介导的，因为在B12辅酶合成和功能中需要核黄素依赖性氧化还原酶系统。在核黄素缺乏的大鼠模型中对B12依赖性酶促反应（5-甲基四氢叶酸-同型半胱氨酸甲基转移酶和甲基丙二酰辅酶A变位酶）的研究表明，肝脏和神经组织中的B12活性正常。此外，对神经脂质的检查以及神经脂肪酸的分离和分析未能揭示在B12缺乏状态下典型出现的奇数链脂肪酸增加的情况。因此，核黄素缺乏的神经组织后遗症似乎与B12辅酶功能无关。
