Abstract
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 riboflavin-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.
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