Riboflavin (Vitamin B2)
Riboflavin normally combines in the tissues with phos-phoric acid to form two coenzymes, flavin mononu-cleotide (FMN) and flavin adenine dinucleotide (FAD).
They operate as hydrogen carriers in important oxida-tive systems of the mitochondria. NAD, operating in association with specific dehydrogenases, usually accepts hydrogen removed from various food substrates and then passes the hydrogen to FMN or FAD; finally, the hydrogen is released as an ion into the mitochon-drial matrix to become oxidized by oxygen.
Deficiency of riboflavin in experimental animals causes severe dermatitis, vomiting, diarrhea, muscle spasticity that finally becomes muscle weakness, coma and decline in body temperature, and then death. Thus, severe riboflavin deficiency can cause many of the same effects as a lack of niacin in the diet; presumably, the debilities that result in each instance are due to gener-ally depressed oxidative processes within the cells.
In the human being, there are no known cases of riboflavin deficiency severe enough to cause the marked debilities noted in experimental animals, but mild riboflavin deficiency is probably common. Such defi-ciency causes digestive disturbances, burning sensations of the skin and eyes, cracking at the corners of the mouth, headaches, mental depression, forgetfulness, and so on.
Although the manifestations of riboflavin deficiency are usually relatively mild, this deficiency frequently occurs in association with deficiency of thiamine, niacin, or both. Many deficiency syndromes, including pellagra,beriberi, sprue, and kwashiorkor, are probably due to acombined deficiency of a number of vitamins, as well as other aspects of malnutrition.
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