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