Vitamin B2 refers to a family of water-soluble flavin vitamins that are critical for metabolism and energy generations in the aerobic cell, through oxidative phosphorylation.
These compounds are synthesized in plants and microorganisms and occur naturally in three forms: the physiologically inactive riboflavin, and the physiologically active coenzymes flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD). FAD accounts for about 90% of the total riboflavin in tissues. Because of their capacity to transfer electrons, FAD and FMN are essential for proton transfer in the respiratory chain, for the dehydration of fatty acids, the oxidative deamination of amino acids, and for other redox processes.
The effects of riboflavin deficiency on growth and development have generally been explained in terms of these functions. Flavin derivatives ingested with the diet (FAD, FMN) are dissociated by gastric acid from their protein binding, transformed by phosphatases to riboflavin, and absorbed in the small intestines. The reconversion of riboflavin to the coenzymes FMN and FAD occurs in the cytoplasm in many different tissues.
Vitamin B2 is involved in the metabolism of folate, vitamin B12, vitamin B6, and other vitamins. Plasma vitamin B2 is a determinant of plasma homocysteine level, which is associated with cardiovascular disease, pregnancy complications, and cognitive impairment. \
Recent studies have suggested that riboflavin may play an important role in the determination of cell fate, which would have implications for growth and development. Specifically, riboflavin deficiency impairs the normal progression of the cell cycle, probably through effects on the expression of regulatory genes, exerted at both the transcriptional and proteomic level.
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Vitamin B2 deficiency is common in many parts of the world, particularly in developing countries. Several studies have indicated that vitamin B2 deficiency may be widespread in industrialized countries as well, both in the elderly and in young adults. Dietary deficiency of riboflavin is characterized by lesions on the lips and the angles of the mouth, fissured and magenta-colored tongue, corneal vascularization and normocytic, normochromic anemia.
Skin lesions include red scaly, greasy patches on the nose, eyelids, scrotum, and labia and seborrheic dermatitis. These symptoms are a consequence of oxidation stress due to the accumulation of lipid peroxides. Vitamin B2 deficiency leads to reduced activity of the flavin-containing enzymes (glutathione reductase and glutathione peroxidase) which, in turn, allows these peroxidase to express their deleterious effects.
No case of riboflavin toxicity in humans has been reported.
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