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.
References:
1. Ball GFM. Vitamins: their role in the human body. Oxford: Blackwell Publishing; 2004:289-299.
2. Rivlin RS, Pinto JT. Riboflavin (vitamin B2). In: Rucker RB, Suttie JW, McCormick DB, Machlin LJ, eds. Handbook of Vitamins. 3rd ed. New York, NY: Marcel Dekker; 2001:255-273.
3. Powers HJ. Riboflavin (vitamin B-2) and health. Am J Clin Nutr. 2003 Jun;77(6):1352-1360. PubMed 12791609
4. Powers HJ, Corfe BM, Nakano E. Riboflavin in development and cell fate. Subcell Biochem. 2012;56:229-245. PubMed 22116702
5. Bamji MS, Sarma KV, Radhaiah G. Relationship between biochemical and clinical indices of B-vitamin deficiency. A study in rural school boys. Br J Nutr. 1979 May;41(3):431-441. PubMed 465434
6. Boisvert WA, Castañeda C, Mendoza I, et al. Prevalence of riboflavin deficiency among Guatemalan elderly people and its relationship to milk intake. Am J Clin Nutr. 1993 Jul;58(1):85-90. PubMed 8317395
7. Bailey AL, Maisey S, Southon S, Wright AJ, Finglas PM, Fulcher RA. Relationships between micronutrient intake and biochemical indicators of nutrient adequacy in a ‘free-living’ elderly UK population. Br J Nutr. 1997 Feb;77(2):225-242. PubMed 9135369
8. Madigan SM, Tracey F, McNulty H, et al. Riboflavin and vitamin B-6 intakes and status and biochemical response to riboflavin supplementation in free-living elderly people. Am J Clin Nutr. 1998 Aug;68(2):389-395. PubMed 9701198
9. Benton D, Haller J, Fordy J. The vitamin status of young British adults. Int J Vitam Nutr Res. 1997;67(1):34-40. PubMed 9119611
10. Hustad S, Ueland PM, Vollset SE, Zhang Y, Bjørke-Monsen AL, Schneede J. Riboflavin as a determinant of plasma total homocysteine: effect modification by the methylenetetrahydrofolate reductase C677T polymorphism. Clin Chem. 2000 Aug;46(8 Pt 1):1065-1071. PubMed 10926884
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.
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No case of riboflavin toxicity in humans has been reported.
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Antiparietal Cell Antibody, Calcitriol (1,25 di-OH Vit D), Copper, Pl, Intrinsic Factor Antibodies (Serum), Intrinsic Factor Blocking Antibody, Manganese, Methylmalonic Acid, Serum, Nicotinamide, Nicotinic Acid, Phosphate (Phosphorus), Vitamin A, Vitamin B1 (Thiamine), Vitamin B12, Vitamin B2 (Riboflavin), Plasma, Vitamin B2, Whole Blood, Vitamin B3 (Niacin), Vitamin B6, Vitamin B9 (Folate), Vitamin C, Vitamin D, 25-Hydroxy, Vitamin E (Tocopherol), Vitamin K, Zinc, RBC