Riboflavin is built on an isoalloxazin ring, which contains three sixcarbon rings: benzoic, pyrazine and pyrimidine. Riboflavin is synthesized by some bacteria, but among humans and animals, the only source of flavin coenzymes (FAD, FMN) is exogenous riboflavin. Riboflavin transport in enterocytes takes place via three translocators encoded by the SLC52 gene. Deficiency of dietary riboflavin has wide ranging implications for the efficacy of other vitamins, the mechanism of cellular respiration, lactic acid metabolism, hemoglobin, nucleotides and amino acid synthesis. In studies it was found that, pharmacologic daily doses (100 mg) have the potential to react with light, which can have adverse cellular effects. Extrene caution should be exercised when using riboflavin as phototherapy in premature newborns. At the cellular level, riboflavin deficiency leads to increased oxidative stress and causes disorders in the glutathione recycling process. Risk factors for developing riboflavin deficinecy include pregnancy, malnutrition (including anorexia and other eating disorders, vegitarianism, veganism and alcoholism. Furthermore, elderly people and atheletes are also at risk of developing this deficiency. Widespread use of riboflavin in medicine, cancer therapy, treatment of neurodegenerative diseases, corneal ectasia and viral infections has resulted in the recent increased interest in this flavina.