Riboflavin, a vitamin derived from many plant and animal sources, is important for the synthesis of flavin nucleotides, which play an important role in electron transport and other reactions in which the transfer of energy is crucial.

Riboflavin is converted within the body to flavin mononucleotides and dinucleotides.

Riboflavin itself and flavin mononucleotides are absorbed from the proximal small bowel, where as flavin adenine dinucleotide must be degraded to flavin mononucleotide prior to absorption.

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The conjugated and unconjugated forms circulate bound to serum proteins, but storage sites have not been clearly defined.

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Clinical symptoms of riboflavin deficiency are uncommon.

They are usually seen only in debilitated patients with a variety of diseases and in poorly nourished alcoholics.

Deficiency of thiamine, riboflavin, and niacin are unusual in the industrialized countries because bread and cereals are fortified with these vitamins.

Occasionally a mild deficiency of riboflavin is seen during pregnancy and lactation or during the period of growth of childhood and adolescence, when increased demands are combined with moderate nutritional deprivation.

Riboflavin deficiency is manifested principally by lesions of the facial skin and the corneal epithelium.

Cheilosis, a term used for fissures in the skin at the angles of the mouth, is a characteristic feature. These cracks in the skin may be painful and often become infected.

Microcopically, hyperkeratosis and a mild mononuclear infiltrate of the skin are noted.

Seborrheic dermatitis, an inflammation of the skin that exhibits a greasy, scaling appearance, typically involves the cheeks and the areas behind the ears.

The tongue is smooth and a purplish (magenta) color owing to atrophy of the mucosa.

The most troubling lesion may be an interstitial keratisis of the cornea.

The conjunctivae are injected and severe photophobia is a problem.

The cornea is initially vascularized by numerous sprouting capillaries.

This process is followed by opacification of the cornea and eventual ulceration.

The localization of the lesions in riboflavin deficiency is not explained by biochemistry.

Thiamin, riboflavin and vitamin B6: impact of restricted intake on physical performance in man.J Am Coll Nutr. 1994 (6):629-40.

OBJECTIVE: A combined marginally deficient status of thiamin, riboflavin, vitamin B6 and vitamin C may affect physical performance, but the relative contribution of each vitamin can only be speculated. In a previous study we did not find any effect of restricted intake of vitamin C individually. Therefore, the functional effect of restriction of thiamin, riboflavin or vitamin B6, individually or in conjunction, was investigated. METHODS: A double-blind, 2 x 2 x 2 complete factorial experiment on the effects of thiamin, riboflavin and vitamin B6 restriction on physical performance was executed with 24 healthy men. During 11 weeks of low vitamin intake, the subjects were given a daily diet of regular food products providing no more than 55% of the Dutch Recommended Dietary Allowances (RDA) for thiamin, riboflavin and vitamin B6. Other vitamins were supplemented at twice the RDA level. RESULTS: In vitamin-restricted subjects, blood vitamin levels, erythrocytic enzyme activities and urinary vitamin excretion decreased and in vitro erythrocytic enzyme stimulation increased. Short-time vitamin restriction had no harmful effects on health. A significant overall decrease was observed in aerobic power (VO2-max; 11.6%), onset of blood lactate accumulation (OBLA; 7.0%) and oxygen consumption at this power output (VO2-OBLA; 12.0%), peak power (9.3%), mean power (6.9%) and related variables (p < 0.01). However, the observed performance decrements could not be attributed to marginal deficiency for any of the vitamins studied. CONCLUSION: The absence of vitamin-specific effects on performance decrements due to thiamin, riboflavin and vitamin B6 restriction suggests quantitatively similar but non-additive effects of these B-vitamins on mitochondrial metabolism.

Riboflavin deficiency is associated with selective preservation of critical flavoenzyme-dependent metabolic pathways.Biofactors. 1992 Jan;3(3):185-90.

Riboflavin is a water soluble vitamin that serves as a precursor of flavin mononucleotide and flavin adenine dinucleotide. These two compounds are coenzymes in a variety of electron transfer reactions that occur in energy producing, biosynthetic, detoxifying and electron scavenging pathways. When an organism is confronted with inadequate dietary riboflavin, characteristic changes occur in the cellular distribution of the various flavin fractions as well as in the activities of flavin-dependent enzymes. These changes suggest a specific hierarchic response to riboflavin deficiency, e.g. the core electron transfer chain required for ATP synthesis is preserved while the enzymes required for the first step of fatty acid beta-oxidation are diminished. The mechanisms by which the specific changes in enzyme activity are mediated have not been completely identified, but appear to result from a combination of diminished access of normal or near normal levels of apoenzyme to coenzyme and diminished abundance of apoenzyme. The changes in apoenzyme content potentially result from alterations in either protein stability or gene expression. The response to riboflavin deficiency of several key enzyme systems and the pathways affected will be discussed and a hierarchic order by which specific enzyme activities are preserved while others are decreased will be proposed. The current understanding of the molecular mechanisms by which these changes are mediated will be discussed.

Riboflavin requirement of Filipino women.Eur J Clin Nutr. 1992 Apr;46(4):257-64.

The level of riboflavin intake that will correct riboflavin deficiency in seven non-pregnant and in twelve pregnant Filipino women was determined in order to reassess the adequacy of the current Recommended Dietary Allowance (RDA) for riboflavin in Filipinos. Increasing levels of riboflavin were given to the subjects who were rated as riboflavin-deficient based on an initial erythrocyte glutathione reductase activation coefficient (EGR-AC) of greater than or equal to 1.3 in screening. The minimum riboflavin requirement, defined as the intake of riboflavin required to achieve an EGR-AC of less than 1.3, was estimated from the regression of EGR-AC on riboflavin intake (mg/1000 kcal). The estimates of minimum riboflavin requirement from the non-pregnant women ranged from 0.16 to 0.42 with a mean of 0.35 +/- 0.09 (SD) mg/1000 kcal. For the pregnant subjects, the estimates of minimum riboflavin requirement ranged from 0.36 to 0.81 with a mean of 0.58 +/- 0.18 (SD) mg/1000 kcal. Adding 30% to the mean, to cover the upper limits of 97.5% of the population, the estimated RDA for non-pregnant women is 0.46/1000 kcal. This value is approximately equal to the 1976 Philippine RDA of 0.5 mg riboflavin/1000 kcal. For pregnant women, adding 30% to the mean minimum requirement of 0.58 mg/1000 kcal, the estimated RDA is 0.75 mg/1000 kcal or 1.75 mg/day computed at the energy allowance of 2350 kcal during pregnancy. This value is 25% higher than the current Philippine RDA of 1.4 mg/day for pregnant women.

Riboflavin deficiency and iron absorption in adult Gambian men.Ann Nutr Metab. 1992;36(1):34-40.

Iron absorption from 3.38 mg 58Fe was measured in riboflavin-deficient Gambian men with haemoglobin (Hb) less than 11.5 g/dl before and after oral riboflavin therapy, and the results compared with a group not receiving riboflavin. Riboflavin status (as determined by erythrocyte glutathione reductase activation coefficient) and Hb increased in teh riboflavin-supplemented but not placebo group. Plasma ferritin levels were low and did not change in either group. There was very wide variation in percentage iron absorption between individuals and also within single individuals on two separate occasions but no measurable change with riboflavin supplementation. The results of the study indicate that the efficiency of iron utilization is impaired in riboflavin deficiency, but that iron absorption is unaffected.

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Significance of phototherapy-induced riboflavin deficiency in the full-term neonate.Biol Neonate. 1992;61(2):76-81.

As a result of impaired fatty acid oxidation, a characteristic urinary dicarboxylic aciduria occurs in the riboflavin deficient animal. We compared the occurrence of riboflavin deficiency induced by phototherapy with changes in urinary organic acid profiles in 8 full-term, breast-fed neonates who received phototherapy for hyperbilirubinemia, and in 10 full-term, breastfed controls. Riboflavin status was assessed by measuring flavin adenine dinucleotide saturation of erythrocyte glutathione reductase. All 8 neonates exposed to phototherapy developed riboflavin deficiency (p less than 0.001). Riboflavin deficiency was progressive with the duration of phototherapy. None of the controls was riboflavin deficient. Urine organic acid profiles indicative of mitochondrial acyl-CoA dehydrogenase activity (fatty acid beta-oxidation, quantitated by gas chromatography mass spectrometry) showed no changes between the study and control groups in mono-, di-, or tricarboxylic acids or other organic acids. The riboflavin deficiency induced by phototherapy in full-term neonates was not of sufficient severity to limit riboflavin-dependent fatty acid oxidation.

Intramitochondrial fatty acid metabolism: riboflavin deficiency and energy production. Biochem Cell Biol. 1991 Jul;69(7):490-7.

Inborn errors of fatty acid beta-oxidation have contributed significantly to our understanding of intracellular fatty acid metabolism. The first intramitochondrial step in beta-oxidation of fatty acyl-CoA of different chain lengths is catalyzed by the three chain length specific acyl-CoA dehydrogenases. Inherited deficiency of these enzymes has been reported. Some are riboflavin responsive. The first step of fatty acid oxidation is reviewed with specific emphasis on beta-oxidation in newborn infants, rendered riboflavin deficient by phototherapy. Given that medium chain fatty acids are not stored as triacylglycerols and undergo rapid beta-oxidation, they have been proposed as superior substrates compared with long chain triglycerides in times of metabolic stress. This review also examines medium chain triglycerides as an alternate energy source. When medium chain triglycerides were fed as 50% of total energy, glucose sparing was present with little loss of energy as dicarboxylic acids.

Recurrent aphthous ulceration: vitamin B1, B2 and B6 status and response to replacement therapy. J Oral Pathol Med. 1991 Sep;20(8):389-91.

An evaluation of the thiamine, riboflavin and pyridoxine (vitamin B1, B2 and B6) status of 60 patients with recurrent mouth ulcers was performed. Seventeen patients (28.2%) were found to be deficient in one or more of these vitamins. Replacement therapy of these vitamins was given to a study group of deficient patients and a non-deficient group for one month. At the end of therapy and after a follow-up period of 3 months, only those patients who had a B complex deficiency had a significant sustained clinical improvement in their mouth ulcers. Vitamin B1, B2 and B6 deficiencies should, therefore, be considered as another possible precipitating factor in recurrent aphthous ulceration.

Vitamin B1, B2 and B6 status of vegetarians.: J Med Assoc Thai. 1991 Oct;74(10):465-70.

The vitamin B1, B2 and B6 status was determined in 132 healthy vegetarians, age range 25-57 years who have been practising vegetarianism for 1-22 years. Sixty-eight healthy non-vegetarians were chosen as controls. The conventional methods to measure the activation coefficient alpha ETK, alpha EGR and alpha EAST were applied to assess the vitamin status of B1, B2 and B6 respectively. The value of 1.25 alpha ETK, 1.5 alpha EGR and 2.0 alpha EAST and above indicate a deficiency in the vitamin status. The results showed significantly poorer vitamin B1 and B6 status in vegetarians than in non-vegetarians, whereas, no significant difference in vitamin B2 status was found. None of the non-vegetarians were deficient in vitamin B1 but 3 of them (4.4%) were deficient in vitamin B6. On the other hand, 10 of vegetarians (7.6%) were deficient in vitamin B1; 38 (28.8%) in vitamin B6. A high prevalence of riboflavin deficiency was found in 32 (24.2%) of the vegetarians; as well as in 15 (22.2%) of the non-vegetarians. Only riboflavin status was significantly related with the duration of vegetarianism practiced. Vegetarians should be considered as the vulnerable group for vitamin B2 and vitamin B6 deficiencies. B-vitamins status should be checked and efforts should be made to improve through dietary counselling and nutritional education should be included and stress in the health education program in order to improve nutritional deficiencies.

Riboflavin deficiency caused by treatment with adriamycin.: J Nutr Sci Vitaminol (Tokyo). 1991 Oct;37(5):473-7.

The present study was undertaken to determine whether administration of adriamycin causes the depletion of riboflavin content. Rats received intraperitoneal injections of adriamycin (4 mg per kg body weight) for 6 consecutive days. Urinary riboflavin excretion began to increase after 2 days of treatment with adriamycin. Erythrocyte FAD levels decreased gradually and plasma lipid peroxide contents increased markedly at the 6th day. The activity coefficient of erythrocyte glutathione reductase showed a significant increase before the decrease of flavin content and the elevation of lipid peroxide level. Therefore, the value of this coefficient obtained from erythrocyte appears to be a reliable index of riboflavin deficiency, particularly during the early stage.

Effect of riboflavin or pyridoxine deficiency on inflammatory response.Indian J Biochem Biophys. 1991 Oct-Dec;28(5-6):481-4.

Inflammatory response has been assessed in riboflavin or pyridoxine deficient rats. Edema was increased by 54% in pyridoxine deficiency as compared to weight-matched control rats. Food restriction per se reduced the volume of edema by 63%. In pyridoxine deficiency, concentrations of thiobarbituric acid reactive substances (which indicate the extent of lipid peroxidation) increase by 30 and 43% respectively in the edematous tissues of the paw as well as in the wounded skin. Both these parameters were not affected by riboflavin deficiency. Activities of NADPH oxidase and superoxide dismutase in elicited leukocytes from peritoneal cavity were reduced by 54 and 52%, respectively, in riboflavin deficiency but were unaltered in pyridoxine deficiency. Superoxide level and acid phosphatase activity were not influenced by either of the deficiencies, whereas hydrogen peroxide level was increased by 48% in riboflavin deficiency. Food restriction did not affect leukocyte enzymes or the levels of reduced oxygen species. The data suggest that inflammation is enhanced in pyridoxine deficiency but not in riboflavin deficiency.

Riboflavin deficiency: mucocutaneous signs of acute and chronic deficiency. Semin Dermatol. 1991 Dec;10(4):293-5.

Mucocutaneous lesions are present in both acute and chronic riboflavin deficiency. The distribution of the lesions varies with the age and gender of the patient. Lesions of acute riboflavin deficiency are similar to those observed in protein-energy malnutrition of the kwashiorkor type. In chronic riboflavin deficiency the cutaneous lesions resemble monilial intertrigo and the mucous membrane lesions include a characteristic glossitis. Prompt resolution of lesions after therapeutic doses of the vitamin are given confirms the diagnosis. Biochemical changes caused by riboflavin deficiency, which explain the dermatoses and mucous membrane lesions, have not as yet been determined. Lack of information in this area is explained by the difficulty of separating cutaneous changes caused by the deficiency from those caused by trauma or other proximate etiologic agents.

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