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Results for “VITAMIN B2 DEFICIENCY”

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At least 19 recordsLinked to original sources
PubMedDate not supplied

[Metabolism of 25-hydroxyvitamin D3 in the kidney and nuclear receptors of 1,25-dihydroxyvitamin D3 in small intestine mucosa of rats with vitamin B2 deficiency].

Effect of vitamin B2 deficiency on metabolism, reception and biochemical functions of vitamin D was studied in young rats. Deficiency in vitamin B2 was shown to cause a moderate hypocalcemia as well as a decrease in the active transport of calcium in small intestine and in concentration of 25-OH D in blood serum, lowered formation of 24,25 (OH)2D3 in kidney slices and decreasing content of nuclear receptors for 1,25 (OH)2D3 (fre and bound in vivo) in small intestine mucose. After administration of cholecalciferol into the animals deficient in vitamins D and B2 within 24 hrs or 6 days before death restoration of the calcium metabolism parameters was retarded as a result of less distinct stimulation of I-hydroxylase and of low activity of 24-hydroxylase 25-OH D3 in kidney as well as due to a moderate increase in content of bound receptors of 1,25 (OH)2D3 in small intestine mucose and, apparently, because of reduced production of the proteins dependent on vitamin D in the tissue (Ca2+-ATPase and alkaline phosphatase). The data obtained suggest the possible importance in rickets of vitamin B2 deficiency mediated via its influence on metabolism and reception of vitamin D.

Animals↗
PubMed1991

Effect of vitamin B2 deficiency on rat liver dihydropyrimidine dehydrogenase activity.

Effect of vitamin B2 deficiency on rat liver dihydropyrimidine dehydrogenase was investigated. It was found that the purified enzyme contains 2 mol flavin per molecule, which consists of equal proportions of flavin-adenine dinucleotide (FAD) and riboflavin 5'-phosphate (FMN). When rats were fed on a vitamin B2-deficient diet for 5 weeks, dihydropyrimidine dehydrogenase activity in the liver was diminished, followed by a decrease in enzyme concentration. Moreover, the addition of exogenous FAD or FMN did not restore the activity. Thus endogenous flavin may regulate the enzyme half-life or synthesis. Lowering of dihydropyrimidine dehydrogenase activity in the livers of rats fed on a vitamin B2-deficient diet did not affect the uridine, uracil and sigma UMP (the sum of acid soluble uracil 5'-nucleotides) pool in liver.

Animals↗
PubMed1990

Influence of vitamin B2 deficiency on polychlorinated biphenyls-induced liver lipid peroxides formation in rats.

The present study is carried out to explore whether the liver microsomal drug-metabolizing enzymes induced by PCB are associated with the PCB-induced liver lipid peroxide formation in rats. For this purpose, variations of the drug-metabolizing enzyme activities mediated by vitamin B2 deficiency were utilized. The administration of PCB to rats induced the liver microsomal cytochrome P-450 and vitamin B2 deficiency promoted the induction. The cytochrome b5 was also induced by PCB but no further induction by vitamin B2 deficiency was observed. The flavoenzyme, NADPH-cytochrome c reductase, was induced by PCB when the vitamin B2-supplemented PCB diet was fed to rats, but the activity of the enzyme was decreased by vitamin B2 deficiency and PCB further decreased the activity. The liver lipid peroxide levels increased in PCB groups with and without vitamin B2 compared with each PCB-free group, but the lipid peroxide level in vitamin B2-deficient PCB group was significantly lower than in vitamin B2-supplemented PCB group. From these results, the PCB-induced liver lipid peroxide formation was not necessarily related to the variations of the liver microsomal drug-metabolizing enzymes.

Animals↗
PubMedDate not supplied

[Metazid-inducible vitamin B2 deficiency in rats and its prevention].

Rectal administration of metaside (20 mg per 100 g body weight) as suppositories for 10 days was found to cause vitamin B2 deficiency both in rats on low-vitamin B2 diet and in those on balanced diet. This appeared as decreased vitamin B2 levels in the liver and plasma. The design and application of suppositories containing the mixed preparation of metaside and riboflavin drug (in a dose of 100 micrograms per rat, which corresponds to the recommended daily requirement) completely prevents vitamin B2 deficiency.

Animals↗
PubMedDate not supplied

Methazid-induced vitamin B2 deficiency in rats and its prevention.

It has been estimated that ten-day rectal administration of metazid in the form of suppositories (20 mg per 100 g of body mass) gives rise to vitamin B2 deficiency both in rats with initial vitamin B2 insufficiency and in those adequately supplied. This is confirmed by a decrease in the vitamin B2 content both in the liver and in the blood plasma. Development and use of suppositories containing combined preparation of metazid and riboflavin (in the dose of 100 micrograms per a rat according to the daily recommended allowance) completely prevent metazid-induced vitamin B2 deficiency.

Animals↗
PubMed1979

[Vitamin B2 deficiency and total parenteral nutrition].

A 15 year old adolescent with Crohn's disease who received total parenteral nutrition for three months developed riboflavin deficiency. The aetiology, the clinical picture and the method of diagnosis of this unusual deficiency are reviewed. The importance of an adequate intake of vitamin B2 and the other B group vitamins, particularly in the malnourished, is emphasied.

Adolescent↗