Hormonal Regulation of Riboflavin Metabolism

Rivlin, Richard S.

doi:10.1007/978-1-4613-4419-3_12

Cited by 12 publications

(8 citation statements)

References 69 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, riboflavin plasma riboflavin concentrations may decrease in pregnancy [15] and in response to treatment with antimalarial drugs [1]. Moreover, evidence has been provided that hypothyroidism impairs the conversion of riboflavin to its coenzyme forms [30,31].…”

Section: Discussionsupporting

confidence: 41%

Riboflavin deficiency causes protein and DNA damage in HepG2 cells, triggering arrest in G1 phase of the cell cycle

Manthey

Rodriguez-Melendez

Hoi

et al. 2006

The Journal of Nutritional Biochemistry

View full text Add to dashboard Cite

Eukaryotes convert riboflavin to flavin adenine dinucleotide, which serves as a coenzyme for glutathione reductase and other enzymes. Glutathione reductase mediates the regeneration of reduced glutathione, which plays an important role in scavenging free radicals and reactive oxygen species. Here we tested the hypothesis that riboflavin deficiency decreases glutathione reductase activity in HepG2 liver cells, causing oxidative damage to proteins and DNA, and cell cycle arrest. As a secondary goal, we determined whether riboflavin deficiency is associated with gene expression patterns indicating cell stress. Cells were cultured in riboflavin-deficient and riboflavin-supplemented media for 4 days. Activity of glutathione reductase was not detectable in cells cultured in riboflavin-deficient medium. Riboflavin deficiency was associated with an increase in the abundance of damaged (carbonylated) proteins and with increased incidence of DNA strand breaks. Damage to proteins and DNA was paralleled by increased abundance of the stress-related transcription factor GADD153. Riboflavin-deficient cells arrested in G1 phase of the cell cycle. Moreover, oxidative stress caused by riboflavin deficiency was associated with increased expression of clusters of genes that play roles in cell stress and apoptosis. For example, the abundance of the pro-apoptotic pleiomorphic adenoma gene-like 1 gene was 183% greater in riboflavin-deficient cells compared with riboflavin-sufficient controls. We conclude that riboflavin deficiency is associated with oxidative damage to proteins and DNA in liver cells, leading to cell stress and G1 phase arrest.

show abstract

Section: Discussionsupporting

confidence: 41%

Riboflavin deficiency causes protein and DNA damage in HepG2 cells, triggering arrest in G1 phase of the cell cycle

Manthey

Rodriguez-Melendez

Hoi

et al. 2006

The Journal of Nutritional Biochemistry

View full text Add to dashboard Cite

show abstract

“…Thyroid hormones also change the FAD content in liver; this may be due to regulation of flavokinase activity (214). The increase in flavokinase activity induced by thyroxine is not blocked by actinomycin D (214,217). This fi nding, plus the observation that an unidentifi ed small molecule (possibly riboflavin) in liver extracts from hyperthyroid animals apparently stabilizes the enzyme, suggests that thy roxin increases activity by modifying fl avokinase degradation.…”

Section: Conversion To Coenzymatic Formssupporting

confidence: 40%

“…Co-administra tion of aldosterone and riboflavin analogues [7,8-dimethyl-1O-formylmethyl isoalloxazine or 7,S-dimethyl-1O-(2'-hydroxyethyl) isoalloxazine] decreased the formation of renal FMN while increasing the urinary output of Na+, compared to aldosterone alone (253); hence, it was concluded that stimula tion of FMN (and FAD) synthesis by aldosterone may be a causative factor in the increased reabsorption of Na+. Thyroid hormones also change the FAD content in liver; this may be due to regulation of flavokinase activity (214). The increase in flavokinase activity induced by thyroxine is not blocked by actinomycin D (214,217).…”

Section: Conversion To Coenzymatic Formscontrasting

confidence: 40%

See 1 more Smart Citation

Formation and Mode of Action of Flavoproteins

et al. 1981

View full text Add to dashboard Cite

“…These and a number of more recent investigations suggest that the enhancement of carcinogenesis by azo dyes in riboflavin deficient animals is likely due to the fact that flavin containing enzymes are involved in demethylation of these drugs and in cleavage of their azo linkage. In riboflavin deficiency, the hepatic concentration of FAD is reduced to one-third of normal [17], and it is likely that under these conditions there is diminished degradation of azo dyes by azo reductase. In the special case of azo compounds attached to benzidine, azo reduction leads to a more potent mutagenic compound, rather than to an inactivated one [18].…”

Section: Riboflavinmentioning

confidence: 44%

Nutrition and cancer: state of the art relationship of several nutrients to the development of cancer.

Rivlin¹

1982

Journal of the American College of Nutrition

View full text Add to dashboard Cite

Nutrition and cancer interact in a number of important ways and nutritional factors are increasingly recognized as relevant to both the prevention and treatment of cancer. The role of several nutrients in cancer development is considered briefly here. Deficiency of riboflavin (Vitamin B2) prolongs the survival of tumor-bearing animals, but may accelerate carcinogenesis caused by certain agents, as flavin cofactors are involved in drug and carcinogen metabolism. Deficiency of Vitamin A may enhance the development of tumors of epithelial origin, particularly lung. Evidence is accumulating that Vitamin A and/or its precursors, the B-carotenes, may possibly have an effect in chemoprevention of certain of these epithelial cancers both in animals and in man. The consumption of dietary fat among various nations is correlated closely with increased development of cancers of the breast, colon, and prostate, and possibly of other organs. Studies of migrant populations from Japan to the United States show changes in prevalence of stomach and colon cancer in the direction of the native United States population. Sources of nitrites are of concern because of their potential conversion to carcinogenic nitrosamines. Limitation of the delivery of nitrites may be difficult to accomplish so investigators are exploring the blockade of conversion of nitrites to nitrosamines. Nutrition should not be viewed as the sole means of cancer prevention and treatment but rather as a vital component of any treatment plan.

show abstract

Hormonal Regulation of Riboflavin Metabolism

Cited by 12 publications

References 69 publications

Riboflavin deficiency causes protein and DNA damage in HepG2 cells, triggering arrest in G1 phase of the cell cycle

Riboflavin deficiency causes protein and DNA damage in HepG2 cells, triggering arrest in G1 phase of the cell cycle

Formation and Mode of Action of Flavoproteins

Nutrition and cancer: state of the art relationship of several nutrients to the development of cancer.

Contact Info

Product

Resources

About