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1
Yamanaka, Gaku, Shinji Suzuki, Natsumi Morishita, Mika Takeshita, Kanako Kanou, Tomoko Takamatsu, Shinichiro Morichi, et al. "Experimental and Clinical Evidence of the Effectiveness of Riboflavin on Migraines." Nutrients 13, no. 8 (July 29, 2021): 2612. http://dx.doi.org/10.3390/nu13082612.
Abstract:
Riboflavin, a water-soluble member of the B-vitamin family, plays a vital role in producing energy in mitochondria and reducing inflammation and oxidative stress. Migraine pathogenesis includes neuroinflammation, oxidative stress, and mitochondrial dysfunction. Therefore, riboflavin is increasingly being recognized for its preventive effects on migraines. However, there is no concrete evidence supporting its use because the link between riboflavin and migraines and the underlying mechanisms remains obscure. This review explored the current experimental and clinical evidence of conditions involved in migraine pathogenesis and discussed the role of riboflavin in inhibiting these conditions. Experimental research has demonstrated elevated levels of various oxidative stress markers and pro-inflammatory cytokines in migraines, and riboflavin’s role in reducing these marker levels. Furthermore, clinical research in migraineurs showed increased marker levels and observed riboflavin’s effectiveness in reducing migraines. These findings suggest that inflammation and oxidative stress are associated with migraine pathogenesis, and riboflavin may have neuroprotective effects through its clinically useful anti-inflammatory and anti-oxidative stress properties. Riboflavin’s safety and efficacy suggests its usefulness in migraine prophylaxis; however, insufficient evidence necessitates further study.
2
Purnakarya, Idral. "Defisiensi Riboflavin dan Demensia pada Usia Lanjut." Kesmas: National Public Health Journal 6, no. 3 (December 1, 2011): 99. http://dx.doi.org/10.21109/kesmas.v6i3.99.
Abstract:
Demensia Alzheimer menempati urutan kesembilan penyebab kematian di Amerika Serikat. Demensia adalah kondisi yang sering dialami yang berhubungan dengan berbagai faktor dan gaya hidup terutama diet. Penelitian ini bertujuan untuk mengetahui hubungan defisiensi asupan riboflavin (vitamin B12) dengan demensia pada usia lanjut (usila). Penelitian ini menggunakan desain studi cross sectional dan dilaksanakanpada bulan September 2007 sampai dengan Januari 2008. Sampel penelitian adalah 141 lansia berumur lebih dari sama dengan 60 tahun yang diambil secara purposive sampling. Demensia diukur menggunakan kuesioner MMSE (² 24, skor maksimum 30) dan asupan riboflavin diukur menggunakan form Semi Quantitative – FFQ. Penelitian ini memperlihatkanbahwa 47,5% usila mengalami demensia. Hasil uji statistik menunjukkan bahwa terdapat hubungan yang signifikan antara umur, tingkat pendidikan, dan asupan riboflavin dengan kejadian demensia pada usila (nilai p < 0,05).Kata kunci: Demensia, defisiensi riboflavin, usia lanjutAbstractDementia Alzheimer’s was ranked the ninth leading cause of death in The United States. Dementia can not be avoided as related to several factors and lifestyle especially the diet. The objective of this research is to know relation the deficiency of riboflavine (vitamin B12) intake and incidence of dementiaat elderly. A cross-sectional study was conducted betweenSeptember 2007 and January 2008. The sample obtained was 141 elderly which it was conducted to purposive sampling. Dementia was measured by using questionnaire MMSE (² 24, maximum score was 30), and riboflavine intake was measure by Semi Quantitative – FFQ form. This study shows that dementia in elderly was 47,5%. Statistical test showed that Statistical test showed that incidence of dementia had significantly associated with ages, level of education, and riboflavine intake (p value < 0,05).Key words: Dementia, deficiency of riboflavine, elderl
3
Pinto, John T., and Janos Zempleni. "Riboflavin." Advances in Nutrition 7, no. 5 (September 1, 2016): 973–75. http://dx.doi.org/10.3945/an.116.012716.
4
&NA;. "Riboflavin." Reactions Weekly &NA;, no. 1365 (August 2011): 40. http://dx.doi.org/10.2165/00128415-201113650-00151.
5
&NA;. "Riboflavin." Reactions Weekly &NA;, no. 1411 (July 2012): 38–39. http://dx.doi.org/10.2165/00128415-201214110-00139.
6
&NA;. "Riboflavin." Reactions Weekly &NA;, no. 893 (March 2002): 13. http://dx.doi.org/10.2165/00128415-200208930-00050.
7
&NA;. "Riboflavin." Reactions Weekly &NA;, no. 1430 (December 2012): 28. http://dx.doi.org/10.2165/00128415-201214300-00101.
8
White, H. B., J. Armstrong, and C. C. Whitehead. "Riboflavin-binding protein. Concentration and fractional saturation in chicken eggs as a function of dietary riboflavin." Biochemical Journal 238, no. 3 (September 15, 1986): 671–75. http://dx.doi.org/10.1042/bj2380671.
Abstract:
The concentration of riboflavin and riboflavin-binding protein were determined in the plasma, egg yolk and albumen from hens fed a riboflavin-deficient diet (1.2 mg/kg) supplemented with 0, 1, 2, 3, 10 and 40 mg of riboflavin/kg. We observed that the deposition of riboflavin in egg yolk and albumen is dependent on dietary riboflavin and reaches half-maximal values at about 2 mg of supplemental riboflavin/kg. The maximal amount of riboflavin deposited in the yolk is limited stoichiometrically by the amount of riboflavin-binding protein, whereas the maximum amount of riboflavin deposited in albumen is limited by other factors before saturation occurs. The amount of riboflavin-binding protein in yolk and albumen is independent of dietary riboflavin. If there is a specific oocyte receptor for riboflavin-binding protein, it cannot distinguish between the apo and holo forms of the protein. Riboflavin-binding protein is about six times more concentrated in yolk than in plasma.
9
Mack, Matthias, and Simon Grill. "Riboflavin analogs and inhibitors of riboflavin biosynthesis." Applied Microbiology and Biotechnology 71, no. 3 (July 2006): 265–75. http://dx.doi.org/10.1007/s00253-006-0421-7.
10
Golbach, Jennifer L., Steven C. Ricke, Corliss A. O'Bryan, and Philip G. Crandall. "Riboflavin in Nutrition, Food Processing, and Analysis - A Review." Journal of Food Research 3, no. 6 (July 29, 2014): 23. http://dx.doi.org/10.5539/jfr.v3n6p23.
Abstract:
<p>Riboflavin is an essential micronutrient in the human diet. Because riboflavin is water soluble and not stored in appreciable amounts in the body, sources of riboflavin must be constantly consumed. In the United States many cereal grains are being fortified with riboflavin. In this review we briefly discuss the chemistry of riboflavin, the role of riboflavin in nutrition and health, effects of food processing and storage and means of measuring riboflavin in food and animal feeds.</p>
11
Petrovska, Yana, Oleksii Lyzak, Justyna Ruchala, Kostyantyn Dmytruk, and Andriy Sibirny. "Co-Overexpression of RIB1 and RIB6 Increases Riboflavin Production in the Yeast Candida famata." Fermentation 8, no. 4 (March 25, 2022): 141. http://dx.doi.org/10.3390/fermentation8040141.
Abstract:
Riboflavin or vitamin B2 is a water-soluble vitamin and a precursor of flavin coenzymes, flavin mononucleotide, and flavin adenine dinucleotide, which play a key role as enzyme cofactors in energy metabolism. Candida famata yeast is a promising producer of riboflavin, as it belongs to the group of so-called flavinogenic yeasts, capable of riboflavin oversynthesis under conditions of iron starvation. The role of the particular structural genes in the limitation of riboflavin oversynthesis is not known. To study the impact of overexpression of the structural genes of riboflavin synthesis on riboflavin production, a set of plasmids containing genes RIB1, RIB6, and RIB7 in different combinations was constructed. The transformants of the wild-type strain of C. famata, as well as riboflavin overproducer, were obtained, and the synthesis of riboflavin was studied. It was found that overexpression of RIB1 and RIB6 genes coding for enzymes GTP cyclohydrolase II and 3,4-dihydroxy-2-butanone-4-phosphate synthase, which catalase the initial steps of riboflavin synthesis, elevated riboflavin production by 13–28% relative to the parental riboflavin-overproducing strains.
12
Vergani, Lodovica, Maria Barile, Corrado Angelini, Alberto B. Burlina, Leo Nijtmans, Maria Pia Freda, Carmen Brizio, Elisabetta Zerbetto, and Federica Dabbeni-Sala. "Riboflavin therapy." Brain 122, no. 12 (December 1999): 2401–11. http://dx.doi.org/10.1093/brain/122.12.2401.
13
&NA;. "Ketorolac/riboflavin." Reactions Weekly &NA;, no. 1421 (September 2012): 33. http://dx.doi.org/10.2165/00128415-201214210-00109.
14
Burgess, Catherine M., Dirk Jan Slotboom, Eric R. Geertsma, Ria H. Duurkens, Bert Poolman, and Douwe van Sinderen. "The Riboflavin Transporter RibU in Lactococcus lactis: Molecular Characterization of Gene Expression and the Transport Mechanism." Journal of Bacteriology 188, no. 8 (April 15, 2006): 2752–60. http://dx.doi.org/10.1128/jb.188.8.2752-2760.2006.
Abstract:
ABSTRACT This study describes the characterization of the riboflavin transport protein RibU in the lactic acid bacterium Lactococcus lactis subsp. cremoris NZ9000. RibU is predicted to contain five membrane-spanning segments and is a member of a novel transport protein family, not described in the Transport Classification Database. Transcriptional analysis revealed that ribU transcription is downregulated in response to riboflavin and flavin mononucleotide (FMN), presumably by means of the structurally conserved RFN (riboflavin) element located between the transcription start site and the start codon. An L. lactis strain carrying a mutated ribU gene exhibits altered transcriptional control of the riboflavin biosynthesis operon ribGBAH in response to riboflavin and FMN and does not consume riboflavin from its growth medium. Furthermore, it was shown that radiolabeled riboflavin is not taken up by the ribU mutant strain, in contrast to the wild-type strain, directly demonstrating the involvement of RibU in riboflavin uptake. FMN and the toxic riboflavin analogue roseoflavin were shown to inhibit riboflavin uptake and are likely to be RibU substrates. FMN transport by RibU is consistent with the observed transcriptional regulation of the ribGBAH operon by external FMN. The presented transport data are consistent with a uniport mechanism for riboflavin translocation and provide the first detailed molecular and functional analysis of a bacterial protein involved in riboflavin transport.
15
Astanov, S. Kh, M. Z. Sharipov, and G. K. Kasimova. "HIPOCHROMIC EFFECT IN RIBOFLAVIN SOLUTIONS." Eurasian Physical Technical Journal 16, no. 1 (June 14, 2019): 12–17. http://dx.doi.org/10.31489/2019no1/12-17.
16
Duerden, Julia M., and C. J. Bates. "Effect of riboflavin deficiency on reproductive performance and on biochemical indices of riboflavin status in the rat." British Journal of Nutrition 53, no. 1 (January 1985): 97–105. http://dx.doi.org/10.1079/bjn19850014.
Abstract:
1. Young female rats were made riboflavin-deficient by feeding a purified diet containing casein (210 g/kg). This basal diet provided 0.40 mg riboflavin/kg diet, to which was added additional riboflavin at 0, 0.12 or 0.25 mg/kg diet. Control animals received the same diet with 15 mg added riboflavin/kg. The diets were given for 4 weeks before mating, then throughout pregnancy and for 15 d of lactation.2. With no added riboflavin in the diet, reproduction was severely impaired and fetal resorption was usually observed. With 0.12 mg added riboflavin/kg diet, however, reproduction was usually successful, and the growth of dams and pups was only marginally depressed in comparison with pair-fed controls optimally supplied with riboflavin.3. The activation coefficient (stimulated: basal activity) of erythrocyte glutathione reductase (NAD(P)H) (EC 1.6.4.2)was high, and the concentration of riboflavin in the liver was correspondingly low in the dams receiving diets containing 0.12 or 0.25 mg added riboflavin/kg and in their sucking pups at 15 d post partum. Riboflavin levels in the milk from both groups of dams were about eightfold lower than in controls. There was little evidence that the sucking pups could maintain their riboflavin level at the expense of that in the maternal tissues.
17
Mazur-Bialy, Agnieszka Irena, Beata Buchala, and Barbara Plytycz. "Riboflavin deprivation inhibits macrophage viability and activity – a study on the RAW 264.7 cell line." British Journal of Nutrition 110, no. 3 (February 18, 2013): 509–14. http://dx.doi.org/10.1017/s0007114512005351.
Abstract:
Riboflavin, or vitamin B2, as a precursor of the coenzymes FAD and FMN, has an indirect influence on many metabolic processes and determines the proper functioning of several systems, including the immune system. In the human population, plasma riboflavin concentration varies from 3·1 nm(in a moderate deficiency, e.g. in pregnant women) to 10·4 nm(in healthy adults) and 300 nm(in cases of riboflavin supplementation). The purpose of the present study was to investigate the effects of riboflavin concentration on the activity and viability of macrophages, i.e. on one of the immunocompetent cell populations. The study was performed on the murine monocyte/macrophage RAW 264.7 cell line cultured in medium with various riboflavin concentrations (3·1, 10·4, 300 and 531 nm). The results show that riboflavin deprivation has negative effects on both the activity and viability of macrophages and reduces their ability to generate an immune response. Signs of riboflavin deficiency developed in RAW 264.7 cells within 4 d of culture in the medium with a low riboflavin concentration (3·1 nm). In particular, the low riboflavin content reduced the proliferation rate and enhanced apoptotic cell death connected with the release of lactate dehydrogenase. The riboflavin deprivation impaired cell adhesion, completely inhibited the respiratory burst and slightly impaired phagocytosis of the zymosan particles. In conclusion, macrophages are sensitive to riboflavin deficiency; thus, a low riboflavin intake in the diet may affect the immune system and may consequently decrease proper host immune defence.
18
Brandsch, R., and V. Bichler. "Riboflavin-dependent expression of flavoenzymes of the nicotine regulon of Arthrobacter oxidans." Biochemical Journal 270, no. 3 (September 15, 1990): 673–78. http://dx.doi.org/10.1042/bj2700673.
Abstract:
In cells of an Arthrobacter oxidans riboflavin-dependent mutant the specific activity of the DL-nicotine-inducible nicregulon enzymes nicotine dehydrogenase (NDH, EC 1.5.99.4), 6-hydroxy-L-nicotine oxidase (6-HLNO, EC 1.5.3.5) and 6-hydroxy-D-nicotine oxidase (6-HDNO, EC 1.5.3.6) was shown to be dependent on the supply of the vitamin in the growth medium. Experiments designed to identify at which level riboflavin directs the biosynthesis of these flavoenzymes revealed that the steady-state levels of enzyme protein analysed on Western blots correlated directly with riboflavin supply from the minimal concentration of 0.5 microns-riboflavin required for growth up to 8 microns-riboflavin. Mutant cells grown at the higher riboflavin concentration showed on dot-blots increased levels of RNA which hybridized to 32P-labelled probes derived from the nic-regulon genes. When cells grown at 2 microns-riboflavin were shifted to 8 microns-riboflavin, 6-HDNO expression increased as indicated by elevated enzyme and RNA levels. When the rates of synthesis of the 6-HDNO and 6-HLNO polypeptides after DL-nicotine induction was analysed in cells grown at 0.5 microns and 8 microns-riboflavin, only cells grown at the higher riboflavin concentration showed on Western blots an accumulation of the polypeptides. No 6-HDNO or 6-HLNO polypeptide was identified in cell extracts from cells grown on 0.5 microns-riboflavin. Pulse-chase experiments with [35S]methionine showed that 6-HDNO- and 6-HLNO synthesis was prevented in cells grown at the low riboflavin concentration. The absence of detectable enzyme levels seemed not to be caused by proteolytic breakdown. Incubation in vitro of apo-6HDNO with low- or high-riboflavin-grown-cell extracts showed no increased proteolytic activity in 0.5 microns-riboflavin-grown cells. From these results it is concluded that riboflavin supply co-regulates the expression of the nicregulon genes at the level of transcription and/or mRNA turnover.
19
Vogl, Christian, Simon Grill, Oliver Schilling, Jörg Stülke, Matthias Mack, and Jürgen Stolz. "Characterization of Riboflavin (Vitamin B2) Transport Proteins from Bacillus subtilis and Corynebacterium glutamicum." Journal of Bacteriology 189, no. 20 (August 10, 2007): 7367–75. http://dx.doi.org/10.1128/jb.00590-07.
Abstract:
ABSTRACT Riboflavin (vitamin B2) is the direct precursor of the flavin cofactors flavin mononucleotide and flavin adenine dinucleotide, essential components of cellular biochemistry. In this work we investigated the unrelated proteins YpaA from Bacillus subtilis and PnuX from Corynebacterium glutamicum for a role in riboflavin uptake. Based on the regulation of the corresponding genes by a riboswitch mechanism, both proteins have been predicted to be involved in flavin metabolism. Moreover, their primary structures suggested that these proteins integrate into the cytoplasmic membrane. We provide experimental evidence that YpaA is a plasma membrane protein with five transmembrane domains and a cytoplasmic C terminus. In B. subtilis, riboflavin uptake was increased when ypaA was overexpressed and abolished when ypaA was deleted. Riboflavin uptake activity and the abundance of the YpaA protein were also increased when riboflavin auxotrophic mutants were grown in limiting amounts of riboflavin. YpaA-mediated riboflavin uptake was sensitive to protonophors and reduced in the absence of glucose, demonstrating that the protein requires metabolic energy for substrate translocation. In addition, we demonstrate that PnuX from C. glutamicum also is a riboflavin transporter. Transport by PnuX was not energy dependent and had high apparent affinity for riboflavin (Km 11 μM). Roseoflavin, a toxic riboflavin analog, appears to be a substrate of PnuX and YpaA. We propose to designate the gene names ribU for ypaA and ribM for pnuX to reflect that the encoded proteins function in riboflavin uptake and that the genes have different phylogenetic origins.
20
Adelekan, D. A., and D. I. Thurnham. "Glutathione peroxidase (EC 1.11.1.9) and superoxide dismutase (EC 1.15.1.1) activities in riboflavin-deficient rats infected with Plasmodium berghei malaria." British Journal of Nutrition 79, no. 3 (March 1998): 305–9. http://dx.doi.org/10.1079/bjn19980048.
Abstract:
Riboflavin deficiency interferes with the growth and multiplication of malaria parasites as well as the host response to malaria. The objective of the present work was to determine the effects of riboflavin deficiency on erythrocyte glutathione peroxidase (EC1.11.1.9; GPx) and superoxide dismutase (EC1.15.1.1; SOD) in rats infected withPlasmodium bergheimalaria. Riboflavin in its co-enzyme form, FAD, is required by glutathione reductase (EC1.6.4.1) to regenerate GSH and GSH is an important cellular antioxidant both in its own right and also as a substrate for the enzyme GPx. Weanling rats were deprived of riboflavin for 8 weeks before intraperitoneal injection of 1 × 106P. bergheiparasites. Control animals were weight-matched to the respective riboflavin-deficient group. At 10d post-infection, parasite counts were higher in the weight-matched control group than the riboflavin-deficient group (P= 0.004). GPx activity was higher in erythrocytes of rats parasitized withP. bergheithan comparable non-infected rats regardless of riboflavin status (P< 0.05). As mature erythrocytes do not synthesize new protein, the higher GPx activities were probably due to the presence of the parasite protein. In erythrocytes from riboflavin-deficient rats, GPx activity tended to be lower than in those rats fed on diets adequate in riboflavin (weight-matched controls) whether parasitized or not, but the difference was not significant. Neither riboflavin deficiency nor malaria had any effect on erythrocyte SOD activity. It was concluded that riboflavin deficiency has no marked effect on erythrocyte GPx or SOD activity in the rat.
21
Radchenko, M. M., N. E. Beyko, G. S. Andriiash, О. О. Тigunova, and С. М. Shulga. "Isolation and identification of a strain producing riboflavin." Faktori eksperimental'noi evolucii organizmiv 24 (August 30, 2019): 154–59. http://dx.doi.org/10.7124/feeo.v24.1094.
Abstract:
Aim. Aim of investigation was to receive riboflavin strain-producers using natural sources for development of riboflavin technology. Methods. Strain-producers were isolated by the method of imprints (replica). The identification of stains was done by commonly used techniques using the «Bergey's Manual of Systematic Bacteriology». The resulting clones were tested for accumulation of riboflavin by fluorometric method. Results. 9 natural sources (seeds of corn and potato tubers) were investigated, pure cultures of microorganisms werr isolated and their identification was carried out. Two types of bacterial colonies of the genus Bacillus were identified. Selected strains weretested for antibiotic susceptibility and for the ability to accumulate riboflavin. Conclusions. As a result of the research, strain-producing riboflavin is isolated, the strain is classified as B. subtilis. The strain accumulated 4.3 g / l of riboflavin in a sucrose medium during a 72 hours cultivation. This strain was accepted as a source for the development of riboflavin technology.
Keywords: riboflavin, stain, microbial synthesis, Bacillus subtilis.
22
Szczuko, Małgorzata, Maciej Ziętek, Danuta Kulpa, and Teresa Seidler. "Riboflavin - properties, occurrence and its use in medicine." Pteridines 30, no. 1 (February 1, 2019): 33–47. http://dx.doi.org/10.1515/pteridines-2019-0004.
Abstract:
Abstract 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.
23
Mosegaard, Signe, Graziana Dipace, Peter Bross, Jasper Carlsen, Niels Gregersen, and Rikke Katrine Jentoft Olsen. "Riboflavin Deficiency—Implications for General Human Health and Inborn Errors of Metabolism." International Journal of Molecular Sciences 21, no. 11 (May 28, 2020): 3847. http://dx.doi.org/10.3390/ijms21113847.
Abstract:
As an essential vitamin, the role of riboflavin in human diet and health is increasingly being highlighted. Insufficient dietary intake of riboflavin is often reported in nutritional surveys and population studies, even in non-developing countries with abundant sources of riboflavin-rich dietary products. A latent subclinical riboflavin deficiency can result in a significant clinical phenotype when combined with inborn genetic disturbances or environmental and physiological factors like infections, exercise, diet, aging and pregnancy. Riboflavin, and more importantly its derivatives, flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), play a crucial role in essential cellular processes including mitochondrial energy metabolism, stress responses, vitamin and cofactor biogenesis, where they function as cofactors to ensure the catalytic activity and folding/stability of flavoenzymes. Numerous inborn errors of flavin metabolism and flavoenzyme function have been described, and supplementation with riboflavin has in many cases been shown to be lifesaving or to mitigate symptoms. This review discusses the environmental, physiological and genetic factors that affect cellular riboflavin status. We describe the crucial role of riboflavin for general human health, and the clear benefits of riboflavin treatment in patients with inborn errors of metabolism.
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Lozano Aguirre, Luis Fernando, Juan Carlos Salazar, José Ignacio Vásquez, and Víctor Antonio García-Angulo. "Interdependency of regulatory effects of iron and riboflavin in the foodborne pathogen Shigella flexneri determined by integral transcriptomics." PeerJ 8 (September 15, 2020): e9553. http://dx.doi.org/10.7717/peerj.9553.
Abstract:
Shigella flexneri is the causative agent of dysentery. For pathogens, iron is a critical micronutrient as its bioavailability is usually low in bacterial niches. This metal is involved in critical physiological processes mainly as a component of important metabolic molecules involved in redox reactions. Usually bacteria respond to fluctuations in iron availability to regulate iron acquisition and other iron-related functions. Recently the close metabolic feedback between iron and riboflavin, another pivotal biological redox agent, began to draw attention in bacteria. This is a widespread biological phenomenon, partly characterized by the coordination of regulatory responses to iron and riboflavin, probably owed to the involvement of these cofactors in common processes. Nonetheless, no systematic analyses to determine the extent of this regulatory effect have been performed in any species. Here, the transcriptomics responses to iron, riboflavin, iron in the presence of riboflavin and riboflavin in the presence of iron were assessed and compared in S. flexneri. The riboflavin regulon had a 43% overlap with the iron regulon. Notably, the presence of riboflavin highly increased the number of iron-responsive genes. Reciprocally, iron drastically changed the pool of riboflavin-responsive genes. Gene ontology (GO) functional terms enrichment analysis showed that biological processes were distinctively enriched for each subgroup of responsive genes. Among the biological processes regulated by iron and riboflavin were iron uptake, amino acids metabolism and electron transfer for ATP synthesis. Thus, iron and riboflavin highly affect the transcriptomics responses induced by each other in S. flexneri. GO terms analysis suggests that iron and riboflavin coordinately regulate specific physiological functions involving redox metabolism.
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Hustad, Steinar, Michelle C. McKinley, Helene McNulty, Jørn Schneede, JJ Strain, John M. Scott, and Per Magne Ueland. "Riboflavin, Flavin Mononucleotide, and Flavin Adenine Dinucleotide in Human Plasma and Erythrocytes at Baseline and after Low-Dose Riboflavin Supplementation." Clinical Chemistry 48, no. 9 (September 1, 2002): 1571–77. http://dx.doi.org/10.1093/clinchem/48.9.1571.
Abstract:
Abstract Background: Vitamin B2 exists in blood as riboflavin and its cofactors, flavin mononucleotide (FMN) and FAD. The erythrocyte glutathione reductase activation coefficient (EGRAC) has traditionally been used to assess vitamin B2 status in humans. We investigated the relationships of EGRAC and plasma and erythrocyte concentrations of riboflavin, FMN, and FAD in elderly volunteers and their responses to riboflavin administration. Methods: EGRAC and plasma and erythrocyte concentrations of riboflavin, FMN, and FAD were determined in 124 healthy individuals with a mean age of 69 years. The same measurements were made in a subgroup of 46 individuals with EGRAC ≥1.20 who participated in a randomized double-blind 12-week intervention study and received riboflavin (1.6 mg/day; n = 23) or placebo (n = 23). Results: Median plasma concentrations were 10.5 nmol/L for riboflavin, 6.6 nmol/L for FMN, and 74 nmol/L for FAD. In erythrocytes, there were only trace amounts of riboflavin, whereas median FMN and FAD concentrations were 44 and 469 nmol/L, respectively. Erythrocyte FMN and FAD correlated with each other and with EGRAC and plasma riboflavin (P <0.05). All variables except plasma FAD responded significantly to riboflavin supplementation compared with placebo (P ≤0.04). The strongest increases were for riboflavin in plasma (83%) and for FMN in erythrocytes (87%). Conclusions: Concentrations of all B2 vitamers except plasma FAD are potential indicators of vitamin B2 status, and plasma riboflavin and erythrocyte FMN may be useful for the assessment of vitamin B2 status in population studies.
26
Juarez del Valle, M., J. E. Laiño, A. de Moreno de LeBlanc, G. Savoy de Giori, and J. G. LeBlanc. "Soyamilk fermented with riboflavin-producingLactobacillus plantarumCRL 2130 reverts and prevents ariboflavinosis in murine models." British Journal of Nutrition 116, no. 7 (September 19, 2016): 1229–35. http://dx.doi.org/10.1017/s0007114516003378.
Abstract:
AbstractIt has been previously shown thatLactobacillus plantarumCRL 2130 is able to produce riboflavin in soyamilk. The aim of the present study was to evaluate the efficiency of this riboflavin-bio-enriched soyamilk to revert and/or prevent the nutritional deficiency of riboflavin using different animal models. When used to supplement the diets of previously depleted animals, it was shown that the growth, riboflavin status and morphology of the small intestines reverted to normal parameters and were similar to animals supplemented with commercial riboflavin. In the prevention model, the same tendency was observed, where animals that received soyamilk fermented withL. plantarumCRL 2130 did not show signs of riboflavin deficiency. This new bio-fortified soya-based product could be used as part of normal diets to provide a more natural alternative to mandatory fortification with riboflavin for the prevention of its deficiency.
27
Ge, Ying-Ying, Jia-Rong Zhang, Harold Corke, and Ren-You Gan. "Screening and Spontaneous Mutation of Pickle-Derived Lactobacillus plantarum with Overproduction of Riboflavin, Related Mechanism, and Food Application." Foods 9, no. 1 (January 14, 2020): 88. http://dx.doi.org/10.3390/foods9010088.
Abstract:
Riboflavin, also known as vitamin B2, plays an important role in human cell metabolism and participates in various redox reactions and in energy utilization. In this study, 90 riboflavin-producing lactic acid bacteria (LAB) were screened out from pickle juices. The yields of riboflavin in these LAB were about 0.096–0.700 mg/L, and one strain, Lactobacillus plantarum RYG-YYG-9049, was found to produce the highest riboflavin content. Next, roseoflavin was used to induce the spontaneous mutation of RYG-YYG-9049, and selected roseoflavin-resistant colonies generally produced higher riboflavin contents, ranging from 1.013 to 2.332 mg/L. The No. 10 mutant, L. plantarum RYG-YYG-9049-M10, had the highest riboflavin content. Next, the molecular mechanism of enhancing riboflavin production in RYG-YYG-9049-M10 was explored, leading to the finding that roseoflavin treatment did not change the rib operons including the ribA, ribB, ribC, ribH, and ribG genes. Unexpectedly, however, this mechanism did induce an insertion of a 1059-bp DNA fragment in the upstream regulatory region of the rib operon, as compared to the wild-type RYG-YYG-9049. To the best of our knowledge, this is the first report that roseoflavin could induce an insertion of DNA fragment in LAB to increase riboflavin content, representing a new mutation type that is induced by roseoflavin. Finally, in order to fortify riboflavin content in soymilk, RYG-YYG-9049 and RYG-YYG-9049-M10 were used to ferment soymilk, and several fermentation parameters were optimized to obtain the fermented soymilk with riboflavin contents of up to 2.920 mg/L. In general, roseoflavin induction is an economical and feasible biotechnological strategy to induce riboflavin-overproducing LAB, and this strategy can be used to develop LAB-fermented functional foods that are rich in riboflavin.
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Darguzyte, Milita, Natascha Drude, Twan Lammers, and Fabian Kiessling. "Riboflavin-Targeted Drug Delivery." Cancers 12, no. 2 (January 27, 2020): 295. http://dx.doi.org/10.3390/cancers12020295.
Abstract:
Active targeting can improve the retention of drugs and drug delivery systems in tumors, thereby enhancing their therapeutic efficacy. In this context, vitamin receptors that are overexpressed in many cancers are promising targets. In the last decade, attention and research were mainly centered on vitamin B9 (folate) targeting; however, the focus is slowly shifting towards vitamin B2 (riboflavin). Interestingly, while the riboflavin carrier protein was discovered in the 1960s, the three riboflavin transporters (RFVT 1-3) were only identified recently. It has been shown that riboflavin transporters and the riboflavin carrier protein are overexpressed in many tumor types, tumor stem cells, and the tumor neovasculature. Furthermore, a clinical study has demonstrated that tumor cells exhibit increased riboflavin metabolism as compared to normal cells. Moreover, riboflavin and its derivatives have been conjugated to ultrasmall iron oxide nanoparticles, polyethylene glycol polymers, dendrimers, and liposomes. These conjugates have shown a high affinity towards tumors in preclinical studies. This review article summarizes knowledge on RFVT expression in healthy and pathological tissues, discusses riboflavin internalization pathways, and provides an overview of RF-targeted diagnostics and therapeutics.
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Mack, Matthias, Adolphus P. G. M. van Loon, and Hans-Peter Hohmann. "Regulation of Riboflavin Biosynthesis inBacillus subtilis Is Affected by the Activity of the Flavokinase/Flavin Adenine Dinucleotide Synthetase Encoded byribC." Journal of Bacteriology 180, no. 4 (February 15, 1998): 950–55. http://dx.doi.org/10.1128/jb.180.4.950-955.1998.
Abstract:
ABSTRACT This work shows that the ribC wild-type gene product has both flavokinase and flavin adenine dinucleotide synthetase (FAD-synthetase) activities. RibC plays an essential role in the flavin metabolism of Bacillus subtilis, as growth of aribC deletion mutant strain was dependent on exogenous supply of FMN and the presence of a heterologous FAD-synthetase gene in its chromosome. Upon cultivation with growth-limiting amounts of FMN, this ribC deletion mutant strain overproduced riboflavin, while with elevated amounts of FMN in the culture medium, no riboflavin overproduction was observed. In a B. subtilis ribC820mutant strain, the corresponding ribC820 gene product has reduced flavokinase/FAD-synthetase activity. In this strain, riboflavin overproduction was also repressed by exogenous FMN but not by riboflavin. Thus, flavin nucleotides, but not riboflavin, have an effector function for regulation of riboflavin biosynthesis in B. subtilis, and RibC seemingly is not directly involved in the riboflavin regulatory system. The mutation ribC820 leads to deregulation of riboflavin biosynthesis in B. subtilis, most likely by preventing the accumulation of the effector molecule FMN or FAD.
30
Dong, H., and S. V. Beer. "Riboflavin Induces Disease Resistance in Plants by Activating a Novel Signal Transduction Pathway." Phytopathology® 90, no. 8 (August 2000): 801–11. http://dx.doi.org/10.1094/phyto.2000.90.8.801.
Abstract:
The role of riboflavin as an elicitor of systemic resistance and an activator of a novel signaling process in plants was demonstrated. Following treatment with riboflavin, Arabidopsis thaliana developed systemic resistance to Peronospora parasitica and Pseudomonas syringae pv. Tomato, and tobacco developed systemic resistance to Tobacco mosaic virus (TMV) and Alternaria alternata. Riboflavin, at concentrations necessary for resistance induction, did not cause cell death in plants or directly affect growth of the culturable pathogens. Riboflavin induced expression of pathogenesis-related (PR) genes in the plants, suggesting its ability to trigger a signal transduction pathway that leads to systemic resistance. Both the protein kinase inhibitor K252a and mutation in the NIM1/NPR1 gene which controls transcription of defense genes, impaired responsiveness to riboflavin. In contrast, riboflavin induced resistance and PR gene expression in NahG plants, which fail to accumulate salicylic acid (SA). Thus, riboflavin-induced resistance requires protein kinase signaling mechanisms and a functional NIM1/NPR1 gene, but not accumulation of SA. Riboflavin is an elicitor of systemic resistance, and it triggers resistance signal transduction in a distinct manner.
31
Gupta, Anju, Poornima Kalyanram, and Istvan Stadler. "Interaction of Riboflavin-5-Phosphate With Liposome Bilayers." Journal of Nanotoxicology and Nanomedicine 3, no. 1 (January 2018): 49–59. http://dx.doi.org/10.4018/jnn.2018010103.
Abstract:
Riboflavin presents tremendous potential as a photosensitizing agent for photodynamic therapy (PDT) for treating microbial infection and cancer therapy. Encapsulation of riboflavin can improve its bioavailability and stability while making the clinical applications more efficient. The authors' detailed study on cellular inhibition of liposome encapsulated riboflavin-5-phosphate investigation, and the effect of unencapsulated riboflavin on liposome bilayers aims to improve the efficiency of cellular delivery of riboflavin. Nano-sized liposomes composed of 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC) and cholesterol were used in this study. Cell studies demonstrate high inhibition rates for the lipsome-encapsualted high concentration riboflavin formulations in the presence of blue light, despite the lower encapsulation lading.
32
M Hemalatha and C Subathra Devi. "Bio prospecting of Riboflavin producing bacteria from different riboflavin enriched food sources." Bioscience Journal 38 (September 30, 2022): e38088. http://dx.doi.org/10.14393/bj-v38n0a2022-62495.
Abstract:
Riboflavin is an essential, water-soluble vitamin (B2) and a component of basic cellular metabolism. The aim of the present study is to isolate and characterize riboflavin producing bacteria from different food sources. Ten different riboflavin enriched food sources were collected from Vellore district. Totally 72 bacterial strains were isolated and cultured on nutrient agar plates. Out of these, 43 strains were identified as riboflavin producers. Isolated bacterial strains HDS27, HDS07, HDS14, HDS18, HDS38 and HDS54 isolated from milk, mushroom, spinach, lamb kidney, beef liver and mackerel fish were found to be potent riboflavin producers. Based on morphological, biochemical and molecular characterization, the potent strains were identified as Lactobacillus plantarum (HDS27), Bacillus cereus (HDS07), Delftia tsuruhatensis (HDS14), Citrobacter freundii (HDS18), Enterobacter cloacae (HDS38) and Bacillus cereus (HDS54). The selected potent isolates HDS27 from milk and HDS07 from mushroom showed a maximum riboflavin production of 3.69 mg/L and 2.9mg/L respectively. The present study explores the riboflavin producing novel bacteria from different food sources. This is the first report that the Enterobacter cloacae isolated from beef liver, Delftia tsuruhatensis from spinach and Citrobacter freundii from lamb kidney has the ability to produce riboflavin. These potent strains could be a better starter for substituting the conventional bacteria for large scale production of riboflavin in industry.
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Tsyrulnyk, A. O., D. V. Fedorovych, S. M. Sobchuk, K. V. Dmytruk, and A. A. Sibirny. "Lactose Inducible Expression of Transcription Factor Gene SEF1 Increases Riboflavin Production in the Yeast Candida famata." Mikrobiolohichnyi Zhurnal 83, no. 5 (October 17, 2021): 3–10. http://dx.doi.org/10.15407/microbiolj83.05.003.
Abstract:
Riboflavin (vitamin B2) is required for synthesis of the flavin coenzymes: riboflavin-5’-phosphate (flavin mononucleotide) and flavin adenine dinucleotide. Riboflavin is important biotechnological commodity with annual market around 250 million US dollars. It is mostly used as component of feed premixes for animals (80%), in food industry as food colorant, in medicine and component of multivitamin mixtures and as drug for treatment of some diseases. Over the past two decades, the microbial production of riboflavin by fermentation completely replaces the chemical synthetic route. The main producers of riboflavin in industry are engineered strains of the bacterium Bacillus subtilis and of the mycelial fungus Ashbya gossypii. Flavinogenic yeast Candida famata has great biosynthetic potential. Using combination of classical selection and metabolic engineering (overexpression of SEF1, RIB1 and RIB7 genes coding the positive regulator, the first and the last structural enzymes of riboflavin synthesis) resulted in the construction of genetically stable strain of C. famata that produces 16 gram of riboflavin per liter in bioreactor. However, the productivity of riboflavin biosynthesis remains still insufficient for industrial production of this vitamin. Studies of transcriptional regulation of genes involved in riboflavin synthesis and using of strong promoters of C. famata for construction of efficient producers of vitamin B2 are areas of both scientific and industrial interest. Aim. The aim of the current work was to improve riboflavin oversynthesis by the available C. famata strains in synthetic and natural lactose-containing media. Methods. The plasmid DNA isolation, restriction, ligation, electrophoresis in agarose gel, electrotransformation, and PCR were carried out by the standard methods. Riboflavin was assayed fluorometrically using solution of synthetic riboflavin as a standard. The cultivation of yeasts was carried out in YNB or YPD media containing different source of carbon and on whey. Results. The strains of C. famata expressed additional copy of central regulatory gene SEF1 under control of the promoter of LAC4 gene (coding for β–galactosidase) C. famata were constructed. The influence of SEF1 gene expression under control of lactose inducible promoter of CfLAC4 gene on riboflavin production was studied. It was shown that the C. famata strains containing “pLAC4_cf-SEF1_cf” expression cassette revealed 1.6-2.1-fold increase in riboflavin yield on lactose when compared to the parental strain. The riboflavin production constructed strains on whey reached 1.69 gram per liter in flask batch culture. Conclusions. The constructed strains containing additional copy of SEF1 gene under the control of LAC4 promoter is a perfect platform for development of industrial riboflavin production on by-product of dairy industry, whey.
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McAuley, E., H. McNulty, C. Hughes, J. J. Strain, and M. Ward. "Riboflavin status, MTHFR genotype and blood pressure: current evidence and implications for personalised nutrition." Proceedings of the Nutrition Society 75, no. 3 (May 12, 2016): 405–14. http://dx.doi.org/10.1017/s0029665116000197.
Abstract:
Clinical deficiency of the B-vitamin riboflavin (vitamin B2) is largely confined to developing countries; however accumulating evidence indicates that suboptimal riboflavin status is a widespread problem across the developed world. Few international data are available on riboflavin status as measured by the functional biomarker, erythrocyte glutathione reductase activation coefficient, considered to be the gold standard index. One important role of riboflavin in the form of flavin dinucleotide is as a co-factor for the folate-metabolising enzyme methylenetetrahydrofolate reductase (MTHFR). Homozygosity for the common C677T polymorphism in MTHFR, affecting over 10 % of the UK and Irish populations and up to 32 % of other populations worldwide, has been associated with an increased risk of CVD, and more recently with hypertension. This review will explore available studies reporting riboflavin status worldwide, the interaction of riboflavin with theMTHFRC677T polymorphism and the potential role of riboflavin in personalised nutrition. Evidence is accumulating for a novel role of riboflavin as an important modulator of blood pressure (BP) specifically in individuals with theMTHFR677TT genotype, with results from a number of recent randomised controlled trials demonstrating that riboflavin supplementation can significantly reduce systolic BP by 5–13 mmHg in these genetically at risk adults. Studies are however required to investigate the BP-lowering effect of riboflavin in different populations and in response to doses higher than 1·6 mg/d. Furthermore, work focusing on the translation of this research to health professionals and patients is also required.
35
TOYOSAKI, TOSHIYUKI, and TAKESHI MINESHITA. "Antioxidant Effects of Protein-Bound Riboflavin and Free Riboflavin." Journal of Food Science 53, no. 6 (November 1988): 1851–53. http://dx.doi.org/10.1111/j.1365-2621.1988.tb07859.x.
36
Insińska-Rak, Małgorzata, Ewa Sikorska, Jose L. Bourdelande, Igor V. Khmelinskii, Wiesław Prukała, Krzysztof Dobek, Jerzy Karolczak, et al. "New photochemically stable riboflavin analogue—3-Methyl-riboflavin tetraacetate." Journal of Photochemistry and Photobiology A: Chemistry 186, no. 1 (February 2007): 14–23. http://dx.doi.org/10.1016/j.jphotochem.2006.07.005.
37
Akompong, Thomas, Saliha Eksi, Kim Williamson, and Kasturi Haldar. "Gametocytocidal Activity and Synergistic Interactions of Riboflavin with Standard Antimalarial Drugs against Growth of Plasmodium falciparum In Vitro." Antimicrobial Agents and Chemotherapy 44, no. 11 (November 1, 2000): 3107–11. http://dx.doi.org/10.1128/aac.44.11.3107-3111.2000.
Abstract:
ABSTRACT Our previous studies have shown that riboflavin has activity against Plasmodium falciparum asexual-stage parasites in vitro. In the present study we examine the gametocytocidal activity of riboflavin and the interaction of riboflavin with some commonly used antimalarial drugs against the asexual forms of P. falciparum in vitro. The addition of riboflavin to P. falciparum cultures killed gametocytes at all stages, even those at late stages (III to V), which are not affected by many of the commonly used antimalarials. Combinations of riboflavin with mefloquine, pyrimethamine, and quinine showed a marked potentiation of the activities of these drugs against asexual-stage parasites in vitro. The combination of riboflavin with artemisinin was additive, while that with chloroquine was mildly antagonistic. High doses of riboflavin are used clinically to treat several inborn errors of metabolism with no adverse side effects. Its efficacy in combination with standard antimalarial drugs in treating and preventing the transmission ofP. falciparum malaria can therefore be evaluated in humans.
38
LeBlanc, Jean Guy, Catherine Burgess, Fernando Sesma, Graciela Savoy de Giori, and Douwe van Sinderen. "Lactococcus lactisis capable of improving the riboflavin status in deficient rats." British Journal of Nutrition 94, no. 2 (August 2005): 262–67. http://dx.doi.org/10.1079/bjn20051473.
Abstract:
Lactococcus lactisis a commonly used starter strain that can be converted from a vitamin B2consumer into a vitamin B2‘factory’ by over-expressing its riboflavin biosynthesis genes. The present study was conducted to assess in a rat bioassay the response of riboflavin produced by GM or native lactic acid bacteria (LAB). The riboflavin-producing strains were able to eliminate most physiological manifestations of ariboflavinosis such as stunted growth, elevated erythrocyte glutathione reductase activation coefficient values and hepatomegalia that were observed using a riboflavin depletion–repletion model. Riboflavin status and growth rates were greatly improved when the depleted rats were fed with cultures ofL. lactisthat overproduced this vitamin whereas the native strain did not show the same effect. The present study is the first animal trial with food containing living bacteria that were engineered to overproduce riboflavin. These results pave the way for analysing the effect of similar riboflavin-overproducing LAB in human trials.
39
Yoshimatsu, Hiroki, Atsushi Yonezawa, Yoshiaki Yao, Kumiko Sugano, Shunsaku Nakagawa, Tomohiro Omura, and Kazuo Matsubara. "Functional involvement of RFVT3/SLC52A3 in intestinal riboflavin absorption." American Journal of Physiology-Gastrointestinal and Liver Physiology 306, no. 2 (January 15, 2014): G102—G110. http://dx.doi.org/10.1152/ajpgi.00349.2013.
Abstract:
Riboflavin, also known as vitamin B2, is transported across the biological membrane into various organs by transport systems. Riboflavin transporter RFVT3 is expressed in the small intestine and has been suggested to localize in the apical membranes of the intestinal epithelial cells. In this study, we investigated the functional involvement of RFVT3 in riboflavin absorption using intestinal epithelial T84 cells and mouse small intestine. T84 cells expressed RFVT3 and conserved unidirectional riboflavin transport corresponding to intestinal absorption. Apical [3H]riboflavin uptake was pH-dependent in T84 cells. This uptake was not affected by Na+ depletion at apical pH 6.0, although it was significantly decreased at apical pH 7.4. The [3H]riboflavin uptake from the apical side of T84 cells was prominently inhibited by the RFVT3 selective inhibitor methylene blue and significantly decreased by transfection of RFVT3-small-interfering RNA. In the gastrointestinal tract, RFVT3 was expressed in the jejunum and ileum. Mouse jejunal and ileal permeabilities of [3H]riboflavin were measured by the in situ closed-loop method and were significantly reduced by methylene blue. These results strongly suggest that RFVT3 would functionally be involved in riboflavin absorption in the apical membranes of intestinal epithelial cells.
40
Franch, Antonella, Federica Birattari, Gloria Dal Mas, Zala Lužnik, Mohit Parekh, Stefano Ferrari, and Diego Ponzin. "Evaluation of Intrastromal Riboflavin Concentration in Human Corneas after Three Corneal Cross-Linking Imbibition Procedures: A Pilot Study." Journal of Ophthalmology 2015 (2015): 1–5. http://dx.doi.org/10.1155/2015/794256.
Abstract:
Purpose. To compare stromal riboflavin concentration after three corneal cross-linking (CXL) imbibition procedures: standard (EpiOff), transepithelial corneal (EpiOn), and iontophoresis-assisted technique (Ionto) using 0.1% hypotonic riboflavin phosphate.Methods. Randomized open-label pilot clinical study. Twelve corneas/12 patients with advanced keratoconus were randomly divided into 4 groups for CXL (n=3). The corneas underwent imbibition with standard riboflavin EpiOff and with enhanced riboflavin solution (RICROLIN+) EpiOff, EpiOn, and iontophoresis techniques. Thereafter, deep anterior lamellar keratectomy procedure was performed and the obtained debrided corneal tissues were frozen. The maximal intrastromal riboflavin concentration was measured by high-performance liquid chromatography/mass spectrometry (mcg/dg).Results. The mean stromal concentration of riboflavin was2.02±0.72mcg/dg in EpiOff group,4.33±0.12mcg/g in EpiOff-RICROLIN+ group,0.63±0.21mcg/dg in EpiOn-RICROLIN+ group, and1.15±0.27mcg/dg in iontophoresis RICROLIN+ group. A 7-fold decrease in intrastromal riboflavin concentration was observed comparing EpiOn-RICROLIN+ and EpiOff-RICROLIN+ groups.Conclusion. The present pilot study indicates that both transepithelial CXL techniques in combination with hypotonic enhanced riboflavin formulation (RICROLIN+) were still inferior to the standard CXL technique; however, larger clinical studies to further validate the results are needed and in progress.
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Venkatesh, Ramarao, and S. Kent Harrison. "Photolytic degradation of 2,4-D onZea maysleaves." Weed Science 47, no. 3 (June 1999): 262–69. http://dx.doi.org/10.1017/s004317450009175x.
Abstract:
Growth chamber experiments were conducted to determine the effects of UV light and riboflavin on photolysis of 2,4-D applied toZea maysleaves. Droplets of 100 mg L−114C-2,4-D were applied toZ. maysleaves with and without 10 mg L−13H-riboflavin and exposed to either UV-enhanced or UV-attenuated polychromatic light in a time-course assay. Photolysis of nonabsorbed14C-2,4-D residues onZ. maysleaves was sensitized by riboflavin regardless of UV light regime, but a larger percentage of nonabsorbed herbicide was degraded under UV-enhanced light compared to UV-attenuated light. Riboflavin was almost completely photolyzed during the first 10 h of exposure; yet, photolysis of14C-2,4-D surface residues in treatments containing riboflavin increased from 59% at 10 h of exposure to 87% at 42 h of exposure. In corresponding treatments without riboflavin, photolysis of14C-2,4-D surface residues was 37% at 10 h of exposure and 84% at 42 h of exposure. In contrast, only 7% of the14C-2,4-D deposited on glass microscope slides was degraded after 42 h of exposure in the absence of riboflavin, whereas 59% was degraded in the presence of riboflavin. Photolysis of 2,4-D onZ. maysleaves in treatments without riboflavin suggests that certain epicuticular component(s) ofZ. maysacted as photosensitizers or catalytic agents that promoted photolysis of nonabsorbed 2,4-D residues.
42
PUEYO, José J., Paul G. CURLEY, and Stephen G. MAYHEW. "Kinetics and thermodynamics of the binding of riboflavin, riboflavin 5′-phosphate and riboflavin 3′,5′-bisphosphate by apoflavodoxins." Biochemical Journal 313, no. 3 (February 1, 1996): 855–61. http://dx.doi.org/10.1042/bj3130855.
Abstract:
The reactions of excess apoflavodoxin from Desulfovibrio vulgaris, Anabaena variabilis and Azotobacter vinelandii with riboflavin 5´-phosphate (FMN), riboflavin 3´,5´-bisphosphate and riboflavin are pseudo-first-order. The rates increase with decreasing pH in the range pH 5–8, and, in general, they increase with increasing ionic strength to approach a maximum at an ionic strength greater than 0.4 M. The rate of FMN binding in phosphate at high pH increases to a maximum at an ionic strength of about 0.1 M, and then decreases as the phosphate concentration is increased further. The dissociation constants for the complexes with FMN and riboflavin decrease with an increase of ionic strength. Inorganic phosphate stabilizes the complex with riboflavin. The effects of phosphate on riboflavin binding suggest that phosphate interacts with the apoprotein at the site normally occupied by the phosphate of FMN. Redox potentials determined for the oxidized/semiquinone and semiquinone/ hydroquinone couples of the riboflavin and FMN complexes were used with Kd values for the complexes with the oxidized flavins to calculate values for Kd for the semiquinone and hydroquinone complexes. The hydroquinone complexes are all less stable than the complexes with the two other redox forms of the flavin. Destabilization of the hydroquinone is less marked in the complexes with riboflavin, supporting a proposal that the terminal phosphate group of FMN plays a role in decreasing the stability of the hydroquinone complex and in decreasing the redox potential of the semiquinone/hydroquinone couple.
43
Soares, M. J., K. Satyanarayana, M. S. Bamjlt, C. M. Jacob, Y. Venkata Ramana, and S. Sudhakar Rao. "The effect of exercise on the riboflavin status of adult men." British Journal of Nutrition 69, no. 2 (March 1993): 541–51. http://dx.doi.org/10.1079/bjn19930054.
Abstract:
Six sedentary to moderately active men with biochemical signs of riboflavin deficiency were studied under metabolic ward conditions to examine the effects of physical activity on riboflavin status. All participants were subjected to additional exercise (EXER) for an 18 d period between two maintenance (Ml and M2) periods (16 and 13 d respectively) of habitual physical activity. Energy balance and riboflavin intake were maintained throughout the study. Riboflavin status, as judged by a significant reduction in erythrocyte glutathione reductase (EC1.6.4.2) activation coefficient (EGR-AC), improved on changing from home (1.53 (SD 0.14)) to period M1 (1.36 (SD 0.21)) diets. The exercise period, however, resulted in a significant deterioration in riboflavin status (1.57 (SD 0.31)) which persisted in the subsequent period M2 (1.54 (SD 0.15)). There was a concomitant fall in the urinary excretion of riboflavin only in the EXER period, when results were expressed as a percentage of the dietary intake of riboflavin. These results suggest an increased demand for the vitamin for selective biochemical functions during exercise. However, the energy cost of walking (treadmill 4 km/h), 50 W and 100 W work-loads (bicycle ergometer) as well as delta mechanical efficiency (DME) did not change during the three metabolic periods. The urinary excretion of riboflavin was inversely related to DME (r— 0.49;P< 0.05) and directly correlated with haemoglobin levels (r0.63;P< 0.005). The present study suggests that riboflavin status further deteriorates during a short period of increased physical activity in individuals whose riboflavin status is marginal.
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Aljaadi, Abeer M., Ru En How, Su Peng Loh, Shannon E. Hunt, Crystal D. Karakochuk, Susan I. Barr, Liadhan McAnena, et al. "Suboptimal Biochemical Riboflavin Status Is Associated with Lower Hemoglobin and Higher Rates of Anemia in a Sample of Canadian and Malaysian Women of Reproductive Age." Journal of Nutrition 149, no. 11 (July 18, 2019): 1952–59. http://dx.doi.org/10.1093/jn/nxz151.
Abstract:
ABSTRACT Background Riboflavin is required for several redox reactions. Clinical riboflavin deficiency occurs mainly in low-income countries, where it is associated with anemia. The functional significance of suboptimal riboflavin status in different populations and its role in anemia is not well understood. Objectives We assessed the biomarker status of riboflavin and its association with hemoglobin concentration and anemia in women living in Vancouver, Canada, and Kuala Lumpur, Malaysia. Methods Healthy nonpregnant, nonbreastfeeding women (19–45 y) were recruited from Canada ( n = 206) and Malaysia (n = 210) via convenience sampling. Fasting blood was collected to assess riboflavin status [erythrocyte glutathione reductase activity coefficient (EGRac)], hematological indicators, soluble transferrin receptor (sTfR), ferritin, vitamin A, folate, and vitamin B-12 concentrations. Linear and logistic regression models were used to assess the association of riboflavin status with hemoglobin concentration and anemia. Results EGRac (mean ± SD) values were higher, indicating poorer riboflavin status, in Malaysian compared with Canadian women (1.49 ± 0.17 compared with 1.38 ± 0.11). Likewise, riboflavin biomarker deficiency (EGRac ≥1.40) was significantly more prevalent among Malaysians than Canadians (71% compared with 40%). More Malaysian than Canadian women were anemic (hemoglobin <120 g/L; 18% compared with 7%). With use of linear regression (pooled sample; n = 416), EGRac values were negatively associated with hemoglobin concentration (r = −0.18; P < 0.001). This relation remained significant (P = 0.029) after adjusting for age, parity, ethnicity, vitamin B-12, folate, sTfR, ferritin, and vitamin A. Women with riboflavin deficiency (EGRac ≥1.40) were twice as likely to present with anemia (adjusted OR: 2.38; 95% CI: 1.08, 5.27) compared with women with EGRac <1.40. Conclusions Biochemical riboflavin deficiency was observed in Canadian and Malaysian women, with higher rates of deficiency among Malaysian women. Deficient biomarker status of riboflavin was a weak but significant predictor of hemoglobin and anemia, suggesting that the correction of riboflavin deficiency may potentially play a small protective role in anemia, but this requires further investigation.
45
Rohner, Fabian, Michael B. Zimmermann, Rita Wegmueller, Andreas B. Tschannen, and Richard F. Hurrell. "Mild riboflavin deficiency is highly prevalent in school-age children but does not increase risk for anaemia in Côte d'Ivoire." British Journal of Nutrition 97, no. 5 (May 2007): 970–76. http://dx.doi.org/10.1017/s0007114507665180.
Abstract:
There are few data on the prevalence of riboflavin deficiency in sub-Saharan Africa, and it remains unclear whether riboflavin status influences the risk for anaemia. The aims of this study were to: (1) measure the prevalence of riboflavin deficiency in children in south-central Côte d'Ivoire; (2) estimate the riboflavin content of the local diet; and (3) determine if riboflavin deficiency predicts anaemia and/or iron deficiency. In 5- to 15-year-old children (n281), height, weight, haemoglobin (Hb), whole blood zinc protoporphyrin (ZPP), erythrocyte glutathione reductase activity coefficient (EGRAC), serum retinol, C-reactive protein (CRP) and prevalence ofPlasmodiumspp. (asymptomatic malaria) andSchistosoma haematobium(bilharziosis) infections were measured. Three-day weighed food records were kept in twenty-four households. Prevalence of anaemia in the sample was 52 %; 59 % were iron-deficient based on an elevated ZPP concentration, and 36 % suffered from iron deficiency anaemia.Plasmodiumparasitaemia was found in 49 % of the children. Nineteen percent of the children were infected withS. haematobium. Median riboflavin intake in 5- to 15-year-old children from the food records was 0·42 mg/d, ~47 % of the estimated average requirement for this age group. Prevalence of riboflavin deficiency was 65 %, as defined by an EGRAC value >1·2. Age, elevated CRP and iron deficiency were significant predictors of Hb. Riboflavin-deficient children free of malaria were more likely to be iron deficient (odds ratio; 3·07; 95 % CI 1·12, 8·41). In conclusion, nearly two-thirds of school-age children in south-central Côte d'Ivoire are mildly riboflavin deficient. Riboflavin deficiency did not predict Hb and/or anaemia, but did predict iron deficiency among children free of malaria.
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Crossley, Rachel A., Duncan J. H. Gaskin, Kathryn Holmes, Francis Mulholland, Jerry M. Wells, David J. Kelly, Arnoud H. M. van Vliet, and Nicholas J. Walton. "Riboflavin Biosynthesis Is Associated with Assimilatory Ferric Reduction and Iron Acquisition by Campylobacter jejuni." Applied and Environmental Microbiology 73, no. 24 (October 26, 2007): 7819–25. http://dx.doi.org/10.1128/aem.01919-07.
Abstract:
ABSTRACT One of the pathways involved in the acquisition of the essential metal iron by bacteria involves the reduction of insoluble Fe3+ to soluble Fe2+, followed by transport of Fe2+ to the cytoplasm. Flavins have been implicated as electron donors in this poorly understood process. Ferrous iron uptake is essential for intestinal colonization by the important pathogen Campylobacter jejuni and may be of particular importance under low-oxygen conditions. In this study, the links among riboflavin biosynthesis, ferric reduction, and iron acquisition in C. jejuni NCTC11168 have been investigated. A riboflavin auxotroph was generated by inactivation of the ribB riboflavin biosynthesis gene (Cj0572), and the resulting isogenic ribB mutant only grew in the presence of exogenous riboflavin or the riboflavin precursor diacetyl but not in the presence of the downstream products flavin adenine dinucleotide and flavin mononucleotide. Riboflavin uptake was unaffected in the ribB mutant under iron-limited conditions but was lower in both the wild-type strain and the ribB mutant under iron-replete conditions. Mutation of the fur gene, which encodes an iron uptake regulator of C. jejuni, resulted in an increase in riboflavin uptake which was independent of the iron content of the medium, suggesting a role for Fur in the regulation of the as-yet-unknown riboflavin transport system. Finally, ferric reduction activity was independent of iron availability in the growth medium but was lowered in the ribB mutant compared to the wild-type strain and, conversely, increased in the fur mutant. Taken together, the findings confirm close relationships among iron acquisition, riboflavin production, and riboflavin uptake in C. jejuni.
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Brijlal, Sangeetha, A. V. Lakshmi, Mahtab S. Bamji, and P. Suresh. "Flavin metabolism during respiratory infection in mice." British Journal of Nutrition 76, no. 3 (September 1996): 453–62. http://dx.doi.org/10.1079/bjn19960050.
Abstract:
Previous control studies carried out in children showed that respiratory infection alters riboflavin metabolism and leads to excessive urinary losses of the vitamin. In order to understand the nature of biochemical changes in riboflavin metabolism during respiratory infection, a study was carried out using the mouse as the experimental model, andKlebsiella pneumonjueas the infective organism. Mice were fed on either a low(0·5 mg/kg)- or high(13·3 mg/kg)-riboflavin semi-synthetic diet. Infection resulted in a 5–6-fold higher excretion of riboflavin in the urine of mice fed on the low-riboflavin diet. Higher erythrocyte FAD levels and lower liver FAD levels were also observed during infection. Of the four enzymes involved in the synthesis and breakdownof the flavin coenzymes studied, the activity of hepatic flavokinase (ATP: riboflavin 5'-phosphotransferase;EC2.7.1.26) was significantly lower, and that of FAD synthetase (ATP: FMN adenylyltransferase;EC2.7.7.2) was higher during riboflavin restriction and infection. The activity of FMN (acid) phosphatase (EC3.1.3.2) was unchanged, whereas FAD (nucleotide) pyrophosphatase (EC3.6.1.9) activity was significantly higher both with the low-riboflavin diet and during infection. Thyroid hormone is known to modulate flavokinase activity and, hence, thyroid status was assessed. Plasma triiodothyronine (T3) levels were not affected, but thyroxine levels were lower in the mice fed on the low-riboflavin diet. However, plasma T3 was significantly lower during infection, suggesting a mechanistic role for the hormone in the reduction of flavokinase activity.
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Kim, Joo-Yun, Eun-Jung Choi, Jae-Ho Lee, Myeong-Seok Yoo, Keon Heo, Jae-Jung Shim, and Jung-Lyoul Lee. "Probiotic Potential of a Novel Vitamin B2-Overproducing Lactobacillus plantarum Strain, HY7715, Isolated from Kimchi." Applied Sciences 11, no. 13 (June 22, 2021): 5765. http://dx.doi.org/10.3390/app11135765.
Abstract:
Vitamin B2, also known as riboflavin, is essential for maintaining human health. The purpose of this study was to isolate novel lactic acid bacteria that overproduce vitamin B2 and to validate their potential as probiotics. In this study, Lactobacillus plantarum HY7715 (HY7715) was selected among lactic acid bacteria isolated from Kimchi. HY7715 showed a very high riboflavin-producing ability compared to the control strain due to the high expression of ribA, ribB, ribC, ribH, and ribG genes. HY7715 produced 34.5 ± 2.41 mg/L of riboflavin for 24 h without consuming riboflavin in the medium under optimal growth conditions. It was able to produce riboflavin in an in vitro model of the intestinal environment. In addition, when riboflavin deficiency was induced in mice through nutritional restriction, higher levels of riboflavin were detected in plasma and urine in the HY7715 administration group than in the control group. HY7715 showed high survival rate in simulated gastrointestinal conditions and had antibiotic resistance below the cutoff MIC value suggested by the European Food Safety Authority; moreover, it did not cause hemolysis. In conclusion, HY7715 could be considered a beneficial probiotic strain for human and animal applications, suggesting that it could be a new alternative to address riboflavin deficiency.
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Vukomanovic, Dragic, Zongchao Jia, Kanji Nakatsu, Graeme N. Smith, and Terence R. S. Ozolinš. "Riboflavin and pyrroloquinoline quinone generate carbon monoxide in the presence of tissue microsomes or recombinant human cytochrome P-450 oxidoreductase: implications for possible roles in gasotransmission." Canadian Journal of Physiology and Pharmacology 98, no. 5 (May 2020): 336–42. http://dx.doi.org/10.1139/cjpp-2019-0376.
Abstract:
Carbon monoxide (CO), an endogenously produced gasotransmitter, regulates inflammation and vascular tone, suggesting that delivery of CO may be therapeutically useful for pathologies like preeclampsia where CO insufficiency is implicated. Our strategy is to identify chemicals that increase the activity of endogenous CO-producing enzymes, including cytochrome P-450 oxidoreductase (CPR). Realizing that both riboflavin and pyrroloquinoline quinone (PQQ) are relatively nontoxic, even at high doses, and that they share chemical properties with toxic CO activators that we previously identified, our goal was to determine whether riboflavin or PQQ could stimulate CO production. Riboflavin and PQQ were incubated in sealed vessels with rat and human tissue extracts and CO generation was measured with headspace-gas chromatography. Riboflavin and PQQ increased CO production ∼60% in rat spleen microsomes. In rat brain microsomes, riboflavin and PQQ increased respective CO production approximately fourfold and twofold compared to baseline. CO production by human placenta microsomes increased fourfold with riboflavin and fivefold with PQQ. In the presence of recombinant human CPR, CO production was threefold greater with PQQ than with riboflavin. These observations demonstrate for the first time that riboflavin and PQQ facilitate tissue-specific CO production with significant contributions from CPR. We propose a novel biochemical role for these nutrients in gastransmission.
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Brady, P. S., and C. L. Hoppel. "Hepatic peroxisomal and mitochondrial fatty acid oxidation in the riboflavin-deficient rat." Biochemical Journal 229, no. 3 (August 1, 1985): 717–21. http://dx.doi.org/10.1042/bj2290717.
Abstract:
The effects of riboflavin deficiency on hepatic peroxisomal and mitochondrial palmitoyl-CoA oxidation were examined in weanling Wistar-strain male rats. The specific activities of peroxisomal catalase and palmitoyl-CoA-dependent NAD+ reduction were not affected by up to 10 weeks of riboflavin deficiency. In contrast, the specific activity of mitochondrial carnitine-dependent palmitoyl-CoA oxidation was depressed by 75% at 10 weeks of deficiency. The amount of peroxisomal protein per g of liver was not affected by riboflavin deficiency, whereas, expressed per liver, both riboflavin-deficient and pair-fed controls showed decreased peroxisomal protein compared with controls fed ad libitum. Hepatic mitochondria, but not peroxisomes, were sensitive to riboflavin deficiency.