Mechanism of impaired skin collagen maturity in riboflavin or pyridoxine deficiency

Rudraraju, Lakshmi; Lakshmi, A.V.; Bamji, Mahtab S.

doi:10.1007/bf02702670

Cited by 11 publications

(7 citation statements)

References 22 publications

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“…MTHFR activity and hepatic 5MeTHF concentrations are lower in riboflavindeficient rats than in controls (6 ). Increased homocysteine in the skin of riboflavin-deficient rats has also been reported (7 ). Recently, plasma riboflavin has been reported to be an independent predictor of tHcy in a group of healthy blood donors.…”

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confidence: 91%

Effect of Riboflavin Status on the Homocysteine-lowering Effect of Folate in Relation to the MTHFR (C677T) Genotype

et al. 2003

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Background: Riboflavin (vitamin B 2 ) is the precursor for FAD, the cofactor for methylenetetrahydrofolate reductase (MTHFR). MTHFR catalyzes the formation of 5-methyltetrahydrofolate, which acts as a methyl donor for homocysteine remethylation. Individuals with the MTHFR 677C3 T mutation have increased plasma total homocysteine (tHcy) concentrations, particularly in association with low folate status. It has been proposed that riboflavin may act together with folate to lower plasma tHcy, particularly in individuals with the thermolabile MTHFR T variant. Methods: We measured B-vitamin status and plasma tHcy in 126 healthy individuals 20 -63 years of age (42 CC, 42 CT, and 42 TT MTHFR genotypes) at baseline and after three interventions (4 months): placebo plus natural diet; daily 400 g folic acid supplement plus natural diet; and increased dietary folate to 400 g/day. Results: At baseline and after nutritional intervention, lower riboflavin status was associated with increased plasma tHcy concentrations. Plasma tHcy was 2.6 mol/L higher in the lowest plasma riboflavin quartile compared with the highest (P <0.02) and was 4.2 mol/L higher in the highest erythrocyte glutathione reductase activation coefficient (EGRAC) quartile compared with the lowest (P <0.001). This effect was not restricted to those with the T allele. Folic acid given as a 400 g/day supplement appeared to exacerbate a tendency toward riboflavin deficiency, as suggested by an increase in the

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confidence: 91%

Effect of Riboflavin Status on the Homocysteine-lowering Effect of Folate in Relation to the MTHFR (C677T) Genotype

et al. 2003

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“…It is also widely recognized that plasma homocysteine (tHcy) concentrations increase with age (Selhub et al, 1993;Andersson et al, 1992). In support of the possibility that riboflavin may be an important determinant of tHcy, Lakshmi et al (1990) noted a 2 -4-fold increase in the concentration of tHcy in the skin of rats in response to an experimentally induced riboflavin deficiency. Sparse and conflicting data exist, however, on the effect of riboflavin intake and status on plasma tHcy in humans.…”

Section: Introductionmentioning

confidence: 99%

Effect of riboflavin supplementation on plasma homocysteine in elderly people with low riboflavin status

et al. 2002

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Objective: To investigate the effect of riboflavin supplementation on plasma homocysteine (tHcy) concentrations in healthy elderly people with sub-optimal riboflavin status. Design: A double-blind, randomized, placebo-controlled riboflavin supplementation trial. Setting: Community based study in Northern Ireland. Subjects: From a screening sample of 101 healthy elderly people, 52 had sub-optimal riboflavin status (erythrocyte glutathione reductase activation coefficient, EGRAC ! 1.20) and were invited to participate in the study. Intervention: The intervention had two parts. Part 1 was a 12 week randomized double blind, placebo-controlled intervention with riboflavin (1.6 mg=day). Following completion of part 1, the placebo group went on to part 2 of the study which involved supplementation with folic acid (400 mg=day) for 6 weeks followed by folic acid and riboflavin (1.6 mg=day) for a further 12 weeks, with a 16 week washout period post-supplementation. The purpose of part 2 was: (a) to address the possibility that homocysteine-lowering in response to riboflavin may be obscured by a much greater effect of folate, and that, once folate status was optimized, a dependence of homocysteine on riboflavin might emerge; and (b) to demonstrate that these subjects had homocysteine concentrations which could be lowered by nutritional intervention. Results: Although riboflavin supplementation significantly improved riboflavin status in both parts 1 and 2 of the study (P < 0.001 for each), tHcy concentrations were unaffected (P ¼ 0.719). In contrast, folic acid supplementation (study part 2) resulted in a homocysteine lowering of 19.6% (P ¼ 0.001). Conclusion: Despite the metabolic dependency of tHcy on riboflavin, it did not prove to be an effective homocysteine-lowering agent, even in the face of sub-optimal riboflavin status.

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“…Impaired collagen maturity in vitamin B2, B6, and B8 deficiency has been reported in earlier studies. [ 4 5 6 7 8 ] Pyridoxine deficiency is known to affect the metabolism of sulfur-containing amino acids such as homocysteine and raise their levels in tissue. In a different study reported that these amino acids are known to interfere with the process of collagen cross-linking.…”

Section: Discussionmentioning

confidence: 99%

To Evaluate the Effect of Vitamin B Complex on Wound Healing – A Clinical and Microbiological Study

Kalsi,

Bhushan,

Mathur

et al. 2024

Journal of Pharmacy and Bioallied Sciences

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Background: The purpose of this study is to explore the effect of vitamin B complex supplementation following periodontal flap surgery on clinical and microbiological parameters. Materials and Methods: A randomized controlled trial on 10 patients with periodontitis in split-mouth design was undertaken to find the effect of vitamin B complex supplementation with open flap debridement on periodontal wound healing. Multiplex polymerase chain reaction (PCR) for Tannerella forsythus and Porphyromonas gingivalis was done using subgingival plaque samples at 0 and 90th day. Results: The results showed a significant reduction (P < 0.01) of clinical (plaque index, gingival index, gingival bleeding index, probing pocket depth, and relative attachment level) and microbial profile in both treatment groups, whereas on intergroup analysis, more reduction in all clinical parameters were observed in the test group, but statistically, the results were insignificant.

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Mechanism of impaired skin collagen maturity in riboflavin or pyridoxine deficiency

Cited by 11 publications

References 22 publications

Effect of Riboflavin Status on the Homocysteine-lowering Effect of Folate in Relation to the MTHFR (C677T) Genotype

Effect of Riboflavin Status on the Homocysteine-lowering Effect of Folate in Relation to the MTHFR (C677T) Genotype

Effect of riboflavin supplementation on plasma homocysteine in elderly people with low riboflavin status

To Evaluate the Effect of Vitamin B Complex on Wound Healing – A Clinical and Microbiological Study

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