Riboflavine
Riboflavin is an easily absorbed micronutrient with a key role in maintaining health in humans and other animals. Riboflavine exhibits anti-inflammatory, hepatoprotective, and antioxidant properties, can treat the regression of neurological impairment.
Riboflavine deficiency may lead to angular conjunctivitis.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com
The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Can J Microbiol. 2014 Nov;60(11):753-9.
Riboflavine-shuttled extracellular electron transfer from Enterococcus faecalis to electrodes in microbial fuel cells.[Pubmed:
25345758]
Great attention has been focused on Gram-negative bacteria in the application of microbial fuel cells.
METHODS AND RESULTS:
In this study, the Gram-positive bacterium Enterococcus faecalis was employed in microbial fuel cells. Bacterial biofilms formed by E. faecalis ZER6 were investigated with respect to electricity production through the Riboflavine-shuttled extracellular electron transfer. Trace Riboflavine was shown to be essential for transferring electrons derived from the oxidation of glucose outside the peptidoglycan layer in the cell wall of E. faecalis biofilms formed on the surface of electrodes, in the absence of other potential electron mediators (e.g., yeast extract).
Arch Pediatr. 1999 Apr;6(4):421-6.
Leigh syndrome and leukodystrophy due to partial succinate dehydrogenase deficiency: regression with riboflavin.[Pubmed:
10230482]
Succinate dehydrogenase (SDH) deficiency is rare. Clinical manifestations can appear in infancy with a marked impairment of psychomotor development with pyramidal signs and extrapyramidal rigidity.
METHODS AND RESULTS:
A 10-month-old boy developed severe neurological features, evoking a Leigh syndrome; magnetic resonance imaging showed features of leukodystrophy. A deficiency in the complex II respiratory chain (succinate dehydrogenase [SDH]) was shown. The course was remarkable by the regression of neurological impairment under treatment by Riboflavine. The delay of psychomotor development, mainly involving language, was moderate at the age of 5 years.
CONCLUSIONS:
The relatively good prognosis of this patient, despite severe initial neurological impairment, may be due to the partial enzyme deficiency and/or Riboflavine administration.
Food Chem Toxicol. 2014 May;67:65-71.
Riboflavine (vitamin B-2) reduces hepatocellular injury following liver ischaemia and reperfusion in mice.[Pubmed:
24560968]
Riboflavine has been shown to exhibit anti-inflammatory and antioxidant properties in the settings of experimental sepsis and ischaemia/reperfusion (I/R) injury.
METHODS AND RESULTS:
We investigated the effect of Riboflavine on normothermic liver I/R injury. Mice were submitted to 60 min of ischaemia plus saline or Riboflavine treatment (30 μmoles/kg BW) followed by 6 h of reperfusion. Hepatocellular injury was evaluated by aminotransferase levels, reduced glutathione (GSH) content and the histological damage score. Hepatic neutrophil accumulation was assessed using the naphthol method and by measuring myeloperoxidase activity. Hepatic oxidative/nitrosative stress was estimated by immunohistochemistry. Liver endothelial and inducible nitric oxide synthase (eNOS/iNOS) and nitric oxide (NO) amounts were assessed by immunoblotting and a chemiluminescence assay. Riboflavine significantly reduced serum and histological parameters of hepatocellular damage, neutrophil infiltration and oxidative/nitrosative stress. Furthermore, Riboflavine infusion partially recovered hepatic GSH reserves and decreased the liver contents of eNOS/iNOS and NO.
CONCLUSIONS:
These data indicate that Riboflavine exerts antioxidant and anti-inflammatory effects in the ischaemic liver, protecting hepatocytes against I/R injury. The mechanism of these effects appears to be related to the intrinsic antioxidant potential of Riboflavine/dihydroriboflavin and to reduced hepatic expression of eNOS/iNOS and reduced NO levels, culminating in attenuation of oxidative/nitrosative stress and the acute inflammatory response.
Int Immunopharmacol. 2014 Aug;21(2):383-8.
Carbon tetrachloride-induced hepatotoxicity in rat is reversed by treatment with riboflavine.[Pubmed:
24874442]
Liver is a vital organ for the detoxification of toxic substances present in the body and hepatic injury is associated with excessive exposure to toxicants.
METHODS AND RESULTS:
The present study was designed to evaluate the possible hepatoprotective effects of Riboflavine against carbon tetrachloride (CCl4) induced hepatic injury in rats. Rats were divided into six groups. Hepatotoxicity was induced by the administration of a single intraperitoneal dose of CCl4 in experimental rats. Riboflavine was administered at 30 and 100mg/kg by oral gavage to test its protective effect on hepatic injury biochemically and histopathologically in the blood/liver and liver respectively. The administration of CCl4 resulted in marked alteration in serum hepatic enzymes (like AST, ALT and ALP), oxidant parameters (like GSH and MDA) and pro-inflammatory cytokine TNF-α release from blood leukocytes indicative of hepatic injury. Changes in serum hepatic enzymes, oxidant parameters and TNF-α production induced by CCl4 were reversed by Riboflavine treatment in a dose dependent manner. Treatment with standard drug, silymarin also reversed CCl4 induced changes in biomarkers of liver function, oxidant parameters and inflammation. The biochemical observations were paralleled by histopathological findings in rat liver both in the case of CCl4 and treatment groups.
CONCLUSIONS:
In conclusion, Riboflavine produced a protective effect against CCl4-induced liver damage. Our study suggests that Riboflavine may be used as a hepato-protective agent against toxic effects caused by CCl4 and other chemical agents in the liver.
