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Cyanocobalamin supplements

The fibroblasts do not convert cyanocobalamin or hydroxocobalamin to methylcobalamin or adenosyl-cobalamin, resulting in diminished activity of both N5-methyltetrahydrofolate homocysteine methyltransferase and methylmalonyl-CoA mutase. Supplementation with hydroxocobalamin rectifies the aberrant biochemistry. The precise nature of the underlying defect remains obscure. Diagnosis should be suspected in a child with homocystinuria, methylmalonic aciduria, megaloblastic anemia, hypomethioninemia and normal blood levels of folate and vitamin B12. A definitive diagnosis requires demonstration of these abnormalities in fibroblasts. Prenatal diagnosis is possible. [Pg.678]

The name vitamin B12 indicates a group of cobalt-containing corrinoids, also described as cobala-mins. Hydroxycobalamin (HOCbl), adenosylcobalamin (AdoCbl), and methylcobalamin (MeCbl) are the natural occurring forms. Instead, cyanocobalamin (Figure 19.20) is the commercially available form used for supplements and food fortification, thanks to its greater relative stability. Occasionally, sulfitocobalmin can occur in processed foods. Vitamin B,2 functions as a coenzyme and it is linked to human growth, cell development, and is involved in metabolism of certain amino acids. Vitamin B12 is present mainly in meat and diary foods, therefore a deficiency can occur in... [Pg.633]

Cyanocobalamin, or vitamin B12, is in small amounts required for red blood cell production and for the formation of nucleoproteins and proteins. It is also needed for the proper functioning of the nervous system. Folic acid supplements can correct the anemia associated with vitamin B12 deflciency. Unfortunately, folic acid will not correct changes in the nervous system that result from vitamin B12 deficiency. Vitamin B12 is only found in animal sources such as liver and other organs. Some vitamin B12 is obtained from fish, eggs and milk. Folic acid and cyanocobalamin have been discussed in more detail in Chapter 22. [Pg.475]

Vitamin B12 supplement Cyanocobalamin Nascobal Methylcellulose Aqueous... [Pg.223]

Cyanocobalamin (vitamin Bl2) Propionibacterium shermanii. Pseudomonas dentrificans Food and animal feed supplement... [Pg.302]

In pernicious anemia, vitamin B12 should be given as intramuscular injection or high-dose oral supplements. Intramuscular injections of 100 to 1000 pg of cyanocobalamin for 5 d and 100 to 1000 pg of cyanocobalamin each month thereafter is a sufficient protocol for treating pernicious anemia (see Baik and Russell, 1999). [Pg.345]

The ligand attached to the cobalt atom determines the activity of vitamin B12 in human enzymatic reactions. The two active coenzyme forms are methyl-cobalamin and 5 -adenosylcobalamin, the primary form of vitamin B12 in tissues. Cyanocobalamin, the therapeutic form of vitamin B12 contained in vitamin supplements, is produced by the cleavage of the unstable fink... [Pg.305]

Oral vitamin Bj2 supplementation appears to be as effective as parenteral, even in patients with pernicious anemia, because the alternate vitamin Bj2 absorption pathway is independent of intrinsic factor. Oral cobalamin is initiated at 1 to 2 mg daily for 1 to 2 weeks, followed by 1 mg daUy. Parenteral therapy is more rapid acting than oral therapy and should be used if neurologic symptoms are present. A popular regimen is cyanocobalamin 1,000 meg daily for 1 week, then weekly for 1 month, and then monthly. When symptoms resolve, daily oral administration can be initiated. [Pg.367]

Vitamin B]2, cyanocobalamin, is essential for human nutrition. It is concentrated in animal tissue but not in higher plants. Although nutritional requirements for the vitamin are quite low, people who abstain completely from animal products may develop a deficiency anemia. Cyanocobalamin is the form used in vitamin supplements. It contains 4.34% cobalt by mass. Calculate the molar mass of cyanocobalamin, assuming that there is one atom of cobalt in every molecule of cyanocobalamin. [Pg.81]

Vitamin Bij (cyanocobalamin extrinsic factor) is required in folate metabolism for DNA synthesis, and a deficiency leads to pernicious anaemia. It is used to supplement the diet after certain operations that remove the site of production of intrinsic factor, such as total gastrectomy. Deficiency causes megaloblastic haemopoiesis in which there is a marked disorder of formation of erythroblasts, and can be rectified by giving hydroxocobalamin. [Pg.21]

Cyanocobalamin, a water-soluble vitamin (25 meg p.o. daily as a dietary supplement), is indicated in vitamin Bj2 deficiency resulting from any cause except malabsorption related to pernicious anemia or other GI disease (see Figure 106). [Pg.176]

VITAMIN Bj2 therapy Vitamin B is available for injection or oral administration combinations with other vitamins and minerals also can be given orally or parenterally. The choice of a preparation always depends on the cause of the deficiency. Although oral preparations may be used to supplement deficient diets, they are of limited value in the treatment of patients with deficiency of intrinsic factor or deal disease. Even though small amounts of vitamin may be absorbed by simple diffusion, the oral route of administration cannot be rehed upon for effective therapy in the patient with a marked deficiency of vitamin Bj and abnormal hematopoiesis or neurological deficits. Therefore, the treatment of choice for vitamin Bj -deficiency is cyanocobalamin administered by intramuscular or subcutaneous injection. [Pg.945]

Vitamin Bj should be given prophylactically only when there is a reasonable probability that a deficiency exists or wdl exist. Dietary deficiency in the strict vegetarian, the predictable malabsorption of vitamin Bj in patients who have had a gastrectomy, and certain diseases of the small intestine constitute such indications. When GI function is normal, an oral prophylactic supplement of vitamins and minerals, including vitamin Bj, may be indicated. Otherwise, the patient should receive monthly injections of cyanocobalamin. [Pg.945]

Supplements. Cyanocobalamin (readily converted in the body to the bioavailable forms 5-deoxy-adenosyl and methylcobalamin) is the principal form of vitamin B,2 used in supplements but methylcobalamin is also available. Cyanocobalamin is available by prescription in an injectable form and as a nasal gel for the treatment of pernicious anemia. Over the counter preparations containing cyanocobalamin include multivitamin, vitamin B-complex, and vitamin B,2 supplements. ... [Pg.259]

Some forms of MMA may be responsive to vitamin Bjj. Responsiveness can be determined by administration of 1.0 mg hydroxocobalamin (IM or IV) for 5 days. A reduction in serum methylmalonic acid concentrations of 50 % or greater suggests responsiveness [14]. For those with cobalamin-responsive forms of MMA, intramuscular (IM) hydroxocobalamin injections of 1.0-2.0 mg are often administered daily. A decreased frequency of IM injections or use of oral supplements may be appropriate for older individuals. The hydroxocobalamin form rather than the standard cyanocobalamin form must be used [15]. [Pg.225]

We have developed a method for simultaneous analysis of thiamine hydrochloride, pyridoxine hydrochloride and cyanocobalamin in pharmaceuticals and dietary supplements (Marszall et al. 2005) and in fortified food (Lebiedzinska and MarszaH 2006) using HPLC-ED. Vitamins were determined in their free forms, so an extraction step from fortified fruit juice was performed prior to the chromatographic isolations. The extraction procedure was based on a study by Ndaw el al. (2000). The enzymatic digestion prior to the separation and quantification step made it possible to release the vitamins bound to proteins or sugars and converted vitamin esters to free forms thus we were able to obtain the total vitamin contents of the fruit juices. The supernatants were adjusted to pH 4.5 with 2.5 M sodium acetate and a single extraction procedure for all vitamins was carried out using mixture of the enzymes, papain and diastase (Lebiedzinska and MarszaH 2006). [Pg.232]

Using a single LC-MS/MS method to quantify all WSVs at such different levels of concentrations is very difficult. However, quantitation of all the WSVs except cyanocobalamin in a single chromatographic run has been achieved (Chen and Wolf 2007 Chen et al. 2009). Compromises have to be made to accommodate WSVs at different concentration levels. For multi WSV analysis using LC-MS or LC-MS/MS in multivitamin dietary supplements, the instrument may need to be intentionally tuned to lower the sensitivity for pantothenic acid to accommodate higher concentrations if folic acid and biotin need to be analysed together (Chen and Wolf 2007). [Pg.358]

Vitamin B12 must be converted into its coenzyme forms, adenosylcobalamin and methylcobalamin, in the cell. These coenzymes function as cofactors of methylmalonyl-CoA mutase and methionine synthase, respectively. Chronic kidney disease (CKD) may affect the conversion from vitamin B12 to the coenzyme forms. This section describes the intracellular metabolism of cyanocobalamin, which is included in many dietary supplements, in particular, referring to a recently discovered trafficking chaperone called methylmalonic aciduria cdlC type with homocystinuria (MMACHC). Cyanocobalamin is first converted to cob(II)alamin, which has no cyanogen group on the ligand occupying the upper axial position of the cobalamin structure. Cob(II)alamin is further reduced to cob(I)alamin, which can function as a coenzyme in the body. [Pg.819]

Added support for the supposition that the biosynthesis of riboflavin and cyanocobalamin make use of a common precursor comes from the increased synthesis of riboflavin by Ashbya gossypii in cobalt-supplemented media (Hickey, 1954) and from the stimulation of riboflavin formation in a Saccharomyces cerevisiae mutant by purines, glycine, and methionine (Giri and Krishnswamy, 1964). [Pg.123]

A connection between folic acid and Bi displayed in pernicious anemia was also revealed in Shive s (1950) studies of the reversal of sulfanilamide inhibition, as mentioned earlier in the discussion of E. coli 313-3. A more direct approach to folic-Bij relations seems available in certain p-aminobenzoic acid (PAB)-deficient strains of Bacillus stearothermophilus which respond with equal sensitivities, on a molar basis, to pteroic acid and pteroylglutamic acid (Baker et al., 1956). This PAB-folic requirement is satisfied by a combination of thymine, xanthine, and cyanocobalamin. The concentration of cyanocobalamin required under these conditions was high (10 ug. %) as contrasted with the requirement (0.01 ug-%) of a Bi2-requiring strain of B. stearothermophilus. The cobalamin supplement for the PAB-deficient strain was not replaceable by methionine on the other hand, cyanocobalamin for the B 12 deficient strain ivas replaceable by methionine. XTnexpectedly, cyanocobalamin did not reverse inhibition by sulfanilamide of the PAB-deficient strain in the presence of methionine, xanthine, thymine, glycine, serine, threonine, and leucine—the combination found effective by Shive in reversing sulfanilamide inhibition of wild-type E. coli. [Pg.129]

Determination of vitamin B12 by LC—UV is difficult to perform in non-supplemented foodstuffs because of the very low concentrations of the vitamin and the poor sensitivity and selectivity of the detection s)istem employed. These problems were overcome using an immimoaffinity column and monitoring the vitamin at 361 run [58]. The extractive procedure of liebiedzihska et al. [7] was based on an enzymatic digestion with a-amilase and papain after autoclaving salmon samples at 121°C in the presence of cyanide cyanocobalamin was monitored by an electrochemical detector. [Pg.488]


See other pages where Cyanocobalamin supplements is mentioned: [Pg.783]    [Pg.783]    [Pg.387]    [Pg.120]    [Pg.1315]    [Pg.120]    [Pg.274]    [Pg.267]    [Pg.87]    [Pg.292]    [Pg.223]    [Pg.176]    [Pg.738]    [Pg.120]    [Pg.5089]    [Pg.810]    [Pg.425]    [Pg.315]   
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Cyanocobalamin

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