Vitamin catabolism

Approximately 0.05 to 0.2% of vitamin > 2 stores are turned over daily, amounting to 0.5—8.0 )J.g, depending on the body pool size. The half-life of the body pool is estimated to be between 480 and 1360 days with a daily loss of vitamin > 2 of about 1 )J.g. Consequentiy, the daily minimum requirement for vitamin B22 is 1 fig. Three micrograms (3.0 J.g) vitamin B22 are excreted in the bile each day, but an efficient enterohepatic circulation salvages the vitamin from the bile and other intestinal secretions. This effective recycling of the vitamin contributes to the long half-life. Absence of the intrinsic factor intermpts the enterohepatic circulation. Vitamin > 2 is not catabolized by the body and is, therefore, excreted unchanged. About one-half of the vitamin is excreted in the urine and the other half in the bile. 

The nitrogen source in the medium is the amino add glutamate. There are several cations K Mn2, Cn2, Zn2, Mg2, Co2, Fe2, Ca2 Mo6. Phosphate (POi") is the major anionic component. Fumaric add is a TCA cycle intermediate and may improve metabolic balance through the catabolic pathways and oxidation through the TCA cyde. Peptone may improve growth through the provision of growth factors (amino acids, vitamins, nudeotides). 

Since the end products of pyrimidine catabolism are highly water-soluble, pyrimidine overproduction results in few clinical signs or symptoms. In hypemricemia associated with severe overproduction of PRPP, there is overproduction of pyrimidine nucleotides and increased excretion of p-alanine. Since A, A -methyl-ene-tetrahydrofolate is required for thymidylate synthesis, disorders of folate and vitamin Bjj metabofism result in deficiencies of TMP. 

Methylmalonyl CoA mutase, leucine aminomutase, and methionine synthase (Figure 45-14) are vitamin Bj2-dependent enzymes. Methylmalonyl CoA is formed as an intermediate in the catabolism of valine and by the carboxylation of propionyl CoA arising in the catabolism of isoleucine, cholesterol, and, rarely, fatty acids with an odd number of carbon atoms—or directly from propionate, a major product of microbial fer-... 

In an inciteful discussion of insect-microbe relationships, Jones (10) postulated that insect-microbial associations, known to involve catabolic (e.g. cellulose-degrading) and anabolic (e.g. biosynthesis of vitamins, sterols, and amino acids) processes necessary to the survival of the host, could also include detoxification abilities. Most investigations in this area have been limited (11). Nevertheless, some studies indicate detoxification of terpenoids (12,... 

These three compounds exert many similar effects in nucleotide metabolism of chicks and rats [167]. They cause an increase of the liver RNA content and of the nucleotide content of the acid-soluble fraction in chicks [168], as well as an increase in rate of turnover of these polynucleotide structures [169,170]. Further experiments in chicks indicate that orotic acid, vitamin B12 and methionine exert a certain action on the activity of liver deoxyribonuclease, but have no effect on ribonuclease. Their effect is believed to be on the biosynthetic process rather than on catabolism [171]. Both orotic acid and vitamin Bu increase the levels of dihydrofolate reductase (EC 1.5.1.4), formyltetrahydrofolate synthetase and serine hydroxymethyl transferase in the chicken liver when added in diet. It is believed that orotic acid may act directly on the enzymes involved in the synthesis and interconversion of one-carbon folic acid derivatives [172]. The protein incorporation of serine, but not of leucine or methionine, is increased in the presence of either orotic acid or vitamin B12 [173]. In addition, these two compounds also exert a similar effect on the increased formate incorporation into the RNA of liver cell fractions in chicks [174—176]. It is therefore postulated that there may be a common role of orotic acid and vitamin Bj2 at the level of the transcription process in m-RNA biosynthesis [174—176]. 

Additionally, a further study described an increased catabolism and mobilization of vitamin A in the whole body (Kelley et al, 1998). 

As the plasma levels of T4 and T3 fall after the administration of antithyroid drugs, the catabolism of vitamin K-dependent clotting factors decreases, thus reducing... 

Geriatric Considerations - Summary Primidone is poorly tolerated in older adults avoid use if possible. Dosage adjustments are required in renal impairment. Numerous drug interactions with primidone exist. Primidone may reduce bone mineral den-sitybyinterferingwith vitamin D catabolism. Calcium and vitamin D supplementation and monitoring of bone mineral density are recommended for older adults taking this drug. 

Colestipol Binds bile acids in gut prevents reabsorption increases cholesterol catabolism up-regulates LDL receptors Decreases LDL Elevated LDL, digitalis toxicity, pruritus Oral taken with meals not absorbed Toxicity Constipation, bloating interferes with absorption of some drugs and vitamins... 

The oxidation of aciy lic acid can be rationalized in terms of the endogenous catabolism of propionic acid, in which acrylyl coenzyme A is an intermediate. This pathway is analogous with fatty acid 3-oxidation, common to all species and, unlike the corresponding pathway in plants, does not involve vitamin 8,2. 3-Hydroxypropionic acid has been found as an intennediate in the metabolism of acrylic acid in vitro in rat liver and mitochondria (Finch Frederick, 1992). The CO2 excreted derives from the carboxyl carbon, while carbon atoms 2 and 3 are converted to acetyl coenzyme A, which participates in a variety of reactions. The oxidation of acrylic acid is catalysed by enzymes in a variety of tissues (Black Finch, 1995). In mice, the greatest activity was found in kidney, which was five times more active than liver and 50 times more active than skin (Black et al., 1993). 

Pernicious anemia is caused by impaired absorption of vitamin B12. What is the effect of this impairment on the catabolism of amino acids Are all amino acids equally affected (Hint See Box 17-2.)... 

Both statements are valid but the second statement, (b), states more accurately why it is that we need vitamins. Vitamin-deficiency diseases, Such as scurvy, result when certain catabolic and anabolic reactions are not able to proceed efficiently in the absence of these important nutrients. 

While Tetrahymena must have lipoic acid in its diet, we humans can make our own, and it is not considered a vitamin. Lipoic acid is present in tissues in extraordinarily small amounts. Its major function is to participate in the oxidative decarboxylation of a-oxoacids but it also plays an essential role in glycine catabolism in the human body as well as in plants.295 296 The structure is simple, and the functional group is clearly the cyclic disulfide which swings on the end of a long arm. Like biotin, which is also present in tissues in very small amounts, lipoic acid is bound in covalent amide linkage to lysine side chains in active sites of enzymes 2963... 

For this group of aminomutases PLP is required as a second coenzyme. Third, X is attached via a carbon atom the enzymes are called mutases. Methyl-malonyl-Co mutase is required for catabolism of propionate in the human body, and is one of only two known vitamin B12-... 

When present in excess methionine is toxic and must be removed. Transamination to the corresponding 2-oxoacid (Fig. 24-16, step c) occurs in both animals and plants. Oxidative decarboxylation of this oxoacid initiates a major catabolic pathway,305 which probably involves (3 oxidation of the resulting acyl-CoA. In bacteria another catabolic reaction of methionine is y-elimination of methanethiol and deamination to 2-oxobutyrate (reaction d, Fig. 24-16 Fig. 14-7).306 Conversion to homocysteine, via the transmethylation pathway, is also a major catabolic route which is especially important because of the toxicity of excess homocysteine. A hereditary deficiency of cystathionine (3-synthase is associated with greatly elevated homocysteine concentrations in blood and urine and often disastrous early cardiovascular disease.299,307 309b About 5-7% of the general population has an increased level of homocysteine and is also at increased risk of artery disease. An adequate intake of vitamin B6 and especially of folic acid, which is needed for recycling of homocysteine to methionine, is helpful. However, if methionine is in excess it must be removed via the previously discussed transsulfuration pathway (Fig. 24-16, steps h and z ).310 The products are cysteine and 2-oxobutyrate. The latter can be oxidatively decarboxylated to propionyl-CoA and further metabolized, or it can be converted into leucine (Fig. 24-17) and cysteine may be converted to glutathione.2993... 

The evaluation of folic acid status must often also include evaluation of vilamin B1 because of its effect on folate metabolism. A vilamin Bu-dependenl reaction is necessary for an cit/vmc involved in the catabolism of branchcd-chain amino acids (mclhylmalonyl CoA to succinyl CoA). This reaction may provide the basis for a functional assessment method for vitamin Biz status. See also Hormones and Vitamin. 

Biochemically, PLP is the coenzyme form of vitamin B6. As such it participates in many enzymatic reactions involved in amino acid biosynthesis and catabolism. Specific examples include ... 

The effects of vitamin D metabolites on bone itself are somewhat unclear. Some metabolites seem to promote bone resorption and others seem to favor bone formation.10 The overall influence of vitamin D, however, is to enhance bone formation by increasing the supply of the two primary minerals needed for bone formation (calcium and phosphate). Vitamin D also directly suppresses the synthesis and release of PTH from the parathyroid glands, an effect that tends to promote bone mineralization by limiting the catabolic effects of PTH.46,92... 

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