Vitamin from liver

Gel permeation ehromatography (GPC)/normal-phase HPLC was used by Brown-Thomas et al. (35) to determine fat-soluble vitamins in standard referenee material (SRM) samples of a fortified eoeonut oil (SRM 1563) and a eod liver oil (SRM 1588). The on-line GPC/normal-phase proeedure eliminated the long and laborious extraetion proeedure of isolating vitamins from the oil matrix. In faet, the GPC step permits the elimination of the lipid materials prior to the HPLC analysis. The HPLC eolumns used for the vitamin determinations were a 10 p.m polystyrene/divinylbenzene gel eolumn and a semipreparative aminoeyano eolumn, with hexane, methylene ehloride and methyl tert-butyl ether being employed as solvent. 

In the enterocyte, provitamin A carotenoids are immediately converted to vitamin A esters. Carotenoids, vitamin A esters, and other lipophilic compounds are packaged into chylomicrons, which are secreted into lymph and then into the bloodstream. Chylomicrons are attacked by endothelial lipoprotein lipases in the bloodstream, leading to chylomicron remnants, which are taken up by the liver (van den Berg and others 2000). Carotenoids are exported from liver to various tissues by lipoproteins. Carotenes (such as (3-carotene and lycopene) are transported by low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL), whereas xanthophylls (such as lutein, zeax-anthin, and (3-cryptoxanthin) are transported by high-density lipoproteins (HDL) and LDL (Furr and Clark 1997). 

Two things hampered efforts to isolate and purify vitamin B12 from liver first, liver contains little of this vitamin and, secondly, the assay for the activity employed the response of pernicious anemia patients. The work required processing factory quantities of liver and it is not surprising that the preparation of pure crystals of vitamin B12 took until 1948 and was accomplished nearly simultaneously in two industrial laboratories, one in the United States and one in England. 

There are several steps in the absorption of vitamin B. In the stomach and lumen of the small intestine it is hydrolysed from its (peptide) links with the proteins of which it is a component. It then attaches to gastric intrinsic factor, which is a glycoprotein of molecular mass about 50 000 kDa, to form a complex. This protects the vitamin from being damaged by acid in the stomach. The complex is carried into the ileum, where it binds to a receptor on the surface of the absorptive cells and is released from the intrinsic factor within the absorptive cell, hi the portal venous blood, it is transported to the liver bound to the vitamin B 12-binding protein, which also protects the vitamin. 

Dietary forms of vitamin B12 are converted to active forms in the body. Vitamin B12, mainly from liver, eggs and dairy products, is absorbed in terminal ileum. Intrinsic factor from parietal cells is required for absorption. Vitamin B12 is transported in the blood by transcobalamin II and stored in the liver. These stores are such that generally a patient does not become symptomatic until some years after the onset of vitamin B12 deficiency. 

Vitamin B12 Vitamin B12 is an important cobalt complex. The vitamin was isolated from liver after it was found that eating large quantities of raw liver was an effective treatment for pernicious anaemia. The term vitamin B12, refers to cyanocobalamin. Vitamin B12 is a coenzyme, and serves as a... 

Osteitis fibrosa does not occur, as in renal osteodystrophy. The common features that appear to be important in this group of diseases are malabsorption of calcium and malabsorption of vitamin D. Liver disease may, in addition, reduce the production of 25(OH)D from vitamin D, although its importance in all but patients with terminal liver failure remains in dispute. The malabsorption of vitamin D is probably not limited to exogenous vitamin D. The liver secretes into bile a substantial number of vitamin D metabolites and conjugates that are reabsorbed in (presumably) the distal jejunum and ileum. Interference with this process could deplete the body of endogenous vitamin D metabolites as well as limit absorption of dietary vitamin D. 

In 1948, red cobalt-containing crystals of vitamin B12 were obtained almost simultaneously by two pharmaceutical firms. Charcoal adsorption from liver extracts was followed by elution with alcohol and numerous other separation steps. Later fermentation broths provided a richer source. Chemical studies revealed that the new vitamin had an enormous molecular weight, that it contained one atom of phosphorus which could be released as P , a molecule of aminopropanol, and a ribofuranoside of dimethyl benzimidazole with the unusual a configuration. 

The leveisal of the oxidative pathway of vitamin A (retinol —r retinal —>-retinoic add) does not occur in the body, When retinoic acid is feci to animals, even in relatively large doses, there is no storage and, in fact, die molecule is rapidly metabolized and cannot be found several hours after administration. The metabolic products have not been fully identified. Several fractions from liver or intestine, isolated after administering retinoic add marked with carbon-14, have been shown to have biological activity. 

Cyanocobalamin (vitamin B12), a cobalt complex first isolated from liver but now produced commercially from microbiological culture, is needed to maintain normal synthesis of red blood cells in man and animals. Ruminants obtain cyanocobalamin from their symbiotic rumen flora while in other herbivores such as the... 

In healthy adults, the percentage of vitamin B12 absorbed from eggs is 24 to 36% from trout, 25 to 47% and from chicken, mutton, and liver, 60, 65, and 9%, respectively. The bioavailability of vitamin B12 from liver is low because its content of vitamin B12 is high. 

If k2 >> k, then reaction (4) is mostly complete before (3) starts. Large doses of vitamin C have been observed to protect rats from liver tumors induced by aminopyrine and sodium nitrite (26). This inhibition is thought to result, in part, from blockage of in vivo nitrosation, which forms dimethylnitrosamine. 

Pyridoxine is rapidly converted to pyridoxal phosphate in the liver and other tissues. Pyridoxal phosphate does not cross cell membranes, and efflux of the vitamin from most tissues is as pyridoxal. Pyridoxal phosphate is exported from the liver bound to albumin by formation of a Schiff base to lysine (Zhang et al., 1999). Much of the free pyridoxal phosphate in the liver (i.e., that which is not protein bound) is hydrolyzed to pyridoxal, which is also exported, and circulates bound to both albumin and hemoglobin in erythrocytes. 

Vitamin is involved in the manufacture of the red corpuscles of the blood. It can be used for the treatment of pernicious anemia, and it is perhaps the most potent substance known in its physiological activity 1 microgram per day (1 X lO g) of vitamin B g is effective in the control of the disease. The vitamin can be isolated from liver... 

In 1933, R. Kuhn and his co-woikers first isolated riboflavin from eggs in a pure, crystaUine state (1), named it ovoflavin, and determined its function as a vitamin (2). At the same time, impure crystalline preparations of riboflavin were isolated from whey and named lyochrome and, later, lactoflavin. Soon thereafter, P. Karrer and his co-workers isolated riboflavin from a wide variety of animal organs and vegetable sources and named it hepatoflavin (3). Ovoflavin from egg, lactoflavin from milk, and hepatoflavin from liver were all subsequently identified as riboflavin. The discovery of the yeUow enzyme by Warburg and Christian in 1932 and their description of lumiflavin (4), a photochemical degradation product of riboflavin, were of great use for the elucidation of the chemical stmcture of riboflavin by Kuhn and his co-workers (5). The stmcture was confirmed in 1935 by the synthesis by Karrer and his co-workers (6), and Kuhn and his co-workers (7). 

Tho data in Table 9.1 are from an cxporlment involving foly] poly glutamate synthase. The enzyme was obtained in purified form from liver and was mixed with glutamic acid, ATP, and the indicated form of foiate. The mixture was incubated to permit the enzyme to catalyze the attachment of glutamafc residues to the folate. What do you think would be the effect of a vitamin Bij deficiency on the rate of polyglutamation of dietary folates, flint Dietary folates occur in the bloodstream initially as 5-melhyl-l UPteGtu, and enter the cell in this form. 

Pantothenic acid has also been called vitamin Bf. Excellent sources of the vitamin ore liver. egg.s. and cereals. It is found, however, in the form of CoA. This coenzyme cannot be absorbed directly from the gut. Although no experiments have been conducted in humans, studies on animals indicate that the coenzyme must be hydrolyzed to panthenene and pantothenate. " which arc absorbed by passive diffusion. Human intestinal cells contain enzymes tltat can hydrolyze the coenzyme. Pantothenate is the major form circulating in the blood and is absorbed by individual cells. Once inside ihe cell. CoA is synthesized. 

Cyanocobalamin, USP. Cyanocobalamin. vitamin B12. is a cobalt-containing substance usually produced by the growth of suitable organLsms or obtained from liver. It ik-curs as dark red ci stals or an amorphous orci slalline powder. The anhydrous form is very hygroscopic and may absorb about 12% water. One gram is soluble in about 80 mL of water. It is soluble in alcohol but insoluble in chloroform and in ether. 

Pernicious anaemia was a fatal disease first reported in 1880. It was not until 1926 that it was discovered that eating raw liver effected a remission. The active principle was later isolated and called vitamin B12 or cyanocobalamin. It was initially obtained from liver but during the 1960s it was noted that it could be obtained as a by-product of microbial metabolism (Table 25.2). Hydroxycobalamin is the form of choice for therapeutic use and can be derived either by chemical transformation of cyanocobalamin or directly as a fermentation product. 

Rich sources of the coenzyme forms of the vitamin are liver, kidney, and heart. Many vegetables are also good sources, but cereals are rather low in flavin content. However, current practices of fortification and enrichment of cereal products have made these significant contributors to the daily requirement. Milk, from cows ° and humans, is a good source of the vitamin, but considerable loss can occur from exposure to light during pasteurization and bottling or as a result of irradiation to increase the vitamin D content. 

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