Vitamin blood clotting

Blood access devices, 3 719-720 Blood alcohol tests, 12 96 Blood clots, 4 82-83 Blood clotting, vitamin K in, 25 795 Blood coagulation, 4 84-90... 

The fat-soluble vitamins are lipids that are involved in such varied functions as vision, growth, and differentiation (vitamin A), blood clotting (vitamin K), prevention of oxidative damage to cells (vitamin E), and calcium metabolism (vitamin D). 

Vitamin K This vitamin is necessary for the synthesis of four proteins involved in blood clotting, vitamins Those organic compounds essential in the diet in small amounts but with tittle or no caloric value, volatile Tending to vaporize easily, volume The volume of an object is a measure of the amormt of space it occupies. Voliune has units such as m or cm. ... 

Biochemical Reactions. The quinones in biological systems play varied and important roles (21,22). In insects they are used for defense purposes, and the vitamin K family members, eg, vitamin [11104-38-4] (32) and vitamin [11032-49-8] (33), which are based on 2-meth5l-l,4-naphthoquiaone, are blood-clotting agents (see Vitamins, vitamin k). 

FIGURE 18.40 The glutamyl carboxylase reaction is vitamin K-dependent. This enzyme activity is essential for the formation of 7-car-boxyglutamyl residues in several proteins of the blood-clotting cascade (Figure 15.5), accounting for the vitamin K dependence of coagulation. 

An example of a biological Friedel-Crafts reaction occurs during the biosynthesis of phylloquinone, or vitamin Kl( the human blood-clotting factor. Phylloquinone is formed by reaction of 1,4-dihydroxynaphthoic acid with phytyl diphosphate. Phytyl diphosphate first dissociates to a resonance-stabilized allylic carbocation, which then substitutes onto the aromatic ring in the typical way. Several further transformations lead to phylloquinone (Figure 16.10). 

Vitamin K A cofactor for the carboxylase of the hepatic endoplasmic reticulum, which is responsible for completing the synthesis of blood-clotting proteins. 

VITAMIN K IS REQUIRED FOR SYNTHESIS OF BLOOD-CLOTTING PROTEINS... 

Prothrombin and several other proteins of the blood clotting system (Factors VII, IX and X, and proteins C and S) each contain between four and six y-carboxygluta-mate residues which chelate calcium ions and so permit the binding of the blood clotting proteins to membranes. In vitamin K deficiency or in the presence of warfarin, an abnormal precursor of prothrombin (preprothrombin) containing little or no y-carboxyglutamate, and incapable of chelating calcium, is released into the circulation. 

A number of iron-containing, ascorbate-requiring hydroxylases share a common reaction mechanism in which hydroxylation of the substrate is linked to decarboxylation of a-ketoglutarate (Figure 28-11). Many of these enzymes are involved in the modification of precursor proteins. Proline and lysine hydroxylases are required for the postsynthetic modification of procollagen to collagen, and prohne hydroxylase is also required in formation of osteocalcin and the Clq component of complement. Aspartate P-hydroxylase is required for the postsynthetic modification of the precursor of protein C, the vitamin K-dependent protease which hydrolyzes activated factor V in the blood clotting cascade. TrimethyUysine and y-butyrobetaine hydroxylases are required for the synthesis of carnitine. 

Compounds showing vitamin K activity are substituted naphthoquinones. The parent compound, 2-methyl-1,4-naphthoquinone, does show some biological activity as do other similar but synthetic compounds. The production of the complete naturally active forms is thought to depend upon the addition of an isoprene chain at position 3 on the aromatic ring. Differences in this side chain produce the various K vitamins (Figure 12.10). A most important physiological role of vitamin K is in the synthesis of the blood clotting factors, II (prothrombin), VII, IX and X. 

The last of the fat-soluble vitamins to be identified was vitamin K, found by Dam to be an anti-hemorrhagic factor for young chicks, distinct from vitamin C. Its structure was determined by Dam in collaboration with Karrer. Interest in the vitamin was intensified when it was discovered (Link, 1941) that dicoumarol, present in spoiled sweet clover, was the agent producing hypothrombinemia (giving prolonged blood-clotting time) in cattle. Since vitamin K is structurally similar to dicoumarol, the vitamin was presumptively implicated in thrombin formation. This has been fully substantiated by recent work on the role of vitamin K in the synthesis of prothrombin in the liver. 

Vitamin K Green leafy vegetables, meats, dairy produce Activation of blood-clotting factors... 

Animals fed spoiled sweet clover were prone to fatal haemorrhages. The canse was traced to the presence of dicoumarol. This compound interferes with the effects of vitamin K in blood coagulation, the blood loses its ability to clot, and minor injnries can lead to severe internal bleeding. Synthetic dicoumarol has been nsed as an oral blood anticoagnlant in the treatment of thrombosis, where the risk of blood clots becomes life threatening. It has since been snperseded by warfarin, a synthetic development based on the natnral prodnct. 

The absorption of vitamins K2, which are found mainly in cheese, curd cheese, and natto, is much higher and may be almost complete. Thus the nutritional importance of menaquinones is often underestimated. The vitamin K activity is related to the activation of specific proteins involved in blood clotting and bone metabolism. Clinical vitamin deficiency due to dietary inadequacy is rare or nonexistent in healthy adults, thanks to the widespread distribution of the vitamin K in foodstuffs and the microbiological flora of the gut, which synthesizes menaquinones. Only infants up to 6 months are at risk of bleeding due to a vitamin K deficiency. No data on negative effects of an overdose of vitamin K are found [417]. 

Deficiency of vitamin K, which Is fat-soluble, is rare and produces only mild symptoms such as a delay in blood clotting (prolongedprothrombin time) In adults. 

In the absence of the vitamin, the blood-clotting time increases, since the post-translational carboxylation of several glutamate residues in prothrombin and other factors involved in blood clotting is impaired. In humans, this disorder is unknown except in cases of faulty vitamin K absorption, since the normal diet covers the need generously. 

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