Vitamin target tissue

Basically, the intravenous application of micronutrients can also be classified as nutritargeting. Specifically, when target tissues like the endothelium of the vessels must be supplied with a higher dose of vitamin E to ensure good protection during surgery with ischemia/reperfusion injury, the parenteral route is superior over the "controlled" oral route (Bartels et al, 2004). 

Vitamin D. The term vitamin D refers to a group of seco-steroids that possess a common conjugated triene system of double bonds. Vitamin I), (10a) and vitamin D, (10b) are the best-known examples (Fig. 2). Vitamin D (10a) is found primarily in vertebrates, whereas vitamin 11 (10b) is found primarily in plants. The term vitamin is a misnomer. Vitamin I) is a prohormonc that is converted into physiologically active form, primarily 1.25-dihydroxy vitamin D3 (11), by successive hydroxylalions in the liver and kidney. This active form is part of a hormonal system that regulates calcium and phosphate metabolism in the target tissues. 

In higher plants, carotenoids are produced in green leaves. In animals, conversion of carotenoids to vitamin A occurs in the intestinal wall. Storage is in the liver also kidney in rat and cat. Target tissues are retina, skin, bone, liver, adrenals, germinal epithelium. Commercial Vitamin A supplements are obtained chemically by extraction of fish liver or synthetically from citral or /3-ionone. 

Factors which tend to decrease bioavailability of pyridoxine include (1) Administration of isoniazid (2) loss in cooking (estimated at 30-45%)—vitamin is water-soluble, (3) diuresis and gastrointestinal diseases (4) irradiation. Availability can be increased by stimulating intestinal bacterial production (very small amount), and storage in liver. The target tissues of Be are nervous tissue, liver, lymph nodes, and muscle tissue. Storage is by muscle phosphorylase (skeletal muscle—small amount). It is estimated that 57% of the vitamin ingested per day is excreted. The vitamin exerts only limited toxicity for humans. 

Although vitamin Bn is essentially considered nontoxic, polycythemia has been reported from excessive dosages. From 30 to 60% of the vitamin is stored in the liver the remainder is found in the kidneys, lungs, and spleen. Target tissues are the central nervous system, kidneys, myocardium, muscle, skin, and bone. 

In the biosynthesis of vitamin D substances, precursors include cholesterol (skin + ultraviolet radiation) in animals ergosterol (algae, yeast + ultraviolet radiation), Intermediates in the biosynthesis include preergocaldferol, tachysterol, and 7-dehydrocholesterol. Provitamins in very small quantities are generated in the leaves, seeds, and shoots of plants. In animals, the production site is the skin. Target tissues in animals are bone, intestine, kidney, and liver. Storage sites in animals are liver and skin. 

Type IE vitamin D-dependent rickets is caused by a target tissue defect in response to l,25(OH)2D. Studies have shown a number of point mutations in the gene for the l,25(OH)2D receptor, which disrupt the functions of this receptor and lead to this syndrome. The serum levels of l,25(OH)2D are very high in type II but not in type I. Treatment with large doses of calcitriol has been claimed to be effective in restoring normocalcemia. Such patients are totally refractory to vitamin D. One recent report indicates a reversal of resistance to calcitriol when 24,25(OH)2D was given. These diseases are rare. 

For nearly 30 years following the discovery of vitamin D3, relatively little was known about its metabolic fate in man. It was thought that vitamin D3 acted directly on the target tissues of intestine and bone. However, the time lag reported by Carlsson (97) between the... 

Vitamin D, along with parathyroid hormone and calcitonin, plays a primary role in calcium and phosphorus homeostasis in the body. Intensive research efforts over the past several years have elucidated a role for vitamin D in many other physiological processes as well. The biological actions of this seco-steroid are mediated primarily through the action of its polar metabolite, 1,25-dihydroxy vitamin D3 (l,25(OH)2D3). There is emerging evidence that l,25(OH)2D3 has many more target tissues than those involved in its classical role in the control of mineral metabolism. In addition, some of the actions of l,25(OH)2D3 may be mediated by mechanisms other than the classical steroid-receptor interaction. In this chapter we will provide a brief overview of the multiple actions of vitamin D3 and the pleiotropic mechanisms by which these actions are accomplished. 

In the past few years, due to a number of technological improvements, l,25(OH)2D3 receptors were able to be identified in a very wide range of tissues and cell lines, extending by far the classical limits of the vitamin D actions upon calcium metabolism (see Ref. 2, page 507). In many of these non-classical target tissues, the reason for the presence of l,25(OH)2D3 receptors is still under active research. We will describe here the possible action of l,25(OH)2D3 in some of those new target tissues in an effort to display the complexity of the vitamin D endocrine system. 

In the intestinal mucosal cells, /3-carotene is cleaved via an oxygenase (an enzyme that introduces molecular 02 into organic compounds) to frans-retinal (aldehyde form of trans-retinol, as shown in Table 6.2), which in turn is reduced to frans-retinol, vitamin Av Retinol is then esterified with a fatty acid, becomes incorporated into chylomicrons, and eventually enters the liver, where it is stored in the ester form until it is required elsewhere in the organism. The ester is then hydrolyzed, and vitamin Ax is transported to its target tissue bound to retinol-binding protein (RBP). Since RBP has a molecular weight of only 20,000 and would be easily cleared by the kidneys, it is associated in the bloodstream with another plasma protein, prealbumin. 

Retinol is released from the liver bound to an a-globulin, retinol binding protein (RBP) this serves to maintain the vitamin in aqueous solution, protects it against oxidation, and also delivers the vitamin to target tissues. RBP binds 1 mol of retinol per mol of protein. 

Type II vitamin D-resistant rickets (Section 3.4.2) is associated with target tissue resistance to calcitriol. Most cases are from either a lack of calcitriol receptors or impaired binding of calcitriol to the receptor. Thus, higher than normal concentrations of calcitriol are required to saturate the receptor. Some affected families show normal binding of calcitriol to the receptor, with an apparent defect in the DNA binding domain (Griffin and Zerwekh, 1983). 

Type 11 vitamin D-resistant rickets is characterized by a lack of responsiveness of target tissues to calcitriol and is caused by a genetic defect in the calcitriol receptor. Affected children develop more or less normally until about 9 months of age, then develop severe rickets with alopecia and a wide variety of disorders, including immune system dysfunction. Three variants are known ... 

A variety of studies have shown that 10% to 20% of the population of developed countries have marginal or inadequate stams, as assessed by erythrocyte transaminase activation coefficient (Section 9.5.36) or plasma pyridoxal phosphate (Section 9.5.1 Bender, 1989b). This may be sufficient to enhance the responsiveness of target tissues to steroid hormones (Section 9.3.3), and may be important in the induction and subsequent development of hormone-dependent cancer of the breast and prostate. Vitamin Be supplementation may be a useful adjunct to other therapy in these common cancers certainly, there is evidence that poor vitamin Be nutritional stams is associated with a poor prognosis in women with breast cancer. 

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