Tissue concentrations, of vitamin

Tissue concentrations of vitamins or trace elements are rarely measured in nutritional assessments because of the lack of availability of suitable tissue however, where such tissue is available, measurement may be helpful (e.g., copper analysis on liver biopsy of patients with suspected Whson s disease). 

The studies on the tissue concentrations of vitamin A in humans and animals have been limited mainly to determinations of the vitamin A content of the liver. In many vertebrates this organ contains over 90 % of the body storage of the vitamin. After a colorimetric procedure was developed for vitamin A analysis, numerous publications on the liver vitamin A content appeared over the period from 1929 to 1942. It should be pointed out t hat most of the observations on the liver vitamin A values were conducted t>ef()ro the modern chromatographic and photoelectric techniques had luH-oine available and that in rec ent years studies on the liver content of vitamin A have been discontinued to a great extent (Moore, 19r>7). In spite of the fa(it that most of the investigations on the liver vitamin A concentrations were performed with the use of rather primitive analytical methods, the information provided by these earlier studies is nevertheless useful and permits certain conclusions with regard to the correlation between age and liver vitamin A levels. 

The significance of the reviewed data is somewhat limited by the fact that several of the available and approved procedures for analysis of the tissue concentrations of vitamins and hormones are not of the highest standard. Although observations made on human tissue samples are of particular importance, it should be pointed out that in the vitamin studies, the measurements on autopsy material are usually made without the opportunity for dietary evaluation. 

The delay in the acquisition of systematic data on the tissue concentrations of vitamins in relation to age is probably to a great extent due to the lack of suitable procedures for the analysis of several of these compounds. When proper techniques for vitamin determinations have been developed, it would be desirable to obtain such information from analyses of both human and animal tissues. 

Hidiroglou, N., Laflamme, L.F. and McDowell, L.R. (1988) Blood plasma and tissue concentrations of vitamin E in beef cattle as influenced by supplementation of various tocopherol compounds. J. Anim. Sci. 66, 3227-3234. 

Recently, we carried out immunohistochemical studies using an antibody directed against oLDL to demonstrate the presence of foam cells and fatty streaks around blood vessels within the sub-intimal lining of rheumatoid synovial tissue [125]. We have also found that the concentration of vitamin E is markedly diminished in synovial fluid from inflamed joints when compared to matched plasma samples, even after correcting for total lipid concentrations [126],... 

Unlike the other fat-soluble vitamins, there is litde or no storage of vitamin D in the liver, except in oily fish. In human liver, concentrations of vitamin D do not exceed about 25 nmol per kg. Significant amounts may be present in adipose tissue, but this is not really storage of the vitamin, because it is released into the circulation as adipose tissue is catabolized, rather than in response to demand for the vitamin. The main storage of the vitamin seems to be as plasma calcidiol, which has a half-life of the order of 3 weeks (Holick, 1990). In temperate climates, there is a considerable seasonal variation, with plasma concentrations at the end of winter as low as half those seen at the end of summer (see Table 3.2). The major route of vitamin D excretion is in the bile, with less than 5% as a variety of water-soluble conjugates in urine. Calcitroic acid (see Figure 3.3) is the major product of calcitriol metabolism but, in addition, there are a number of other hydroxylated and oxidized metabolites. 

Because vitamin E is transported in lipoproteins secreted hy the liver, the plasma concentration depends to a great extent on total plasma lipids. Erythrocytes may also he important in transport, because there is a relatively large amount of the vitamin in erythrocyte membranes, and this is in rapid equilibrium with plasma vitamin E. There are two mechanisms for tissue uptake of the vitamin. Lipoprotein lipase releases the vitamin by hydrolyzing the tri-acylglycerol in chylomicrons and VLDL, whereas separately there is receptor-mediated uptake of LDL-bound vitamin E. Studies in knockout mice suggest that the main mechanism for tissue uptake of vitamin E from plasma lipoproteins is byway of the class B scavenger receptor (Mardones et al., 2002). 

Control over tissue concentrations of riboflavin coenzymes seems to be largely by control of the activity of flavokinase, and the synthesis and catabolism of flavin-dependent enzymes. Almost all the vitamin in tissues is enzyme bound, and free riboflavin phosphate and FAD are rapidly hydrolyzed to riboflavin. If this is not rephosphorylated, it rapidly diffuses out of tissues and is excreted. 

Hyperthyroidism is not associated with elevated tissue concentrations of flavin coenzymes, despite increased activity of flavokinase. Again, this demonstrates the importance of the enzyme binding of flavin coenzymes and the rapid hydrolysis of unbound FAD and riboflavin phosphate in the regulation of tissue concentrations of the vitamin. 

In species for which ascorbate is not a vitamin, riboflavin deficiency can also lead to considerably reduced synthesis and low tissue concentrations of ascorbate, since gulonolactone oxidase, the key enzyme in ascorbate synthesis (Section 13.2), is a flavoprotein. 

Because flavin coenzymes are widely distributed in intermediary metabolism, the consequences of deficiency maybe widespread. Because riboflavin coenzymes are involved in the metabohsm of folic acid, pyridoxine, vitamin K, and niacin, deficiency will affect enzyme systems other than those requiring flavin coenzymes. With increasing riboflavin deficiency, tissue concentrations of FMN and FAD fall, as does flavokinase activity, thus further decreasing FMN concentrations. FMN concentrations are decreased proportionally more than FAD concentrations. Decreases in the activities of enzymes requiring FMN generally follow the fall in tissue concentrations, whereas the FAD-dependent enzymes are more variably affected. ... 

Absorption of vitamin C from the small intestine is a carrier-mediated process that requires sodium at the luminal surface. Transport is most rapid in the ileum and resembles the sodium-dependent transport of sugars and amino acids, but the carrier is distinct for each class of compound. Some ascorbate may also enter by simple diffusion. With dietary intake less than 100 mg/d, efficiency of absorption is 80-90%. With intake equal to the RDA, plasma ascorbate is 0.7-1.2 mg/dL, and the ascorbate pool size is 1500 mg. Scurvy becomes evident when the pool is less than 300 mg, at which point plasma ascorbate is 0.13-0.24 mg/dL. Highest tissue concentrations of ascorbate are in the adrenal gland (cortex > medulla). 

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