Vitamin tissue distribution

Shearer MJ, Bach A, and Kohlmeier M (1996) Chemistry, nutritional sources, tissue distribution and metabolism of vitamin K with special reference to bone health./owrufl/ of Nutrition 126, 1181S-6S. 

Gugger, E. T., Bierer, T. L., Henze, T. M., White, W. S., and Erdman, J.W. (1992). /3-carotene uptake and tissue distribution in ferrets (Mustela putorius fitro). J. Nutr. 122,115-119. Heinonen, O. P., Albanes, D., and the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study Group (1994). The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. N. Engl J. Med. 339,1029-1035. 

Repletion of retinol-deficient rats can also be effectively achieved by the intravenous injection of retinol dispersed in a 20% Tween 40 solution (Smith et al., 1980 Fig. 4). Such an injection produces a rapid, dose-related increase in the serum concentration of RBP. The changes in serum RBP levels seen after the injection of retinol in a 20% Tween 40 solution closely resembled those previously seen after the injection of vitamin A (retinyl esters) in association with lymph chylomicrons. However, the amount of retinol required to stimulate the secretion of a given amount of RBP from the liver was about two to three times that required when retinol (retinyl esters) was injected in chylomicrons. As discussed by Smith et al. (1980), this quantitative difference is probably due to differences in the tissue distribution pattern of retinol when injected in the Tween 40 solution, compared to its administration in the form of chylomicrons. 

Clinical studies investigated the antioxidative effects of antioxidant supplementation of humans on ex vivo LDL oxidation [48-52], We have shown that dietary supplementation of p-carotene of healthy subjects resulted in a moderate inhibitory effect on the susceptibility of LDL to oxidative modification [53-55] in some, but not in all studied subjects. The combination of carotenoids with vitamin E, in contrast, demonstrated a synergistic inhibitory effect on LDL oxidation in all studied cases [56], We showed that supplementation of vitamin E of atherosclerotic apolipoprotein E-deficient mice (25 pg/mouse/day for 3 months) inhibited LDL oxidation by 40% and the atherosclerotic lesion area by 35% [57], In humans, unlike in animal models, both vitamin E and carotenoids did not significantly reduce atherosclerosis in primary prevention trials [58], This result may be related to insufficient absorption, insufficient potency, and inappropriate tissue distribution,... 

RJ Stephens, DS Negi, SM Short, FJGM Van Kuijk, EA Dratz, DW Thomas. Vitamin E distribution in ocular tissues following long-term dietary depletion and supplementation as determined by microdissection and gas chromatography-mass spectrometry. Exp Eye Res 47 237-245, 1988. 

JC LinneU, AV Hoffbrand, HA-A Hussein, U Wise, DM Matthews. Tissue distribution of coenzyme and other forms of vitamin B,2 in control subjects and patients with pernicious anemia. Chn Sci Mol Med 46 163-172, 1974. 

Tocotrienols also appear to have properties that are distinct from those of a-tocopherol. In a very interesting paper, Ikeda et al (2000) examined the tissue distribution of tocotrienols and tocopherols after feeding nude mice (BALB/c Slc-nu) and hairless mice (SKHl) a diet containing a tocotrienol-rich vitamin E extract from palm oil. a-Tocopherol was found in the skin, liver, kidney and... 

Goodman DS, Huang HS, Shiratori T (1965) Tissue distribution and metabolism of newly absorbed vitamin A in the rat. J Lipid Res 6 390-396... 

Navab M, Smith JE, Goodman DS (1977) Rat plasma prealbumin. Metabolic studies on effects of vitamin A status and on tissue distribution. J Biol Chem 252 5107-5114 64 Natarajan V, Holven KB, Reppe S, Blomhoff R, Moskaug JO (1996) The C-terminal RNLL sequence of the plasma retinol-binding protein is not responsible for its intracellular retention. Biochem Biophys Res Commun 221 374-379... 

There is a decrease in the plasma concentration of vitamin Bg with increasing age, and some studies have shown a high prevalence of abnormal transaminase activation coefficient in elderly subjects, suggesting that the elderly may be at risk of vitamin Bg deficiency. It is not known whether this reflects an inadequate intake, a greater requirement, or changes in the tissue distribution and metabolism of the vitamin with increasing age. 

The term vitamin E describes a family of eight antioxidants, four tocopherols, alpha (a), beta ((3), gamma (y) and delta (8), and four tocotrienols (also a, (3, y, and 8). a-Tocopherol is present in nature in only one form, RRR a-tocopherol. The chemical synthesis of a-tocopherol results in eight different forms (SRR, SSR, SRS, SSS, RSR, RRS, RSS, RRR), only one of which is RRR a-tocopherol. These forms differ in that they can be right (R) or left (S) at three different places in the a-tocopherol molecule. RRR a-tocopherol is the only form of vitamin E that is actively maintained in the human body and is therefore the form of vitamin E found in the largest quantities in the blood and tissue. A protein synthesized in the liver (a-TTP alpha-tocopherol transfer protein) preferentially selects the natural form of vitamin E (RRR a-tocopherol) for distribution to the tissues. However, the mechanisms for the regulation of vitamin E in tissues are not known... 

Both intact carotenoids and their apolar metabolites (retinyl esters) are secreted into the lymphatic system associated with CMs. In the blood circulation, CM particles undergo lipolysis, catalyzed by a lipoprotein lipase, resulting in the formation of CM remnants that are quickly taken up by the liver. In the liver, the remnant-associated carotenoid can be either (1) metabolized into vitamin A and other metabolites, (2) stored, (3) secreted with the bile, or (4) repackaged and released with VLDL particles. In the bloodstream, VLDLs are transformed to LDLs, and then HDLs by delipidation and the carotenoids associated with the lipoprotein particles are finally distributed to extrahepatic tissues (Figure 3.2.2). Time-course studies focusing on carotenoid appearances in different lipoprotein fractions after ingestion showed that CM carotenoid levels peak early (4 to 8 hr) whereas LDL and HDL carotenoid levels reach peaks later (16 to 24 hr). 

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