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Monocytes, vitamin

As opposed to an initial human blood monocytic vitamin E content of 4.75 pmol/10 cells, macro-phagic vitamin E levels were undetectable (Visioli et al. 2000). [Pg.263]

Factor VII. This is a vitamin K-dependent serine protease that functions in the extrinsic coagulation pathway and catalyzes the activation of Factors IX and X. Factor VII is present constitutively in the surface membrane of pericytes and fibroblasts in the adventitia of blood vessels, vascular endothehum, and monocytes. It is a single-chain glycoprotein of approximately 50,000 daltons. [Pg.174]

Increases in plasma S-AA levels have previously been reported in patients with coronary disease (57). S-AA and plasma intracellular adhesion molecule-1 were elevated in patients with CAD and hyperhomocysteinemia, but only S-AA decreased after vitamin supplementation (35). Homocysteine activates nuclear factor- in endothelial cells, possibly via oxidative stress (58), and increases monocyte chemoattractant protein-1 expression in vascular smooth muscle cells (59). Additionally, it stimulates interleukin-8 expression in human endothelial cultures (60). These inflammatory factors are known to participate in the development of atherosclerosis. Taken together, these reports suggest an association of elevated tHcy and low-grade inflammation in CAD. [Pg.179]

Deficiency of vitamin B6 (pyridoxine) causes gradual disappearance of the lymphatic system, depressed number of B lymphocytes in peripheral blood, and impaired activity of antibodies and IL-2 (Szponar and Respondek 1998) (Table 2.2.4). Vitamin D3 can produce an immunosupressive effect. The recent literature data suggest that one of metabolites of this vitamin, 1,2,5-dihydroxy D3, by affecting a specific receptor present on monocytes and lymphocytes, can inhibit their proliferation. This effect occurs via retardation of the production of mRNA for GM CSF, IL-2, and IFN-7. At the same time, it has been demonstrated that deficiency of vitamin D3 in food caused impaired cellular-type tolerance (Szponar and Respondek 1998). [Pg.61]

The site of TC II synthesis has been the subject of much study and it has been shown that de novo synthesis occurs in the liver (E3,S7,T1), blood monocytes (R2,R3), and ileal enterocytes (C6,R4). Like intrinsic factor, TC II contains a single vitamin B12 binding site per molecule. However, unlike intrinsic factor, TC II will bind analogs of the vitamin (H6). A number of genetically determined variants of TC II have been described and were recognized by their altered electrophoretic mobility (D2,F3) and these are discussed in Section 8.1. [Pg.170]

The nuclear vitamin D receptor was originally studied in intestinal mucosa, hut has subsequently been found in a variety of other tissues that have therefore been shown to be vitamin D-responsive, including kidneys, bone, parathyroid gland, -islet cells of the pancreas, pituitary, placenta, uterus, mammary glands, skin, thymus, monocytes, macrophages, and activated T lymphocytes. Like other steroid hormone receptors, it is a zinc finger protein it has the same high affinity (of the order of 10 " M) for both calcitriol and ercalcitriol. [Pg.91]

Koschmieder S, Agrawal S, Radomska HS, Huettner CS, Tenen DG, Ottmann OG, Berdel WE, Serve HE, Muller-Tidow C. Decitabine and vitamin D3 differentially affect hematopoietic transcription factors to induce monocytic differentiation. Int. Oneok 2007 30 349-355. [Pg.1153]

Martin, A., Foxall, T., Blumberg, J. B., and Meydani, M. (1997) Vitamin E inhibits low-density lipoprotein-induced adhesion of monocytes to human aortic endothelial cells in vitro. Arterioscler Thromb Vase Biol 17,429-36. [Pg.118]

Wu, D., Koga, T., Martin, K. R., and Meydani, M. (1999) Effect of vitamin E on human aortic endothelial cell production of chemokines and adhesion to monocytes. Atherosclerosis 147,297-307. [Pg.118]

Williams, J. C., Forster, L. A., Tull, S. P., Wong, M., Bevan, R. J., and Ferns, G. A. (1997) Dietary vitamin E supplementation inhibits thrombin-induced platelet aggregation, but not monocyte adhesiveness, in patients with hypercholesterolaemia. Int J Exp Pathol 78,259-66. [Pg.118]

Vitamin K2 (menaquinone) represents a series of compounds in which the phytyl side chain of phytonadione has been replaced by a side chain built up of 1-14 isoprenyl units. It has been reported that vitamin K2 with four isoprenyl units (4) induced the monocytic differentiation of human myeloid leukemia cell lines [58], or apoptosis in isolated osteoclast [59] and human ovary cancer cells [60]. We have recently found that vitamin K2 derivatives (1-3) induced some tumor-specific cytotoxicity and non-apoptotic cell death in oral carcinoma [61]. As an extension of the search for tumor-specific substances targeted against human oral squamous, hepatocellular carcinoma, and promyelocytic leukemia cell lines, we investigated the QSAR of seven vitamin K2 derivatives (1-7) (Fig. 18), by conventional and recent techniques of computation chemistry, such as the concept of absolute hardness [ 16-18]. [Pg.125]

Yano M, Kishida E, Iwasaki M, Shosuke K, Masuzawa Y. Docosahexaenoic acid and vitamin E can reduce human monocytic U937 cell apoptosis induced by tumor necrosis factor. J Nutr 2000 130 1095-1101. [Pg.420]

The current recommended dietary allowance (RDA) for vitamin C (L-ascor-bate) for adult non-smoking individuals is 60 mg day which is based on a mean requirement of 46 mg day to prevent the deficiency disease scurvy [ 14]. It was shown that ascorbate uptake by neutrophils, monocytes, and lymphocytes saturate with a daily supplementation of 100 mg ascorbate and that these cells contain concentrations at least 14-fold higher than those in plasma. Bioavailability was complete for 200 mg of vitamin C as a single dose. [Pg.82]


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See also in sourсe #XX -- [ Pg.121 ]

See also in sourсe #XX -- [ Pg.121 ]

See also in sourсe #XX -- [ Pg.121 ]




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Monocytes

Monocytes monocytic

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