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Vitamin in blood

K. Johansen and P. O. Edlund, Determination of water-soluble vitamins in blood and plasma by coupled-column liquid clrromatography , 7. Chromatogr. 506 471-479 (1990). [Pg.295]

Other investigators have found larger amounts of ascorbic acid were necessary to maintain normal concentrations of the vitamin in blood. For monkeys, 10 (63) and 25 (35) mg of ascorbic acid/kg of body weight were proposed as the minimum required amounts. Recent experiments showed that the trained monkey required only 3-6 mg of ascorbate/kg of body weight (120). Young monkeys (sexually imma-... [Pg.328]

Nutrition Concentrations of fat-soluble vitamins in blood have been measured in a cross-sectional study in 54 patients (19 with acromegaly and 35 with carcinoid tumors) treated with somatostatin analogues (44 octreotide and 10 lanreotide) for at least 18 months [69 ]. There was steatorrhea in... [Pg.711]

K Nakamura, H Toyohira, H Kariyazono, M Ishibashi, H Saigenji, S Shimokawa, A Taira. Anticoagulant effects of warfarin and kinetics of K vitamins in blood and feces. Artery 21(3) 148-160, 1994. [Pg.275]

Protein-binding assays Several enzyme protein-binding assays and radio-protein-binding assays have also been developed and commercialized as kits for rapid evaluation of this vitamin in blood, plasma, and different foodstuffs. Despite their rapidity, these methods lack adequate discrimination between different forms of folates. [Pg.415]

Factors controlling calcium homeostasis are calcitonin, parathyroid hormone(PTH), and a vitamin D metabolite. Calcitonin, a polypeptide of 32 amino acid residues, mol wt - SGOO, is synthesized by the thyroid gland. Release is stimulated by small increases in blood Ca " concentration. The sites of action of calcitonin are the bones and kidneys. Calcitonin increases bone calcification, thereby inhibiting resorption. In the kidney, it inhibits Ca " reabsorption and increases Ca " excretion in urine. Calcitonin operates via a cyclic adenosine monophosphate (cAMP) mechanism. [Pg.376]

Three hormones regulate turnover of calcium in the body (22). 1,25-Dihydroxycholecalciferol is a steroid derivative made by the combined action of the skin, Hver, and kidneys, or furnished by dietary factors with vitamin D activity. The apparent action of this compound is to promote the transcription of genes for proteins that faciUtate transport of calcium and phosphate ions through the plasma membrane. Parathormone (PTH) is a polypeptide hormone secreted by the parathyroid gland, in response to a fall in extracellular Ca(Il). It acts on bones and kidneys in concert with 1,25-dihydroxycholecalciferol to stimulate resorption of bone and reabsorption of calcium from the glomerular filtrate. Calcitonin, the third hormone, is a polypeptide secreted by the thyroid gland in response to a rise in blood Ca(Il) concentration. Its production leads to an increase in bone deposition, increased loss of calcium and phosphate in the urine, and inhibition of the synthesis of 1,25-dihydroxycholecalciferol. [Pg.409]

PTH is the most important regulator of bone remodelling and calcium homeostasis. PTH is an 84-amino acid polypeptide and is secreted by the parathyroid glands in response to reductions in blood levels of ionised calcium. The primary physiological effect of PTH is to increase serum calcium. To this aim, PTH acts on the kidney to decrease urine calcium, increase mine phosphate, and increase the conversion of 25-OH-vitamin D to l,25-(OH)2-vitamin D. PTH acts on bone acutely to increase bone resorption and thus release skeletal calcium into the circulation. However, due to the coupling of bone resorption and bone formation, the longer-term effect of increased PTH secretion is to increase both bone resorption and bone formation. [Pg.279]

Transthyretin (TTR) A protein complex found in blood that binds both retinol (vitamin A) and thyroxine. [Pg.334]

Toxic compounds polychlorinated biphenyls, polycyclic aromatic hydrocarbons, organochlorine pesticides, chlorinated pesticides, dioxins, veterinary drug residues, hormone residues, aflatoxins, toxic compounds in shellfish. Compoimds of nutritional significance in foods vitamins, fat, lipids, carbohydrates, protein, energy-calorific value, proximates, dietary fibre, ash. Other compounds hormones in blood serum... [Pg.22]

Kalafatis M., Swords N. A., Rand M. D Mann K. G. Membrane-dependent reactions in blood coagulation Role of Vitamin K-dependent enzyme complexes. Biochim Biophys Acta 1994 1227,113-29. [Pg.164]

In the future, this test may be replaced by the proteins induced by vitamin K antagonists absence (PIVKA) concentrations in serum. PIVKAs are coagulation factor precursors, normally not detectable in blood but released into the... [Pg.11]

Lead was found to decrease tissue levels of vitamin C in a study in rats (Vij et al. 1998). Since vitamin C is required for the synthesis of heme, the authors suggested that some hematological effects of lead (e.g., inhibition of ALAD) may be due at least partially to a lead-induced decrease in bioavailability or increased demand of vitamin C. Supplementation with vitamin C almost completely restored ALAD activity in blood and liver. [Pg.289]

Sobel AE, Yuska H, Peters DD, et al. 1940. The biochemical behavior of lead I. Influence of calcium, phosphorus, and vitamin-D on lead in blood and bone. J Biol Chem 188 239-265. [Pg.577]

Intrinsic factor is produced by the parietal cells. Within the stomach, it combines with vitamin Bu to form a complex necessary for absorption of this vitamin in the ileum of the small intestine. Vitamin B12 is an essential factor in the formation of red blood cells. Individuals unable to produce intrinsic factor cannot absorb vitamin B12 and red blood cell production is impaired. This condition, referred to as Pernicious anemia, occurs as a result of an autoimmune disorder involving destruction of parietal cells. [Pg.293]

Olas and Wachowicz (2002) investigated the effects of tranx-resveratrol and vitamin C on oxidative stress in blood platelets. The level of 02 in control blood platelets and platelets incubated with resveratrol or vitamin C was recorded using a chemiluminescence method. On the other hand, Oh and others (2006) reported the x02 quenching activities of various freshly squeezed fruit and vegetable juices by measuring their inhibitory effects on the rubrene oxidation induced by x02 from disproportionation of hydrogen peroxide by sodium molybdate in a microemulsion system. [Pg.282]

Olas B and Wachowicz B. 2002. Resveratrol and vitamin C as antioxidants in blood platelets. Thromb Res 106(2) 143-148. [Pg.301]

A large number of reports on the biological activity of antioxidants in blood plasma and cell membranes verify that vitamin E (VE) is the most significant... [Pg.510]

Figure 10 presents the results of assay of VE and ACL in blood plasma of rabbits treated with probucol and two other synthetic antioxidants (S-l, S-2) for 4 weeks. In addition to an improvement in antioxidative blood plasma protection, in the case of compound S-2 a statistically significant (p < 0.01) decrease in vitamin E content was detected, a finding considered physiologically unfavorable. [Pg.512]

An example of the prognostic meaning of vitamin C measurements is given in Figure 13 [33], In this study on neurosurgical patients drastic reduction of the vitamin C concentration in blood during the operation was associated with postoperative brain edema. [Pg.515]

Pantothenate in blood and tissues is bound (R9) and released by autolysis or hydrolysis. More vitamin could be released by use of an alkaline phosphatase and an enzyme from avian liver (L6). This method liberates pantothenate from coenzyme A in a variety of foods and tissues (N3, N4). A comparison of hydrolytic methods in blood suggested autolysis to be the most advantageous method (N3) in our hands, treatment with Clarase gave more reliable results as compared with autolysis, acid hydrolysis, treatment with Mylase P, or combination of Clarase and papain, or liver enzyme and alkaline phosphatase. In urine, pantothenic acid is unbound our results show no increase with Clarase treatment. The vitamin has presumably a low threshold. Pantothenic acid shows the same concentration in blood and cerebrospinal fluid. [Pg.199]

We have developed a direct assay for vitamin Be in blood, serum, urine, cerebrospinal fluid, and tissue, based on the ciliate, Tetrahymena pyriformvs. The techniques are essentially those described for nicotinic acid (see Section 4.1), except that vitamin Be is omitted from the basal medium both nicotinic acid and its amide are added each at 0.1 mg/100 ml of basal medium. The method for blood, serum, urine, cerebrospinal fluid, and tissues is given below. [Pg.214]

Fig. 5. Vitamin Ba-levels in blood upon intramuscular injection of 100 mg pyridoxine-HCl. Fig. 5. Vitamin Ba-levels in blood upon intramuscular injection of 100 mg pyridoxine-HCl.
The ability of the liver to act as a depot for vitamin Bi2 (B28, G13) enables us to use this vitamin as an index of proper hepatic function. Hepatic disorders lead to an increased Bi2-binding in the serum (J5, R3), suggesting that the blood assumes a greater role in the conservation of B12. We have reported that patients with liver disease excreted invariably less than 10 fig of Bi2> 8 hours after a 50-[ig intramuscular load dose of the vitamin. In contrast, normal subjects excreted 24-40 pg, i.e., 50-80% of the vitamin in the same test (B14). These results were correlated with various chemical determinations indicative of hepatic disorders (Bl). In Table 16 the clinical diagnosis and the various liver-... [Pg.233]


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See also in sourсe #XX -- [ Pg.576 ]




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