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Plasma ascorbate

Absorption, Transport, and Excretion. The vitamin is absorbed through the mouth, the stomach, and predominantly through the distal portion of the small intestine, and hence, penetrates into the bloodstream. Ascorbic acid is widely distributed to the cells of the body and is mainly present in the white blood cells (leukocytes). The ascorbic acid concentration in these cells is about 150 times its concentration in the plasma (150,151). Dehydroascorbic acid is the main form in the red blood cells (erythrocytes). White blood cells are involved in the destmction of bacteria. [Pg.22]

The adrenal glands and pituitary glands have the highest tissue concentration of ascorbic acid. The brain, Hver, and spleen, however, represent the largest contribution to the body pool. Plasma and leukocyte ascorbic acid levels decrease with increasing age (152). Elderly people require higher ascorbic acid intakes than children to reach the same plasma and tissue concentration (153). [Pg.22]

Frei B, England L, Amos B (1989) Ascorbate is an outstanding anti-oxidant in human blood plasma. Proc Natl Acad Sci USA 86 6377-6381... [Pg.174]

Vitamin C occurs as L-ascorbic acid and dihydroascorbic acid in fruits, vegetables and potatoes, as well as in processed foods to which it has been added as an antioxidant. The only wholly undisputed function of vitamin C is the prevention of scurvy. Although this is the physiological rationale for the currently recommended intake levels, there is growing evidence that vitamin C may provide additional protective effects against other diseases including cancer, and the recommended dietary allowance (RDA) may be increased in the near future. Scurvy develops in adults whose habitual intake of vitamin C falls below 1 mg/d, and under experimental conditions 10 mg/d is sufficient to prevent or alleviate symptoms (Bartley et al., 1953). The RDA is 60 mg per day in the USA, but plasma levels of ascorbate do not achieve saturation until daily intakes reach around 100 mg (Bates et al., 1979). Most of the ascorbate in human diets is derived from natural sources, and consumers who eat five portions, or about 400-500 g, of fruits and vegetables per day could obtain as much as 200 mg of ascorbate. [Pg.28]

Nowadays, consumers would like those antioxidants present in food products not only to stabilise food lipids, but also to be absorbed through the intestinal wall and protect the lipids of blood plasma against oxidation. This effect is relatively evident in the case of tocopherols (which are liposoluble) or ascorbic acid (which is hydrophilic), but much less evidence is available on antioxidants of medium polarity, such as flavonoids, rosemary oleoresins or green or black tea catechins. [Pg.311]

Ascorbate has multiple antioxidant capacities and may be the most important water-soluble defence against free-radical damage in human plasma. At millimolar concentrations, ascorbate scavenges O2, OH and HOCl (Blake et al., 1983). The latter reaction protects plasma lipids against degradation by activated PMNs. [Pg.101]

Wayner, D.D., Burton, G.W., Ingold, K.U., Barclay, L.R.C. and Locke, S.J. (1987). Antioxidants in human blood plasma. The relative contributions of vitamin E, urate, ascorbate and protein to the total radical trapping antioxidant activity. Biochim. Biophys. Acta 925, 408-413. [Pg.142]

Reduced scavenger capacity is deduced from studies demonstrating low plasma and cellular levels of antioxidants such as glutathione, vitamin E, thiols, magnesium and ascorbic acid, as well as reduced levels of scavenger enzymes such as neutrophil glutathione peroxidase and red cell superoxide dismutase (Lyons, 1991 Sinclair /., 1992). [Pg.185]

Essential hypertension, whose prevalence is increased nearly two-fold in the diabetic population, may be another source of free-radical activity. The vascular lesions of hypertension can be produced by free-radical reactions (Selwign, 1983). In the recent Kuopio Ischaemic Heart Risk Factor Study in Finnish men, a marked elevation of blood pressure was associated with low levels of both plasma ascorbate and serum selenium (Salonen etal., 1988). A few studies report a hypotensive effect of supplementary ascorbate in patients with hypertension, but the actual changes in both systolic and diastolic pressure after ascorbate were not statistically significant in comparison with placebo (Trout, 1991). [Pg.193]

Routine antioxidant vitamin supplementation, e.g. with vitamins C and/or E, of the diabetic diet should be considered. Vitamin C depletion is present in all diabetics irrespective of the presence of vascular disease. A recent study demonstrated no significant difference between the dietary intake of vitamin C (the main determinant of plasma ascorbate) in patients with diabetes and age-matched controls, confirming the view that ascorbate depletion is secondary to the diabetic process and su esting that diabetic patients require additional intakes of the vitamin to maintain optimal levels (Sinclair et /., 1994). Antioxidant supplementation may have additive beneficial effects on a wide variety of processes involved in diabetic vascular damage including blood pressure, immune function, inflammatory reactions. [Pg.194]

Sinclair, A.J. Taylor, P.B., Lunec, J., Girling, A.J. and Barnett, A.H. (1994). Low plasma ascorbate levels in patients with type 2 diabetes mellitus consuming adequate dietary vitamin C. Diabet. Med. 11, 893-898. [Pg.197]

HOCl is one of the oxidants that activated phagocytes have in their arsenal. Hu et al. (1993) have shown that plasma albumin sulphydryl and ascorbic acid both protect against oxidant injury from HOCl. Neutrophils, interestingly, contain about 25 times more ascorbic acid than plasma. This su ests an endogenous self-protection role. This work is important because of the biological emphasis of reactive chlorine by the neutrophil. [Pg.273]

P. Askerlund and C. Larsson, Transmembrane electron transport in plasma membrane vesicles loaded with an NADH-generating system or ascorbate. Plant Phy-.i-iol. 96 1178 (1991). [Pg.87]

A typical time course of PCL with luminol as the photosensitizer is shown in Figure 5, as blank. The presence of a water-soluble antioxidant leads to dose-dependent temporary inhibition of PCL. ACW (antioxidant capacity of water-soluble compounds) represents the effect of human blood plasma (2 p.L) on PCL all tested antioxidants, such as ascorbic acid, uric acid, Trolox, taurine, bilirubin, ceruloplasmin, etc., produced the same effects. [Pg.506]

Basic procedure (ACW kit) Mix 1500 pL of ACW reagent 1 (diluter) with 1000 pL of ACW reagent 2 (buffer) and 25 pL of photosensitizer reagent (lumi-nol based). Start measurement after brief vortexing. Assayed solution (or control) is added before addition of photosensitizer reagent. Volume of ACW reagent 1 is reduced by the volume of assayed plasma sample. Standard substance ascorbic acid. Duration of measurement 2-3 min. Measured parameter effective lag phase = lag-phase sample - lag-phase blank. Assayed amount of human blood plasma 2 pL. [Pg.511]

Modified procedure (ASC kit) Ascorbic acid is isolated from plasma proteins and uric acid in a single-step liquid gel chromatography procedure and its amount... [Pg.513]


See other pages where Plasma ascorbate is mentioned: [Pg.22]    [Pg.486]    [Pg.28]    [Pg.296]    [Pg.583]    [Pg.42]    [Pg.42]    [Pg.42]    [Pg.43]    [Pg.115]    [Pg.129]    [Pg.130]    [Pg.130]    [Pg.186]    [Pg.188]    [Pg.218]    [Pg.223]    [Pg.226]    [Pg.226]    [Pg.227]    [Pg.64]    [Pg.392]    [Pg.444]    [Pg.136]    [Pg.152]    [Pg.127]    [Pg.4]    [Pg.22]    [Pg.219]    [Pg.706]    [Pg.709]    [Pg.709]    [Pg.709]   
See also in sourсe #XX -- [ Pg.340 ]




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Ascorbic acid (vitamin plasma concentration

Plasma and Leukocyte Concentrations of Ascorbate

Plasma ascorbic acid

Plasma ascorbic acid levels

Plasma ascorbic acid specific activity

Relationship between Plasma Ascorbate and Blood Histamine

Requirements Estimated from the Plasma and Leukocyte oncentrations of Ascorbate

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