Ascorbate transport

Banhegyi G, Marcolongo P, Pusk F, Fulceri R, Mandl J, Benedetti A. Dehydroascorbate and ascorbate transport in rat liver microsomal vesicles. J. Biol. Chem. 1998 273 2758-2762. [Pg.400]

Foyer CH and Harbinson J (1997) The photosynthetic electron transport system efficiency and control. In Foyer CH, Quick WP (eds), A molecular approach to primary metabolism in higher plants, pp 3-39. Taylor and Francis, London, UK Foyer CH and Lelandais M (1995) Ascorbate transport into protoplasts, chloroplasts and thylakoid membranes of pea leaves. In Mathis P (ed), Photosynthesis From light to Biosphere, Vol V,pp511-514. Kluwer Academic Publishers, Dordrecht... [Pg.322]

Shields, P. P., Gibson, T. R., and Glembotski, C. C., 1986, Ascorbate transport by AtT-20 mouse pituitary corticotropic tumor cells Uptake and secretion studies. Endocrinology 118 1452-1460. [Pg.310]

Becker, B., 1967, Ascorbate transport in guinea pig eyes. Invest. Ophthalmol. 6 410-415. [Pg.326]

Khatami, M., Stramm, L. E., and Rockey, J. H., 1986a, Ascorbate transport in cultured cat retinal pigment epithelial cells, Exp. Eye Res. 43 607-615. [Pg.327]

When ascorbate acts as an antioxidant or enzyme cofactor, it becomes oxidized to DHAA. Ascorbate and DHAA possess roughly equivalent bioavailability. Bioavailability is determined by the rates of absorption, distribution, and metabolism within the body, and by excretion. Ascorbate and DHAA are absorbed along the entire length of the human intestine (Malo and Wilson, 2000). For both the DHAA and ascorbate transport systems, initial rates of uptake saturate with increasing external substrate concentration, reflecting high-affinity interactions that can be described by Michaelis-Menten kinetics. [Pg.260]

Ascorbate transport is mainly controlled by carriers availability, and thus it depends on the number of SVCT proteins present in the plasma membrane (which in turn is related to enhanced synthesis, slowed degradation, activation of nonfunctional carriers or cellular redistribution), as well as their substrate affinity. So, transcriptional, translational, and post-translational modifications of SVCTs allow a fine-tuned regulation of AA uptake (Liang et al., 2002). [Pg.263]

Dixon, S. J. Wilson, J. X. 1992. Adaptive regulation of ascorbate transport in osteoblastic cells. J. Bone Miner. Res. 7 675-681. [Pg.272]

Kuo, S. M. MacLean, M. E. McCormick, K. Wilson, J. X. 2094. Gender and sodium ascorbate transporters determine ascorbate concentrations in mice. J. Nutr. 134 2216-2221. [Pg.274]

The ascorbate transporter SVCTl has been shown to be inhibited by some flavonols such as quercetin but less so by the related catechins. The absence of the ketone at the 4-position of the C ring has a dramatic negative effect on the potency of inhibition, suggesting that a key hydrogen-bonding... [Pg.361]

Ascorbic acid is involved in carnitine biosynthesis. Carnitine (y-amino-P-hydroxybutyric acid, trimethylbetaine) (30) is a component of heart muscle, skeletal tissue, Uver and other tissues. It is involved in the transport of fatty acids into mitochondria, where they are oxidized to provide energy for the ceU and animal. It is synthesized in animals from lysine and methionine by two hydroxylases, both containing ferrous iron and L-ascorbic acid. Ascorbic acid donates electrons to the enzymes involved in the metabohsm of L-tyrosine, cholesterol, and histamine (128). [Pg.21]

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]

Arrhythmogenic Right Ventricular Dysplasia/ Cardiomyopathy Aiteriogenesis Arteriosclerosis Arylhydrocarbon Receptor L-Ascorbic Acid ASF Family of Transporters Asn-linked Glycosylation ASON... [Pg.1487]

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]

Since many essential nutrients (e.g., monosaccharides, amino acids, and vitamins) are water-soluble, they have low oil/water partition coefficients, which would suggest poor absorption from the GIT. However, to ensure adequate uptake of these materials from food, the intestine has developed specialized absorption mechanisms that depend on membrane participation and require the compound to have a specific chemical structure. Since these processes are discussed in Chapter 4, we will not dwell on them here. This carrier transport mechanism is illustrated in Fig. 9C. Absorption by a specialized carrier mechanism (from the rat intestine) has been shown to exist for several agents used in cancer chemotherapy (5-fluorouracil and 5-bromouracil) [37,38], which may be considered false nutrients in that their chemical structures are very similar to essential nutrients for which the intestine has a specialized transport mechanism. It would be instructive to examine some studies concerned with riboflavin and ascorbic acid absorption in humans, as these illustrate how one may treat urine data to explore the mechanism of absorption. If a compound is... [Pg.48]

M Gilmour Buck, JA Zadunaisky. (1975). Stimulation of ion transport by ascorbic acid through inhibition of 3, 5 -cyclic AMP phosphodiesterase in the corneal epithehum and other tissue. Biochim Biophys Acta 376 82-88. [Pg.388]

In the enterocyte as it enters the absorptive zone near to the villus tips, dietary iron is absorbed either directly as Fe(II) after reduction in the gastrointestinal tract by reductants like ascorbate, or after reduction of Fe(III) by the apical membrane ferrireductase Dcytb, via the divalent transporter Nramp2 (DCT1). Alternatively, haem is taken up at the apical surface, perhaps via a receptor, and is degraded by haem oxygenase to release Fe(II) into the same intracellular pool. The setting of IRPs (which are assumed to act as iron biosensors) determines the amount of iron that is retained within the enterocyte as ferritin, and that which is transferred to the circulation. This latter process is presumed to involve IREG 1 (ferroportin) and the GPI-linked hephaestin at the basolateral membrane with incorporation of iron into apotransferrin. (b) A representation of iron absorption in HFE-related haemochromatosis. [Pg.250]

Tsukaguchi, H., et al. A family of mammalian Na+-dependent L-ascorbic acid transporters. Nature 1999, 399, 70-75. [Pg.283]

Wang, Y., et al. Human vitamin C (L-ascorbic acid) transporter SVCT1. Biochem. Biophys. Res. Commun. 2000, 267, 488-494. [Pg.283]

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