Abstract
ALTHOUGH vitamin C is critical to human physiology1–5, it is not clear how it is taken up into cells. The kinetics of cell and tissue accumulation of ascorbic acid in vitro indicate that the process is mediated by specific transporters at the cell membrane6. Some experimental observations have linked the transport of ascorbic acid with hexose transport systems in mammalian cells, although no clear information is available regarding the specific role(s) of these transporters, if any, in this process7–16. Here we use the Xenopus laevis oocyte expression system to show that the mammalian facilitative hexose transporters are efficient transporters of the oxidized form of vitamin C (dehydroascorbic acid). Two transport pathways, one with low affinity and one with high affinity for dehydroascorbic acid, were found in oocytes expressing the mammalian transporters, and these oocytes accumulated vitamin C against a concentration gradient when supplied with dehydroascorbic acid. We obtained similar results in experiments using normal human neutrophils. These observations indicate that mammalian facilitative hexose transporters are a physiologically significant pathway for the uptake and accumulation of vitamin C by cells, and suggest a mechanism for the accumulation of ascorbic acid against a concentration gradient.
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References
Crandon, J. H. & Lund, C. C. New Engl. J. Med. 223, 353–369 (1940).
Hodges, R. E. Baker, E. M., Hood, J. H., Sauberlich, H. E. & Baker, E. M. Am. J. clin. Nutr. 22, 535–548 (1969).
Hodges, R. E., Baker, E. M., Hod, J. H., Sauberlich, H. E. & Baker, E. M. Am. J. clin. Nutr. 24, 432–443 (1971).
Englard, S. & Steifter, S. A. Rev. Nutr. 6, 365–406 (1986).
Padh, H. Biochem. Cell Biol. 68, 1166–1173 (1990).
Rose, R. C. Biochim. biophys. Acta 947, 335–366 (1988).
Siliprandi, L., Vanni, P., Kessler, M. & Semenza, G. Biochim. biophys. Acta 552, 129–142 (1979).
Toggenburger, G. et al. Biochim. biophys. Acta 646, 433–443 (1981).
Bigley, R., Wirth, M., Layman, D., Riddle, M. & Stankova, L. Diabetes 32, 545–548 (1983).
Bianchi, J., Wilson, F. A. & Rose, R. C. Am. J. Physiol. 250, G461–G468 (1986).
Ingermann, R. L., Stankova, L. & Bigley, R. H. Am. J. Physiol. 250, C637–C641 (1986).
Rose, R. C. Am. J. Physiol. 250, F627–F632 (1986).
Padh, H. & Aleo, J. J. Biochim. biophys. Acta 901, 283–290 (1987).
McLennan, S. et al. Diabetes 37, 359–361 (1988).
Wilson, J. X. & Dixon, J. S. J. Membr. Biol. 111, 83–91 (1989).
Waskho, P. & Levine, M. J. biol. Chem. 267, 23568–23574 (1992).
Winkler, B. S. Biochim. biophys. Acta 925, 258–264 (1987).
Wunderling, M., Paul, H.-H. & Lohmann, W. Biol. Chem. Hoppe-Seyler 367, 1047–1054 (1986)
Birnbaum, M., Haspel, H. & Rosen, O. Proc. natn. Acad. Sci. U.S.A. 83, 5784–5788 (1986).
Vera, J. C. & Rosen, O. Molec. cell. Biol. 9, 4187–4195 (1989).
Vera, J. C. & Rosen, O. Molec. cell. Biol. 10, 743–751 (1990).
Oka, Y. et al. Nature 345, 550–553 (1990).
Jung, C. Y. & Rampal, A. L. J. biol. Chem. 252, 5456–5463 (1977).
Wheeler, T. J. & Hinkle, P. C. A. Rev. Biochem. 47, 503–517 (1985).
Thorens, B., Sarkar, H., Kaback, H. & Lodish, H. Cell 55, 281–290 (1988).
Washko, P., Rotrosen, D. & Levine, M. J. biol. Chem. 264, 18996–19002 (1989).
Dhariwal, K. R., Hartzell, W. O. & Levine, M. Am. J. clin. Nutr. 54, 712–716 (1991).
Moser, U. & Weber, F. Int. J. Vit. Nutr. Res. 54, 47–53 (1984).
Bergsten, P. et al. J. biol. Chem. 265, 2584–2587 (1990).
Bigley, R. H. & Stankova, L. J. exp. Med. 139, 1084–1092 (1974).
Raghoebar, M., Huisman, J. A. M., van den Berg, W. B. & van Ginnekan, C. A. M. Life Sci. 40, 499–510 (1987).
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Vera, J., Rivas, C., Fischbarg, J. et al. Mammalian facilitative hexose transporters mediate the transport of dehydroascorbic acid. Nature 364, 79–82 (1993). https://doi.org/10.1038/364079a0
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DOI: https://doi.org/10.1038/364079a0
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