ASCORBATE FUNCTION AND METABOLISM IN THE HUMAN ERYTHROCYTE

James M. May

Departments of Medicine and Molecular Physiology and Biophysics, 736 Medical Research Building II, Vanderbilt University School of Medicine, Nashville, TN 37232-6303 USA

Received 11/5/97 Accepted 11/9/97

4. ERYTHROCYTE UPTAKE OF ASCORBATE AND DHA

Uptake of ascorbic acid by erythrocytes is very slow, with a half-time of hours, and occurs by simple diffusion (11-14). In contrast, most nucleated cells possess a sodium- and energy-dependent transporter with a high affinity for ascorbate that maintains low millimolar intracellular concentrations of the vitamin (2). Since erythrocytes lack an active transporter for ascorbate, they have intracellular concentrations of the vitamin that are similar to those in plasma, ranging from 20-60 micromolar in humans not taking ascorbate supplements (15, 16).

DHA is taken up by erythrocytes and other cells by facilitated diffusion on the glucose transporter. This was originally shown in human erythrocytes (2, 17), and has been elegantly demonstrated in Xenopus laevis oocytes. Xenopus oocytes naturally lack appreciable transport of glucose, ascorbate, and DHA. By expressing glucose transporters in oocytes, Vera, et al. (18) showed that DHA, but not ascorbate, enters cells via facilitated diffusion on the "GLUT" transporter type. Once it has entered erythrocytes or other cells, DHA is rapidly converted to ascorbate and trapped within the cells (figure 2) (13, 14, 17, 19). Uptake by facilitated diffusion of DHA, followed by reduction to ascorbate does generate at least a transient ascorbate gradient across the erythrocyte cell membrane (20), and probably accounts for plasma DHA concentrations of < 2 micromolar (15, 21, 22).

Figure 2. Erythrocyte recycling of DHA to ascorbate. HMP = hexose monophosphate pathway.