Absorption Transport and Storage

in species for which ascorbate is not a vitamin, intestinal absorption is passive, while in human beings and guinea pigs there is sodium-dependent active transport of the vitamin at the brush border membrane, with a sodium-independent mechanism at the basolateral membrane. Dehydroascorbate is absorbed passively in the intestinal mucosa and is reduced to ascorbate before transport across the basolateral membrane.

At intakes up to about 100mg per day, 80-95% of dietary ascorbate is absorbed, falling from 50% of a 1g dose to 25% of a 6g and 16% of a 12g dose. Unabsorbed ascorbate is a substrate for intestinal bacterial metabolism.

Ascorbate and dehydroascorbate circulate in the bloodstream both in free solution and bound to albumin. About 5% of plasma vitamin C is normally in the form of dehydroascorbate. Ascorbate enters cells by sodium-dependent active transport; dehy-droascorbate is transported by the insulin-dependent glucose transporter and is accumulated intracellu-larly by reduction to ascorbate. In poorly controlled diabetes mellitus, tissue uptake of dehydroascorbate is impaired because of competition by glucose, and there may be functional deficiency of vitamin C despite an apparently adequate intake.

About 70% of blood-borne ascorbate is in plasma and erythrocytes (which do not concentrate the vitamin from plasma). The remainder is in white cells, which have a marked ability to concentrate ascorbate; mononuclear leukocytes achieve 80-fold concentration, platelets 40-fold, and granulocytes 25-fold, compared with the plasma concentration.

There is no specific storage organ for ascorbate; apart from leukocytes (which account for 10% of total blood ascorbate), the only tissues showing a significant concentration of the vitamin are the adrenal and pituitary glands. Although the concentration of ascorbate in muscle is relatively low, skeletal muscle contains much of the body pool of 5-8.5 mmol (900-1500 mg) of ascorbate.

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