Vitamin C is am important in vivo antioxidant that is involved in protecting cellular components from damage by free radicals, in particular hydrogen peroxide and the superoxide radical. Vitamin C is a relatively large polar compound and so its absorption is dependent on the presence of specific transporters that aid its transport into cells. The transporters that aid this process belong to either the glucose family of transporters (GLUT) or the sodium vitamin C cotransporter family (SVCT). The GLUT transporters mediate the facilitated diffusions of vitamin C and the SVCT transporters mediate the active transport of vitamin C. Prior to absorption by GLUT, vitamin C is oxidised to dehydroascorbate (DHA). The DHA is then subsequently reduced back to ascorbate by glutathione in the cell. In contrast, transport by SVCT is coupled to the transport of sodium and vitamin C is in the reduced form (ascorbate).
Dietary vitamin C is absorbed by the epithelial cells of the small intestine via the sodium vitamin C cotransporter-1 (SVCT1). Vitamin C then diffuses across the basolateral membrane into the circulation. The bioavailability of ascorbate is determined by the rate of absorption and the subsequent rate of excretion from the kidneys. Renal excretion is determine by the amount of vitamin C filtered through the bowman’s capsule of the kidneys, minus the vitamin C that is reabsorbed from the SVCT1 transporters in the proximal tubules. Low intakes of vitamin C tend to cause efficient absorption in SVCT1 transporters in both the kidneys and the intestine. Higher intakes of vitamin C saturate the SVCT1 transporter which causes the maximum serum levels of vitamin C to be reached at around 200 µmol/L, if taken orally. High concentrations of vitamin C also down regulate expression of the SVCT1 transporter, further controlling serum levels.
Serum levels of vitamin C are limited to around 200 µmol/L, and the normal plasma range of healthy humans eating a mixed diet is 60 to 100 µmol/L. However, intracellular levels can be much higher because some cells express the SVCT2 tansporter that allows intracellular concentration of vitamin C. At low intakes of around 20mg absorption of vitamin C may be as high as 98%, but as intakes increase absorption is greatly reduced such that at 12g intake the absorption is only around 16%. Most of the daily intake of vitamin C (120 mg) is absorbed, but that which is not is generally metabolised by the gut bacteria. However, it should be noted that total absorption at 12g is still higher than that at 20mg. Pectin may inhibit vitamin C absorption, but the mechanism of action is unknown. High concentrations of iron in the gastrointestinal tract oxidises vitamin C to produce compounds with no ascorbate activity (e.g. diketogluconic acid)
Because vitamin C shares the same transporters as glucose (the GLUT family), vitamin C is competitively inhibited from transport by glucose. Higher levels of glucose in the blood, as might occur with diabetes has been shown to lead to a reduction in the circulating levels of vitamin C. It is known that obesity reduces circulating levels of vitamin C and this might be because of increased levels of inflammation causing free radical generation. However, it might be because glucose levels limit the absorption of vitamin C under hyperglycaemic conditions, that may accompany obesity. Evidence suggests that vitamin C transport is not as efficient in the elderly when compared to younger individuals. However, this age associated decline can be compensated for with increased dietary intake and supplements. Because vitamin C is water soluble and quickly metabolised or excreted, it is important to ensure a high daily intake.
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