The observation that high concentrations of vitamin C are found in phagocytic cells has underpinned the concept that ascorbic acid is an important nutrient for optimal immune function. However, although the role of vitamin C as a key component of antioxidant defense is well established, most studies have shown only minor effects on a range of immune functions, except in cases where the vitamin may be acting by interacting with GSH metabolism. Unlike deficiencies in vitamins B6, E, and riboflavin, deficiency of vitamin C does not cause atrophy of lymphoid tissue. In a study of ultra marathon runners, dietary supplementation with 600mg/day of ascorbic acid reduced the incidence of upper respiratory tract infections after a race by 50% (62). It is interesting to note that strenuous exercise has been shown to deplete tissue glutathione content. The interrelationship between gluta-thione and ascorbic acid may therefore play a role in the effect of exercise on immune function.
When immunological parameters and anti-oxidant status were measured in adult males fed 250 mg/day of vitamin C for 4 days followed by 5 mg/day for 32 days, plasma ascorbic acid and glutathione decreased and impairment of antioxidant status became evident from a doubling in semen 8-hydroxydeoxyguanosine concentration (a measure of oxidative damage to nucleic acids) during the second dietary period (63). A fall in vitamin content in peripheral blood mononuclear cells was noted and the delayed type hypersensitivity reaction to seven recall antigens was significantly reduced in intensity. These results again highlight that the strength of inflammation and immune function is interrelated in an inverse manner.
A further potential facet of the effect of ascorbic acid on immune function, other than by modulating anti-oxidant defenses, was shown in an in vitro study that examined the effects of physiological concentrations of the vitamin on binding of AP1 to its receptor in macrophages. The vitamin enhanced binding. The effect was shown to be independent of the oxidation state of iron, which is important in binding of AP1 to its receptor (64).
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