Folic acid plays a crucial role in DNA synthesis suggesting that every aspect involving cell proliferation might be affected by deficiency in the vitamin. Indeed, cell-mediated immunity is especially affected by deficiency in humans and animals (83). Folate deficiency also impairs natural killer cell activity in rats (84).
As the vitamin is also intimately involved in sulfur amino acid metabolism, it might be expected that the vitamin would modulate anti-oxidant status and immune function. However, there is evidence that only the second of these two effects occurs. Indeed, oxidative stress may impair folate metabolism. In a double-blind, placebo-controlled crossover intervention in healthy subjects, it was found that although a folate rich diet and folate supplements caused a fall in plasma homocysteine concentrations, there was no change in anti-oxidant activity (plasma and red blood cell glutathione peroxidase activity and red cell superoxide dismutase activity) or oxidant damage (plasma malonaldehyde) (85). Infection and inflammation are often associated with hyperhomocysteine-mia, an indicator of folate insufficiency (86). It has been hypothesized that the underlying cause of this effect is that the active form of folate (tetrahydrofolate) is susceptible to oxidation during the oxidative stress involved in infection and inflammatory disease (86). Therefore, folate insufficiency is the result rather than the cause of a weakening in anti-oxidant defenses during the immune response.
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