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Mechanisms and Biomarkers (WG 4) page 62
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Vitamin E, though very effective as a chain-breaking antioxidant in cell membranes, becomes
a prooxidant in the absence of adequate concentrations of cytosolic antioxidants such as
ascorbate and glutathione (Stocker, 1999).Vitamin E deficiency is associated with lowered Bcell
antibody production and T-cell proliferation in response to mitogenic stimulation and an
increase in rate of infection. Substantial protection is best demonstrated in supplementation
studies with Vitamin E depleted subjects and in the elderly (Meydani and Heharka, 1996).The
protective mechanism is thought to involve inhibition of 5-lipoxygenase thus decreasing
leukotriene B4 levels, the agonist for IL-1B (Deveraj and Jialal, 1997). Inhibition of NF-kB
activity per se, or by a feedback mechanism via IL-1B may be another immunoprotective
function of Vitamin E in ROS initiated inflammatory processes (Jackson et al, 1998). β-
carotene has been assessed in a large number of in vitro, in vivo studies and clinical trials, and
may be protective against several cancers, CHD, stroke, ageing, sunburn and macular
degeneration (Mayne 1996). Results are conflicting, but on balance, the major
immunoprotectant mechanism appears to be via increases in T-helper lymphocyte (CD4+)
numbers (Allard et al, 1998) and in increased natural killer cell activity. Again as with
Vitamin E the most significant results are observed with elderly subjects.