γ-Tocopherol, the new vitamin E?

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Abstract
Several lines of evidence support a role for oxidative stress and inflammation in atherogenesis. Epidemiologic studies suggest that low levels of antioxidants are associated with an increased risk of cardiovascular disease and that increased intakes appear to be protective. In supplementation studies in humans, α-tocopherol, the major form of vitamin E, decreased lipid peroxidation (LDL oxidation and F2-isoprostanes), monocyte proatherogenicity, and platelet aggregation and adhesion and was antiinflammatory (1). α-Tocopherol can modulate the inflammatory response by inhibiting 5-lipoxygenase, which in turn decreases monocyte interleukin 1β release. By decreasing adhesion molecule expression on monocytes and endothelial cells, α-tocopherol also decreases monocyte–endothelial cell adhesion in vitro, possibly by α-tocopherol–mediated inhibition of nuclear factor κB activation (2). α-Tocopherol inhibits signaling pathways through protein kinase C (PKC)-mediated mechanisms in model systems such as monocyte superoxide production, smooth muscle cell proliferation (3), and platelet aggregation and adhesion (4). Another key function regulated by α-tocopherol is vascular homeostasis. Normal vascular function requires responsiveness to nitric oxide (NO). α-Tocopherol mediates NO production, and α-tocopherol supplementation in hypercholesterolemic men and smokers preserves endothelium-dependent vasorelaxation (5).

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