Table 1.

Properties of Different Tocopherols

α‐Tocopherol	Decreases lipid peroxidation, monocyte proatherogenicity, and platelet aggregation.33, 34
	Modulates inflammatory response by inhibiting 5‐lipoxygenase, which in turn decreases monocyte IL‐1β release.33, 34
	Decreases monocyte adhesion to ECs in vitro, possibly by inhibiting NF‐κB activation.34
	Inhibits PKC‐mediated monocyte superoxide production, SMC proliferation, and platelet aggregation and adhesion.35, 36
γ‐Tocopherol	Has most of the effects of α‐tocopherol and is more potent.58, 69, 71
	Has additional effect of removing peroxynitrite‐derived RNS.27
	Acts in vivo as a trap for membrane‐soluble electrophilic NOs and other electrophilic mutagens.31
	Has an unique unsubstituted C‐5 position to trap electrophiles, which are enhanced during inflammation. As a result, γ‐tocopherol is superior to α‐tocopherol in detoxifying NO2 and peroxynitrite via formation of 5‐nitro‐γ‐tocopherol.31
	Inhibits SMC proliferation.34
	Decreases platelet aggregation and delays intra‐arterial thrombus formation.58, 62
β‐Tocopherol	Has anti‐inflammatory and antioxidant action, but less is known about it.
δ‐Tocopherol	Has potent anti‐inflammatory and antioxidant action. Inhibits COX‐1, COX‐2, and 5‐lipoxygenase. Inhibits SMC proliferation.

Abbreviations: COX, cyclooxygenase; EC, endothelial cell; IL‐1β, interleukin‐1β; NF‐κB, nuclear factor κB; NO, nitrogen oxide; NO₂, nitroso compounds; PKC, protein kinase C; RNS, reactive nitrogen species; SMC, smooth muscle cell.