|Publication Type||Journal Article|
|Year of Publication||2021|
Vitamin E is a lipid-soluble antioxidant. Specifically, vitamin E acts as an antioxidant by intercepting peroxyl radicals, which are formed instantaneously when a lipid radical reacts with oxygen. During lipid peroxidation, vitamin E reacts with the peroxyl radical before it can attack the PUFA but generates a tocopheroxyl radical that must be reduced by other antioxidants, such as ascorbic acid (1).
Plants synthesize 8 different lipid-soluble molecules with “vitamin E antioxidant” activity. These are α-, β-, γ-, δ-tocopherols and α-, β-, γ-, δ-tocotrienols, which differ in the number of methyl groups on the chromanol head and whether the tail is a phytyl tail or an unsaturated tail. Plants synthesize a specific stereochemical form, RRR, where the 3 chiral carbons are in the R-conformation at positions 2, 4′, and 8′. Chemically synthesized all-racemic (all rac)-α-tocopherol has an approximately equal mixture of 8 different stereoisomers (RRR, RSR, RRS, RSS, SRR, SSR, SRS, SSS). The α-tocopherol 2 position, the junction of the ring and phytyl tail, is critical for in vivo vitamin E biologic activity. Specifically, only 2R-α-tocopherol forms meet human vitamin E requirements.
Vitamin E biologic activity is different from its antioxidant activity. The biological preference for 2R-α-tocopherol is mediated by the α-tocopherol transfer protein (α-TTP) (2). Hepatic α-TTP facilitates the selective incorporation of 2R-α-tocopherol into circulating lipoproteins that distribute the vitamin to nonhepatic tissues. Additionally, other vitamin E (non-α-tocopherol natural) forms and 2S-α-tocopherol are preferentially catabolized and excreted.
|Alternate Journal||Adv Nutr|