TitleVitamin E, antioxidant and nothing more.
Publication TypeJournal Article
Year of Publication2007
AuthorsTraber MG, Atkinson J
JournalFree Radic Biol Med
Date Published2007 Jul 01
KeywordsAntioxidants, Apoptosis, Cell Proliferation, Cytokines, Humans, Oxidative Stress, Oxygenases, Protein Kinase C, Vitamin E, Vitamin E Deficiency

All of the naturally occurring vitamin E forms, as well as those of synthetic all-rac-alpha-tocopherol, have relatively similar antioxidant properties, so why does the body prefer alpha-tocopherol as its unique form of vitamin E? We propose the hypothesis that all of the observations concerning the in vivo mechanism of action of alpha-tocopherol result from its role as a potent lipid-soluble antioxidant. The purpose of this review then is to describe the evidence for alpha-tocopherol's in vivo function and to make the claim that alpha-tocopherol's major vitamin function, if not only function, is that of a peroxyl radical scavenger. The importance of this function is to maintain the integrity of long-chain polyunsaturated fatty acids in the membranes of cells and thus maintain their bioactivity. That is to say that these bioactive lipids are important signaling molecules and that changes in their amounts, or in their loss due to oxidation, are the key cellular events that are responded to by cells. The various signaling pathways that have been described by others to be under alpha-tocopherol regulation appear rather to be dependent on the oxidative stress of the cell or tissue under question. Moreover, it seems unlikely that these pathways are specifically under the control of alpha-tocopherol given that various antioxidants other than alpha-tocopherol and various oxidative stressors can manipulate their responses. Thus, virtually all of the variation and scope of vitamin E's biological activity can be seen and understood in the light of protection of polyunsaturated fatty acids and the membrane qualities (fluidity, phase separation, and lipid domains) that polyunsaturated fatty acids bring about.

Alternate JournalFree Radic. Biol. Med.
PubMed ID17561088
PubMed Central IDPMC2040110
Grant ListR01 ES012249 / ES / NIEHS NIH HHS / United States
R01 DK067930 / DK / NIDDK NIH HHS / United States
R01 DK059576-05 / DK / NIDDK NIH HHS / United States
R01 DK067930-01A1 / DK / NIDDK NIH HHS / United States
ES012249 / ES / NIEHS NIH HHS / United States
R01 DK067930-01A1S1 / DK / NIDDK NIH HHS / United States
DK 067930 / DK / NIDDK NIH HHS / United States
R01 DK059576 / DK / NIDDK NIH HHS / United States