title: Vitamin E and genome stability.
abstract: Free radicals and reactive oxygen species (ROS) which are generated continuously cause mutagenic alterations resulting in cancer, aging and abnormalities in the nervous system. Accumulating evidence indicates that Vitamin E, the most potent lipid peroxyl radical scavenger, may reduce free radical induced chromosomal damages through inhibition of free radical formation, and activation of endonuclease that can be triggered by intracellular oxidative stress, and by increasing the rate of removal of damaged DNA. Although some studies suggest a potential usefulness of Vitamin E in the prevention of mutagenic effects caused by genotoxic free radicals, other studies report no effects. Thus the data are not conclusive enough to be used as a basis to change the current recommended dietary allowances (RDA). Future research should address molecular mechanisms underlying the protective effects of Vitamin E and develop appropriate biologically relevant biomarkers of DNA damage to further help in determining the dietary levels of Vitamin E needed to protect the genetic pool from internally and externally induced DNA damages.
authors: Nutritional Immunology Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, 02111, Boston, MA, USA.
authors: K J
authors: KJ
authors: Claycombe
authors: S N
authors: SN
authors: Meydani
mesh_terms: D000818:Animals; D004247:DNA / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D004249:DNA Damage; D019587:Dietary Supplements; D006801:Humans; D018673:Nutrition Policy; D014810:Vitamin E / Q000494:pharmacology*
chemical_list: D014810:Vitamin E; D004247:DNA