Vitamin E and genome stability

Free radicals and reactive oxygen species (ROS) which are generated continu ously cause mutagenic alterations resulting in cancer, aging and abnormalit ies in the nervous system. Accumulating evidence indicates that Vitamin E, the most potent lipid peroxyl radical scavenger, may reduce free radical in duced chromosomal damages through inhibition of free radical formation, and activation of endonuclease that can be triggered by intracellular oxidativ e stress, and by increasing the rate of removal of damaged DNA. Although so me 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 t o change the current recommended dietary allowances (RDA). Future research should address molecular mechanisms underlying the protective effects of Vi tamin E and develop appropriate biologically relevant biomarkers of DNA dam age to further help in determining the dietary levels of Vitamin E needed t o protect the genetic pool from internally and esternally induced DNA damag es. (C) 2001 Elsevier Science B.V. W lights reserved.