ABSTRACT
Various forms of the fat soluble vitamin, vitamin E, have been shown to be effective in inhibiting certain types of chemically-induced and retrovirus-induced tumor growth in vivo. One possible mechanism that has been proposed for these anti-tumor effects by vitamin E is a direct effect on tumor cell growth. Vitamin E's best characterized function is as a lipid-soluble antioxidant in cell membranes, functioning as a free radical scavenger to prevent lipid peroxidation of polyunsaturated fatty acids. The effects of vitamin E on the rapidly proliferating cells of the established chicken lymphoid cell line, C4#1, transformed by the highly oncogenic replication defective retrovirus, reticuloendotheliosis virus (REV-T) carrying the v-rel oncogene, and its replication competent associated helper virus (REV-A) were examined. Vitamin E's best characterized function is as a lipid-soluble antioxidant in cell membranes, functioning as a free radical scavenger to prevent lipid peroxidation of polyunsaturated fatty acids.
