The elevated level of circulating estradiol increases the risk of breast tumor development. To gain further insight into mechanisms involved in their actions, we investigated the molecular mechanisms of 4-hydroxyestradiol (4-$OHE_2$) to initiate and/or promote abnormal cell growth, and of $alpha$- or $gamma$-tocopherol to inhibit this process. MCF-10A, human breast epithelial cells were incubated with $0.1{mu}M$ 4-$OHE_2$, either with or without $30{mu}M$ tocopherols for 96 h. 4-$OHE_2$ caused the accumulation of intracellular ROS, while cellular GSH/GSSG ratio and MnSOD protein levels were decreased, indicating that there was an oxidative burden. 4-$OHE_2$ treatment also changed the levels of DNA repair proteins, BRCA1 and PARP-1. $gamma$-Tocopherol suppressed the 4-$OHE_2$-induced increases in ROS, GSH/GSSG ratio, and MnSOD protein expression, while $alpha$-tocopherol up-regulated BRCA1 and PARP-1 protein expression. In conclusion, 4-$OHE_2$ increases oxidative stress reducing the level of proteins related to DNA repair. Tocopherols suppressed oxidative stress by scavenging ROS or up-regulating DNA repair elements.