Cancer cell proliferation and apoptosis are induced by overload Ca2+ entry. Transient receptor potential vanilloid 1 (TRPV1) as a Ca2+ permeable cation channel is activated by capsaicin and reactive oxygen species (ROS), although it is blocked by capsazepine and sodium selenite (Na-Se). Bisphenol A (BPA) induces estrogenic action and further stimulates the proliferation of estrogen receptor positive MCF-7 cell through excessive production ROS and Ca2+ influx. However, whether or not Na-Se can influence BPA-induced oxidative stress and apoptosis through modulation of TRPV1 in breast cancer cells has not drawn much attention. The MCF-7 and MDA-MB-231 breast cancer cells were divided into four treatment groups as control, Na-Se (1 mu M for 2 h), and BPA (0.1 mM for 24 h) and BPA + Na-Se. The Na-Se reduced BPA-induced increase of cell number, mitochondria oxidative stress, and TRPV1 channel activity modulation of MCF-7 cells, which was proved by the suppression of cell viability, excessive ROS production, mitochondrial membrane depolarization, lipid peroxidation, early apoptosis (Annexin-V), late apoptosis (propidium iodide) and upregulation of reduced glutathione, glutathione peroxidase, and cell death (propidium iodide/Hoechst rate). The similar effects of Na-Se were observed in the MCF-7 cells by capsazepine treatment. However, the effects of BPA were not observed in the MDA-MB-231 breast cancer cells. In conclusion, cell proliferative and oxidant effects of BPA were increased by activation of TRPV1, but its action on the values was decreased by the Na-Se treatment. The results may be a good set of preliminary data for designing animal studies on estrogenic effect of bisphenol A and antiestrogenic of selenium.