It has been proposed that cancer originates from a rare coincidence where the cell acquires simultaneously deregulated proliferation and suppressed apoptosis (1). The importance of GSH in the pathology of cancer has long been recognized, as well as its central place in the control of vital cell processes of great diversity including cell proliferation (2). Bcl-2, the antiapoptotic protein, promotes the compartimentation of the GSH in the nucleus and thus contributes to the resistance to apoptosis (3). Considering the growing evidence that shows the importance of GSH compartimentation, and its role in numerous processes that occur in the nucleus, we have studied the changes in the GSH distribution throughout the cell cycle in MCF7- (Bcl-2 wild type +/-), and its Bcl-2 over expressing analogue, MCF7+ (Bcl2+/+) in order to see the possible relation between Bcl-2, GSH level, telomerase activity (TA) and cell proliferation. We studied the cell cycle by flow cytometry, total GSH (GSHt) level by spectrophotometry, telomerase activity by TRAP assay and its distribution by confocal microscopy. Triple staining was applied: propidium iodide (PI) to identify dead cells, Hoechst to localize nucleus and CellTracker green 5-chloromethylfluorescein diacetate (CMFDA), which marks GSH (specificity 95%). Our results show that the peak of GSHt in MCF7+ is at 6h (304.9 ±1 8.5 nmol/mg prot, p<0.001 vs 12h) and precedes the peak of TA at 12h (2220 ± 754), while in MCF7- both GSHt (256.8 ± 61.1 nmol/mg prot, p<0.05 vs 24h) and TA (1448 ± 522) have their maximum at 18h after plating. MCF7+ cells show significantly higher level of GSHt and TA. By confocal microscopy we observed a growing tendency of GSH compartimentation in the nucleus of both cell types starting from 24h of culture which coincides with the plateau of high cell proliferation rate and is maintained until 72h after plating. We demonstrate that the level of GSH and TA in MCF7 cells could be, at least in part, Bcl-2 dependent. However, there was no significant difference in GSH distribution or in cell cycle dynamic and proliferation rate between MCF7+ and MCF7- cells.