Endometriosis, an estrogen dependent disease, affects at least 10% of women of reproductive age. The classic “retrograde menstruation” theory has been widely accepted as the initiation of the disease. However, to date, the mechanism of endometriotic cell proliferation is still unexplained although oxidative stress has been implicated as contributing to cell growth. Antioxidants have been shown to inhibit endometriotic cell proliferation, however the molecular mechanisms are poorly understood. In the present study, we determined the effects of oxidant (H2O2)and antioxidant (NAC) on endometriotic cell growth using immortalized human endometriotic epithelial cells (12-z). Cells were treated with the H2O2 (0.5-500 µM) or NAC (0.5-30 mM) for 48 hours. Cells viability was determined by MTT [(3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay and lactate dehydrogenase (LDH) assay. The results show that H2O2 induced cell proliferation at 1 µM, however at high concentrations, it caused significant growth inhibition. In contrast, NAC has been shown to cause cytotoxicity especially at concentrations above 10 mM. In treated cells, the percentages of LDH leakage relative to control were significantly higher when cells were exposed to H2O2 (10-500 µM) and NAC (10-30 mM). Cells were also pretreated with NAC at the above concentrations for 24 hours followed by addition of H2O2 at 1 µM or 10 µM for another 48 hours. Interestingly, the MTT assay shows that NAC significantly suppressed the H2O2 induced proliferation despite the increased concentration of H2O2. We also determined the expression of apoptotic markers in 12-z cells treated with NAC (1-30 mM) for 24 hours. Subcellular fractions were analyzed and activated Caspase 3 (whole cell), Bax (mitochondria fraction) and cytochrome C (cytosolic fraction) were determined by Western blotting. The expression of these markers were significantly increased when cells were treated with NAC at 3 mM. The results of this present study indicate that NAC has antiproliferative effect and could have a potential protective effect against oxidative stress induced proliferation. This antioxidant triggers the cells into apoptosis via a mitochondria-mediated mechanism. Therefore, this antioxidant may be considered as a treatment for endometriosis. Further studies are needed to determine the signaling pathway/s that may be involved in the mechanisms underlying the effects of NAC on inhibiting cell proliferation.