Endometriosis is a complex gynaecological disease characterized by ectopic endometrial tissue outside of the uterus. Several factors have been reported to promote endometriotic cell proliferation. We have shown previously that oxidants and the lipid peroxidation product acrolein can significantly induce endometriotic cell proliferation, and this proliferation is aggravated by estradiol. To date, the precise molecular mechanism by which estrogens act on endometriotic cell proliferation remains obscure. The aims of this study are i) to investigate factors that affect the expression of aromatase (CYP19) and steroid hormone receptors (estradiol and progesterone) and ii) to determine the expression of aromatase (CYP19) in human samples of normal endometrium and from ovarian endometriosis. Immortalized human endometriotic epithelial cells (12-z) (obtained with consent from patients undergoing surgery) were treated with estradiol (10-8 M) alone for 24 hours or in combination with the oxidants H2O2 (1 µM) or menadione (20 µM), or the lipid peroxidation product acrolein (20 µM) for 48 hours. The expression of aromatase in 12-z cells was determined by Western blotting and aromatase activity was determined using an estrone ELISA. The expression and activity of aromatase was found to be significantly higher in 12-z cells treated with oxidants, lipid peroxidation products and estradiol as compared to untreated control. In addition, the expression of aromatase in ovarian endometriosis was significantly higher than in normal endometrium. This suggests that this enzyme may contribute to cell proliferation as aromatase is a key enzyme of local estradiol production. The expression and localization of estradiol-α (ER-α), estradiol- β (ER-β) and progesterone (PR) receptors were determined by Quantitative Reverse Transcriptase-Polymerase Chain Reaction (Q-RT-PCR) and Western blotting. A significant upregulation of ER-α expression was observed in cells treated with oxidants, lipid peroxidation products and estradiol, particularly with the combination of oxidants/acrolein and estradiol. No increase in ER-β and PR expression was observed, indicating that they are not involved in the response to oxidants and estradiol. In summary, changes in gene expression by oxidants and estradiol mimics the physiological situation in endometriosis and provides potential areas for therapeutic intervention.