17β-estradiol stimulates generation of reactive species oxygen and nitric oxide in ovarian adenocarcinoma cells (ovcar 3)

Background: experimental and epidemiological evidence supports a role for steroid hormones in the pathogenesis of ovarian cancer. among steroid hormones, 17β-estradiol (e2) has the most potent effect on proliferation, apoptosis and metastasis. objectives: in the present study, we investigated the effect of e2 on production of ros and no in ovarian cancer cells. materials and methods: ovarian adenocarcinoma cell line (ovcar-3) was cultured and treated with various concentrations of e2, antioxidants (n-acetyle cysteine and ebselen) and ici182780 as an estrogen receptor antagonist. mtt test was performed to evaluate cell viability. no and ros levels were measured by griess and dcfh-da methods, respectively. results: ros levels as well as no levels were increased in ovcar-3 cells treated with e2. the increase in ros production was in parallel with increased cell viability which indicates that estrogen-induced ros can participate in cancer progression. ici182780 abolished e2-induced ros production. progesterone was also effective in reducing ros and no generation. conclusions: no and ros are important molecules in signaling networks in cell. these molecules can be used as therapeutic targets for prevention and treatment of ovary cancer and other estrogen-induced malignancies.