ESTATIONAL trophoblastic diseases/ GTD is a group of disease arising from placental trophoblastic tissue after both normal and abnormal fertilization. World Health Organization (WHO) classified GTD into hydatidiform mole

Background: The pathomechanisms of gestational trophoblastic disease have not yet been able to be extensively understood. It is associated with oxidative damage related to the production of reactive oxygen species (ROS). Estrogen, as well as all of its metabolites, can produce ROS. Therefore it is necessary to analyze how far the involvement of estrogen, in this case 17β estradiol, to the pathological mechanisms of gestational trophoblastic disease by the measurement of total ROS level. Objective: To determine the role of 17β estradiol on the total production of ROS in hydatidiform mole tissue culture. Methods: The study was carried out experimentally in the Laboratory of Cell/Tissue Culture, Central Laboratory of Biomedics and Laboratory of Physiology, Medical Faculty University of Brawijaya, Malang by using Randomized Control Group Design. One group of hydatidiform mole tissue culture supplemented with various doses of estrogen (17β estradiol) compared to a group without supplementation. Results: There were highly significant differences in ROS levels between treatment groups with 17 beta-estradiol 5 g/ml and 17 betaestradiol 40 g/ml (p = 0.000), between treatment groups of 17 betaestradiol 10 g/ml and 17 beta-estradiol 40 g/ml (p = 0.000) and between treatment groups of 17 beta-estradiol 20 g/ml and treatment groups of 17 beta-estradiol 40 g/ml (p = 0.000). Conclusion: The exposure of 17β estradiol significantly affected the total production of H2O2 in hydatidiform mole cell culture in the dose 20 g/ml and 40 g/ml, while it did not occur significantly in the dose 5 g/ml, 10 g/ml, and control group. Synopsis: The exposure of 17β estradiol significantly affected the total production of H2O2 in hydatidiform mole cell culture in various doses. Keywords—ROS, hydatidiform mole, 17-Beta Estradiol.