Polycystic Ovary Syndrome (PCOS) is an endocrine-metabolic pathology related with infertility and recurrent miscarriage. We have previously shown that the endometrium of these patients can exhibit a potentially higher sensitivity to estrogen action, being estrogens important regulators of the cell cycle and tissue homeostasis. The effect of estrogens on tissues depends on their in situ availability, which is in part regulated by the activity of steroid metabolic enzymes within the tissues. Therefore, the objective of the present study was to analyze if the activity and/or expression of steroid metabolic enzymes in endometria from women with PCOS differ from controls. For this purpose, the activity of the enzymes was determined by using radiometric assays and the mRNA levels measured by semi-quantitative RT-PCR. Both assays were assessed in endometria obtained during mid secretory phase from control (CE, n=12) and PCOS women (PCOSE, n=11). For the statistical analyses, Mann-Whitney and Student's t-tests were used to compare CE and PCOSE, considering a p value <0.05 significantly different. The results showed an increase in the sulfatase activity in PCOS respect to control endometria (200+/-28pmol/mg vs. 115+/-13pmol/mgproth; p<0.05), in agreement with the higher mRNA levels found for the enzyme in PCOSE. In addition, a PCOSE exhibited lower activity of sulfotransferase respect to the control group (50+/-21pmol/mg vs. 124+/-10pmol/mgproth; p<0.05), whereas a higher level of 17beta-hydroxysteroid dehydrogenase type 1mRNA was found in PCOSE compared with the control tissues (p<0.05). The activity of 17beta-hydroxysteroid dehydrogenase type 2 and the mRNA levels of sulfotransferase were similar in both groups; meanwhile, the expression of aromatase was undetectable. These data indicate that the sulfatase pathway could play an important role in the local production of estrogens in PCOSE from secretory phase. This potentially higher bioavailability of estrogens in endometria from PCOS women could influence the deregulation of tissue homeostasis that we have previously reported, and could partially explain the poor reproductive performance observed in this group of patients.