title: In situ estrogen metabolism in proliferative endometria from untreated women with polycystic ovarian syndrome with and without endometrial hyperplasia.
abstract: The aim of the present investigation was to study whether the endocrinological status of women bearing polycystic ovarian syndrome (PCOS) affects the endometrial in situ steroid metabolism. For this purpose, we evaluated the mRNA levels (RT-PCR), and the activity of steroid metabolic enzymes: P450 aromatase, steroid sulfatase (STS), estrogen sulfotransferase (EST) and 17beta-hydroxysteroid dehydrogenase (17beta-HSD) in 23 samples of normal endometria (CE), 18 PCOS endometria without treatment (PCOSE), 10 specimens from PCOS women with endometrial hyperplasia (HPCOSE), and 7 endometria from patients with endometrial hyperplasia not associated to PCOS (EH). The data showed lower levels of STS mRNA for PCOSE and HPCOSE (p<0.05, p<0.01, respectively) and of EST for HPCOSE and EH compared to control (p<0.05). However, higher levels for EST mRNA were obtained in PCOSE (p<0.05) versus CE. The mRNA and protein levels for P450 aromatase were undetectable in all analyzed endometria. The relationship between the activities of STS and EST was lower in PCOSE and HPCOSE (p<0.05) versus CE. The ratio between the mRNA from 17beta-HSD type 1/type 2 was higher in PCOSE (p<0.05), whereas, a diminution in the 17beta-HSD type 2 activity was observed in PCOSE (p<0.05). These results indicate that the activity of enzymes related to the steroid metabolism in analyzed PCOSE differ from those found in the CE. Consequently, PCOSE may present an in situ deregulation of the steroid metabolism.
authors.affiliation: Institute of Maternal and Child Research, School of Medicine, University of Chile, Chile; Department of Obstetrics and Gynecology, School of Medicine, University of Chile, Clinical Hospital, Santos Dumont # 999, Santiago, Chile.
authors.forename: K
authors.initials: K
authors.lastname: Bacallao
authors.forename: L
authors.initials: L
authors.lastname: Leon
authors.forename: F
authors.initials: F
authors.lastname: Gabler
authors.forename: E
authors.initials: E
authors.lastname: Soto
authors.forename: C
authors.initials: C
authors.lastname: Romero
authors.forename: L
authors.initials: L
authors.lastname: Valladares
authors.forename: M
authors.initials: M
authors.lastname: Vega
mesh_terms: D015067:17-Hydroxysteroid Dehydrogenases / Q000235:genetics / Q000378:metabolism; D000328:Adult; D001141:Aromatase / Q000235:genetics / Q000378:metabolism; D004714:Endometrial Hyperplasia / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D004717:Endometrium / Q000378:metabolism / Q000473:pathology*; D004967:Estrogens / Q000378:metabolism*; D005260:Female; D006801:Humans; D008875:Middle Aged; D011085:Polycystic Ovary Syndrome / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D043266:Steryl-Sulfatase / Q000235:genetics / Q000378:metabolism; D015238:Sulfotransferases / Q000235:genetics / Q000378:metabolism
chemical_list: D004967:Estrogens; D015067:17-Hydroxysteroid Dehydrogenases; C044256:3 (or 17)-beta-hydroxysteroid dehydrogenase; D001141:Aromatase; D015238:Sulfotransferases; C020122:estrone sulfotransferase; D043266:Steryl-Sulfatase