4.6 Article

Distribution of steroidogenic enzymes involved in androgen synthesis in polycystic ovaries: an immunohistochemical study

期刊

MOLECULAR HUMAN REPRODUCTION
卷 6, 期 5, 页码 443-447

出版社

OXFORD UNIV PRESS
DOI: 10.1093/molehr/6.5.443

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17 alpha hydroxylase; ovarian stroma; ovarian surgery; polycystic ovary; side chain cleavage enzyme

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To find an explanation for the possible working mechanism of laparoscopic ovarian electrocautery for the treatment of anovulation in polycystic ovarian syndrome (PCOS), we evaluated the distribution of steroidogenic enzymes involved in the synthesis of ovarian androgens in surgical pathology specimens of entire polycystic ovaries. A total of 13 formalin-fixed and paraffin-embedded samples of the ovaries of patients with clinically proven PCOS were immunostained with specific antibodies against cholesterol side-chain-cleavage enzyme (P450scc), 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD), 17 alpha-hydroxylase (P450c17) and adrenal 4-binding protein (Ad4BP), a transcription factor of steroidogenic enzymes. Follicular theca cells of all ovaries demonstrated marked immunoreactivity for Ad4BP, P450scc, 3 beta-HSD and P450c17. Granulosa cells of seven ovaries expressed Ad4BP, while granulosa cells of three ovaries also showed P450scc. In the granulosa cells of ail ovaries, 3 beta-HSD and P450c17 immunoreactivity was not observed. In the stroma, luteinized cells of most ovaries demonstrated Ad4BP, P450scc, 3 beta-HSD and P450c17 immunoreactivity, but at a much lower level compared with the follicular theca cells. Non-luteinized stromal cells sporadically demonstrated Ad4BP, P450scc, 3 beta-HSD and P450c17 immunoreactivity. The stromal steroidogenic cells were mainly located in the ovarian cortex, except for some hilus steroidogenic cells. These data demonstrate that in polycystic ovaries, androgens are mainly produced in the follicular theca cells and to some extent in luteinized stromal cells. This suggests that the working mechanism of laparoscopic electrocautery of the ovary is primarily explained through the reduction of ovarian hyperandrogenism by coagulation of follicular theca cells and concomitant stroma.

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