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BACKGROUND: Inhibitors of 5 alpha reductase (5 alpha R), the enzyme that converts testosterone to dihydrotestosterone (DHT), have been shown to retard the growth of hyperplastic prostates. This study evaluates the effects of the 5 alpha R inhibitor, epristeride, on cultured stromal and epithelial cells from benign, hyperplastic adult prostates. METHODS: [3H]-thymidine incorporation was used as a measure of proliferation. Prostate-specific antigen (PSA) was quantified by ELISA and reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: Stromal cell proliferation in response to testosterone was dose-dependently inhibited by epristeride (1 x 10(-9) -3 x 10(-7) M, P < 0.05). However, epristeride had no effect on DHT-induced growth or the growth of androgen-unresponsive stroma. Upregulation of PSA secretion from epithelial cells by androgens was downregulated by epristeride (3 x 10(-9) M, P < 0.05) in testosterone-treated cells. Transforming growth factor beta-1 (TGF beta-1) secretion was downregulated by testosterone treatment and increased following treatment with epristeride (3 x 10(-9) M, P < 0.05). CONCLUSIONS: This demonstrates that epristeride specifically blocks testosterone-induced effects on prostatic cultures. TGF beta-1 may be a marker of 5 alpha reductase activity.


Journal article



Publication Date





259 - 265


5-alpha Reductase Inhibitors, Adult, Androstadienes, Cell Division, Cells, Cultured, Dihydrotestosterone, Enzyme Inhibitors, Enzyme-Linked Immunosorbent Assay, Epithelium, Humans, Immunohistochemistry, Male, Polymerase Chain Reaction, Prostate, Prostate-Specific Antigen, Prostatectomy, Prostatic Hyperplasia, RNA, Messenger, Testosterone, Thymidine, Transcription, Genetic, Transforming Growth Factor beta