| Disease | WE COMPARE TESTOSTERONE (T) METABOLISM IN PRIMARY CULTUARES OF EPITHELLAL CELLS AND FIBROBLASTS SEPARATED FROM BENIGN PROSTATE HYPERTROPHY (BPH) AND PROSTATE CANCER TISSUES. IN ALL CULTURES, ANDROSTENEDIONE(^4) FORMED BY OXIDATION OF T BY 17
BETA-HYDROXYSTEROID DEHYDROGENASE (17-BETA-HSD) REPRESENTED 80% OF THE METABOLITES RECOVERED. THE AMOUNTS OF 5-ALPHA-DIHYDROTESTOSTERONE (DHT), FORMED BY REDUCTION OF T BY 5-ALPHA-REDUCTASE (5-ALPHA-R), WERE SMALL: 5 AND 2% (BPH) AND 8 AND 15%
(ADENOCARCINOMA) FOR EPITHELIAL CELLS AND FIBROBLASTS. RESPECTIVELY. NOTHERN BLOT ANALYSIS OF TOTAL RNA FROM EPITHELIAL CELLS (BPH OR ADENOCARCINOMA) ATTRIBUTED THE REDUCTIVE ACTIVITY TO THE 5-ALPHA REDUCTASE TYPE 1 ISOZYME AND OXIDATIVE ACTIVIT
TO THE 17-BETA-HSD TYPE 2. IN CANCER FIBROBLASTS, ONLY LITTLE 17-BETA-HSD TYPE 2 MRNA WAS DETECTED. THE 5-ALPHA-REDUCTASE INHIBITORS, 4-MA (17-BETA-(N,N-DIETHYL)CARBAMOYL-4-METHYL-4-AZA-5-ALPHA-ANDROSTAN-3-ONE) AND FINASTERIDE, INHIBITED DHT
FORMATION WITH A PREFERENTIAL ACTION OF 4-MA ON EPITHELIAL CELLS (BPH OR ADENOCARCINOMA) AND OF FINASTERIDE ON FIBROBLASTS FROM ADENOCARCINOMA. NEITHER INHIBITOR ACTED ON ^4 FORMATION. ON THE OTHER HAND, THE LIPIDO-STEROL EXTRACT OF SERENOA
REPENS (LSESR, PERMIXON*) INHIBITED THE FORMATION OF ALL THE T METABOLITES STUDIED [IC,- 40 AND 200ML/ML (BPH) AND 90 AND 70 MG/ML (ADENOCARCINOMA) IN EPITHELIAL CELLS AND FIBROBLASTS. RESPECTIVELY]. THESE RESULTS HAVE IMPORTANT THERAPEUTIC
IMPLICATIONS WHEN SELECTING APPROPRIATE TREATMENT OPTIONS FOR BPH. |