Abstract. Because of the well known stromal-epithelial interaction of various urogenital organs, it was of interest to compare quantitatively steroid metabolism and binding in epithelium (E) and stroma (S) of the human benign prostatic hyperplasia (BPH). Testosterone 5α-reductase activity was determined by thin-layer chromatography and androgen as well as oestrogen binding sites by a charcoal adsorption technique after a steroid incubation period of 18 h at 0°C, using methyltrienolone (R1881) and oestradiol-17β as tritiated ligands and unlabelled R1881 and diethylstilboestrol as the respective competitors. The main results were as follows: (1) using biochemical markers (acid phosphatase, hydroxyproline), an on average 17% contamination of E by S and 6% of S by E was found, (2) the molar optimum of NADPH for the enzyme reaction was nearly identical in E and S, ranging between 1 and 0.1 mm, (3) the apparent Michaelis constant (Km) of 5α-reductase was in both fractions identical, the mean being 0.15 (μm, (4) the maximal rate of 5α-reductase activity (pmol 5α-reduced metabolites · mg protein−1 · 1 h−1) was 161 ± 28 (sem; n = 20), 66 ± 4.6 and 148 ± 6.6 in S, E and whole tissue fraction of BPH, respectively. In two normal prostates the means were: 88, 53 and 73, respectively, (5) the androgen binding sites were evenly distributed between the cytosol of E and S, while measurable oestrogen binding sites were found in 42% of the analyzed S but only in 5% of analyzed E. In conclusion: the 2.4 times higher 5·-reductase activity in S compared to E of the BPH is responsible for the about 2 to 2.5 times higher activity in the whole tissue fraction of BPH if compared with the normal prostate. Furthermore, due to our preliminary binding studies, oestrogens might play an important role in the S fraction of BPH.

Twenty-one renal cell carcinomas were analyzed for the presence of androgen progestin and estrogen receptors by agar gel electrophoresis and a dextran-coated charcoal assay. An androgen receptor could be demonstrated in 3 tumors, a progestin or estrogen receptor was not detectable. It was therefore concluded that renal cell carcinoma is generally not a hormone-dependent tumor, and a hormonal treatment of metastatic renal cell carcinoma as first-line therapy does not seem to be justified.

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Histochemical fluorescence techniques could be of great value in order to assay androgen receptors (AR), particularly in punch biopsies from human prostatic carcinoma (PCA). Therefore, prostatic tissue was examined for specific binding of fluorescein-labeled 5 alpha-dihydrotestosterone derivatives (FDHT) to AR. Using a 17 beta-fluoresceinated DHT derivative (17-FDHT), variable fluorescence was found in human and rat prostates at high 17-FDHT concentrations. This fluorescence could be blocked by unlabeled DHT in 11 and 73% of human and rat prostatic tissue, respectively. Control studies of receptor and organ specificity were conducted and showed that preheated slices from rat prostates displayed no decrease of fluorescent staining. No difference in fluorescence intensity could be seen between prostates from castrated and uncastrated rats. Unstained tissue slices frequently showed a considerable intensity of autofluorescence. An appreciable amount of fluorescence in both rat liver and spleen was found. From these results and various general methodical problems inherent in fluorescent receptor assays, we conclude that the fluorescence techniques described are inappropriate for demonstration of AR.

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