Summary A specific antiserum has been generated against inhibin-like material (ILM) of prostatic origin. Using the immunoperoxidase technique, localization of ILM has been examined in a total of 114 prostates including normal (4 specimens), malignant (46) and hyperplastic (55) In the present study, we report immunocytochemical localization of inhibin-like material (ILM) in prostatic tissue. Inhibin is involved in the suppression of FSH synthesis and secretion. Of the various forms of inhibin-like materials (ILM) present in human seminal plasma, a peptide having a molecular weight of 10,400 daltons has been isolated in purified form from this laboratory (Thakur et al., 1981) the amino acid sequence of which has been reported (Sheth et al., 1984a; Johnson et al., 1984;Seidah et al., 1984). This peptide-ILM has been shown to be of prostatic origin (Sheth et al., 1984b;Beksac et al., 1984) and chemically similar (Johansson et al., 1984)
Gonadal functions were evaluated in 92 male patients after treatment for advanced Hodgkin's disease. The patients received six to ten cycles of cyclophosphamide, vincristine, procarbazine, and prednisolone (COPP) chemotherapy. All patients were in remission and were followed for 1 to 17 years (median, 6). Testicular atrophy was noticed in 89 (96.7%) patients. All patients remained azoospermic during the period of follow-up. The testosterone levels did not differ before and after treatment. The follicle stimulating hormone levels rose from pretreatment values (mean +/- standard deviation) of 179.27 +/- 21.99 ng/ml to 578.79 +/- 102.36 ng/ml after the treatment; the rise was significant (P less than 0.001). The luteinizing hormone levels rose from pretreatment values of 106.96 +/- 20.37 ng/ml to 127.37 +/- 32.19 ng/ml after treatment; the rise was significant (P less than 0.05). Testicular biopsy specimens in 19 patients showed germinal aplasia in all cases. It is concluded that six or more cycles of COPP chemotherapy for advanced Hodgkin's disease in men leads to permanent sterility.
In vivo administration of HSPI (10.7 kDa FSH suppressing peptide of prostate) to intact adult male rats was found to suppress the basal levels of incorporation of 3H-thymidine into DNA of ventral and dorsolateral lobes of the prostate, in a dose-dependent manner. Interestingly, microscopic examination of the prostate histology of HSPI treated rats revealed a significantly increased incidence of apoptotic bodies which are indicative of cell death. In another experiment, HSPI was also found to suppress the active DNA synthesis in testosterone-induced regrowth of prostate in castrated rats. Thus HSPI can suppress the basal and stimulated DNA synthesis and also induce apoptotic cell death in rat prostate.
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