Petersson F, Hammar M, Mathson K, Hjertberg H, Varenhorst E
Department of Obstetrics and Gynaecology, University Hospital of Linköping, Sweden.
Scand J Urol Nephrol. 1987;21(4):267-71. doi: 10.3109/00365598709180780.
Nine elderly men with prostatic carcinoma underwent treatment with a LHRH-agonist (Zoladex, ICI) for 3-6 months. At the end of the treatment period the patients underwent subcapsular orchidectomy. Testicular tissue was incubated with different tritiated testosterone precursors. Conversion mediated by several testicular steroidogenic enzymes was compared between Zoladex-treated patients and nineteen non-treated patients who underwent orchidectomy because of prostatic carcinoma. Serum concentrations of LH, FSH and testosterone were determined before and during treatment in the treated patients. The LHRH agonist treatment induced significantly decreased conversion mediated by the enzymes 3 beta-hydroxysteroid dehydrogenase, 17 alpha-hydroxylase and C17-20 lyase. Conversion mediated by 17 beta-ketosteroid reductase was also decreased although not as dramatically as the other enzymes, while conversion mediated by 20 alpha-dehydrogenase was increased. Serum concentrations of testosterone decreased to castration levels. Serum gonadotrophins decreased but remained within normal levels suggesting that "desensitization" at the pituitary level was not the only mechanism of action of the LHRH-agonist.
九名患有前列腺癌的老年男性接受了促性腺激素释放激素(LHRH)激动剂(诺雷德,帝国化学工业公司)治疗3至6个月。在治疗期结束时,患者接受了包膜下睾丸切除术。将睾丸组织与不同的氚标记睾酮前体一起孵育。比较了接受诺雷德治疗的患者与19名因前列腺癌接受睾丸切除术的未治疗患者之间几种睾丸类固醇生成酶介导的转化情况。在接受治疗的患者中,测定了治疗前和治疗期间血清促黄体生成素(LH)、促卵泡生成素(FSH)和睾酮的浓度。LHRH激动剂治疗导致由3β-羟基类固醇脱氢酶、17α-羟化酶和C17-20裂解酶介导的转化显著降低。由17β-酮类固醇还原酶介导的转化也有所降低,尽管不如其他酶明显,而由20αα-脱氢酶介导的转化则增加。血清睾酮浓度降至去势水平。血清促性腺激素减少但仍在正常水平范围内,这表明垂体水平的“脱敏”不是LHRH激动剂的唯一作用机制。