Tanabe E T, Lee C, Grayhack J T
J Urol. 1982 Apr;127(4):826-8. doi: 10.1016/s0022-5347(17)54059-8.
The possibility that an intracellular proteolytic process is activated during castration induced prostatic regression warrants consideration and investigation. We investigated the activities of cathepsin D, a lysosomal proteolytic enzyme, in the prostate of rats at different intervals following castration. The enzyme activity was noted to increase during the period of rapid prostatic involution. Administration of exogenous testosterone in varying doses to castrated rats prevented or retarded prostatic weight loss as well as the increase in cathepsin D activity in a dose related manner. Administration of actinomycin D to castrated rats also retarded ventral prostate regression and decreased cathepsin D activity. These observations suggest that cathepsin D is actively synthesized in the regressing prostate and that the enzyme may play an important role in castration induced prostatic regression.
阉割诱导前列腺退化过程中细胞内蛋白水解过程被激活的可能性值得考虑和研究。我们研究了在阉割后不同时间段大鼠前列腺中溶酶体蛋白水解酶组织蛋白酶D的活性。在前列腺快速退化期间，该酶活性增加。给阉割大鼠给予不同剂量的外源性睾酮，以剂量相关的方式预防或延缓了前列腺重量减轻以及组织蛋白酶D活性的增加。给阉割大鼠给予放线菌素D也延缓了腹侧前列腺退化并降低了组织蛋白酶D活性。这些观察结果表明，组织蛋白酶D在退化的前列腺中被积极合成，并且该酶可能在阉割诱导的前列腺退化中起重要作用。
