Effects of alpha-difluoromethylornithine, an enzyme-activated irreversible inhibitor or ornithine decarboxylase, on testosterone-induced regeneration of prostate and seminal vesicle in castrated rats.
Effects of alpha-difluoromethylornithine, an enzyme-activated irreversible inhibitor or ornithine decarboxylase, on testosterone-induced regeneration of prostate and seminal vesicle in castrated rats.
复制标题
α-二氟甲基鸟氨酸(一种酶激活的不可逆抑制剂或鸟氨酸脱羧酶)对睾酮诱导的去势大鼠前列腺和精囊再生的影响。
作者:
C. Danzin;M. Jung;N. Claverie;J. Grove;A. Sjoerdsma;J. Koch
1. Castration of adult rats markedly decreases the amounts of polyamines (putrescine, spermidine and spermine) and of RNA and DNA in the ventral prostate and the seminal vesicle. 2. Daily injections of testosterone propionate to rats castrated 7 days previously increase polyamine and nucleic acid contents more rapidly in the seminal vesicle than in the ventral prostate. 3. After 7 days of androgen treatment, polyamine and nucleic acid contents of the seminal vesicle are significantly higher than those of intact animals. Nucleic acid, but not polyamine, contents return to normal values during the next 4 days of continued treatment. In the prostate, androgen treatment increases polyamine and nucleic acid contents to, but not above, normal values. 4. Repeated doses of alpha-difluoromethylornithine, a potent enzyme-activated irreversible inhibitor of ornithine decarboxylase, totally blocked the testosterone-induced increase of putrescine and spermidine in the ventral prostate and of putrescine in the seminal vesicle. They slowed significantly the accumulation of spermine in the ventral prostate and of spermidine in the seminal vesicle. alpha-Difluoromethylornithine also retarded the testosterone-induced accumulation of RNA in the ventral prostate. However, no clear correlation was apparent between accumulation of polyamines and of nucleic acids in the two organs. 5. alpha-Difluoromethylornithine markedly slows the testosterone-induced weight gain of the prostate, but not of the seminal vesicle. Cytological studies suggest that this effect on the prostate is due to inhibition of the androgen-induced restoration of the secretion content of prostatic acini.