The terminal electron-transport system (TET) of the human prostate was studied histochemically and biochemically. The estimation of these systems was done with fresh specimens obtained at operation. Prostatic hypertrophy 30, prostatic cancer 5 and normal prostate 3 as a control were used. Among them, in 23 cases of hypertrophy and 4 cases of cancer, testosterone propionate, hexestrol or stilbestrol diphosphate were administered or orchiectomy was performed before removal of the prostatic tumor.
The auther applied Nitro-BT for histochemical reaction and NT for biochemical reaction. On biochemical study, the auther analyzed the TET to 5 groups (endogenous dehydrogenase (ED), succinoxi dase system (SOS), succinic dehydrogenase (SD), cytochrome c-cytochrome oxidase system (COS) and TET) by using antimycin A and amytal as inhibitory agents, and arrived at the following conclusions.
1) On the histochemical reaction, these systems were mainly observed in the glandular epitheriali cells of the normal prostate and hypertrophy, and the cancer cells of prostatic cancer.
2) Biochemically, there were a little TET activities of the prostatic tissue.
3) On the biochemical analysis, the TET reaction took place conjugating about 8% in the step of the SD at the normal prostate, 25% at fibromyomatous type, about 45% at mixed type and about 44% at adenomatous type of the hypertrophy, and 12% at the cancer.
4) The strength of the ED and the TET activities may be arranged as following order; cancer, adenomatous and mixed type of the hypertrophy, normal prostate and fibromyomatous type of the hypertrophy.
5) The SOS and the COS ordered; cancer, mixed type, adenomatous type, normal prostate and fibromyomatous type.
6) As for the SD, the order was as follows: mixed type, adenomatous type, cancer normal prostate and fibromyomatous type. Namely the SD activity of the cancer was not so strong.
7) The activities of these systems on the hypertrophy were changed by the administration of sexhormones, and these changes were stronger at the adenomatous type than the mixed type. In the adenomatous type, testosterone propionate inhibited the SD and accelerated the COS, hexestrol inhibited the every system but the COS, and stilbestrol diphosphate inhibited the every system.
8) According to the difference of the sex-hormonal sensitivities between the adenomatous and the mixed type, the stroma of the hypertrophy has little activity, or if it has activity, that is far different from that of the gland.
9) The activities of the prostatic cancer were markedly inhibited by the administration of stilbestrol diphosphate, being observed the same effect by orchiectomy.
10) Androgen do not antagonized with estrogen in the effect to the SD on the adenomatous type, namely testosterone propionate inhibited the SD as well as hexestrol and stilbestrol diphosphate.
11) In those enzyme systems, the cancer was far different from the hypertrophy and the same relationship was found under the estrogen administration.
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