Male rats were subjected to the following treatment: 1. Castration or treatment with the oestrogens polyoestradiol phosphate (PEP) (estradurin®), polydiethylstilboestrol phosphate (PSP), polyoestriol phosphate (SEP) (triodurin®), oestradiol‐17‐undecylate (EU) (progynon®‐depot), oestradiol‐3‐N‐[bis(2‐chloroethyl)]‐carbamate‐17‐dihydrogenphosphate (E) (estracyt®) or diethylstilboestrol diphosphate (H) (honvan®). PEP, PSP, SEP and EU were given as a single injection intramuscularly in a dose of 8 mg/kg, whereas E and H were given orally as water solutions (8 mg/kg) every second day. 2. Castration and treatment with the oestrogens. 3. Castration and treatment with testosterone‐3‐(p‐hexyloxyphenyl)‐proprionate (A) (andradurin®) (60 mg/kg intramuscularly in a single injection) and the oestrogens. – After 20 days the weight of the ventral prostate in group 1 was reduced to 85% by SEP, to 20% by E and to 10% by castration and the administration of other oestrogens. In group 2 the prostatic weight was reduced to 10%. In 3, A alone or combined with PEP, SEP, EU or E restored the prostatic weight. PSP reduced the prostatic weight to 75% and H to 65%. The alkaline phosphatase activity in group 1 was reduced to 55% by castration and increased to 135% by EU; in group 2 PEP, PSP, EU and E restored the activity; in group 3, A given alone restored the activity and A + PEP, PSP, EU or H increased the activity to 175–350%. The acid phosphatase activity in group 1 was reduced to 45% by castration, to 55% by H and to 70% by PSP. In group 2 PEP, PSP and E partly reversed the decrease brought about by castration; in 3, A given alone restored the activity, which was increased to 115–155% after A + PEP, PSP, H or E. Secretion from the ventral prostate of intact rats or castrated rats treated with A or A + PEP was squeezed out. The alkaline and acid phosphatase activities after A + PEP were approximately doubled. The findings indicate that oestrogen can affect the rat ventral prostate in ways other than by reducing the secretion of testicular androgens.
Male rats were injected intramuscularly with 8 mg/kg polyoestradiol phosphate (PEP) (estradurin®), polydiethylstilboestrol phosphate (PSP), polyoestriol phosphate (SEP) (triodurin®) or oestradiol undecylate (EU) (progynon®‐depot). After 20 days the weight of the spleen was decreased to 70 % by PEP, PSP and EU whereas SEP had no effect. The weight decrease was due to a histochemically demonstrated atrophy of the white pulp, which contained little acid phosphatase. The acid phosphatase activity per spleen was found to be unchanged although the activity per weight unit was increased. Male rats were injected intramuscularly with 100 mg/kg methylprednisolone acetate (D) (depomedrone®). After 20 days the weight of the spleen was decreased to 60 %. The acid phosphatase activity per weight unit was not increased and the activity per spleen was decreased to 70 %. A lower dose of D (10 mg/kg) had no effect on the enzyme activity but reduced the weight of the spleen to 90 %. Adrenalectomized rats were injected intramuscularly with 10 or 1 mg/kg D. No effects on the spleen weight or phosphatase activity were found after 20 days. When PEP (8 mg/kg, intramuscularly) was injected in adrenalectomized rats treated with either 10 or 1 mg/kg D the weight of the spleen was decreased to 75 and 85 %, respectively. The acid phosphatase activity per spleen was unchanged. The results indicate that the polymerized oestrogens and EU, but not D, have a similar action on the spleen. The action of PEP in adrenalectomized rats substituted with D indicates that the effects of PEP are not mediated through the adrenal glands.
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