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Endröczi & Lissák (1962) and Saginor & Horton (1968) have shown that in rabbits the testosterone output in venous testicular blood increases shortly before and after copulation. Drori & Folman (1964) and Folman & Drori (1966) have shown that in male rats mating produces hypertrophy of the accessory reproductive organs and suggested that this is due to increased integral androgen production. Drori, Amir & Folman (1968) have also shown increased fructose levels in the coagulating glands of mated male rats. In this study, the testosterone content in the testes of mated and unmated male rats was compared.
Forty-eight pairs of litter-mate rats aged 40 days were split into two equal groups: in one group the rats were mated and in the other they were unmated. The mated male rats were housed with hysterotomized females in groups of four males to two females; the females were replaced once a week. The
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SUMMARY
Interaction in the immature mouse of potent oestrogens with the weak utero-vaginotrophic (UV) compounds, coumestrol, genistein, dimethyl-stilboestrol, norethisterone acetate and megestrol acetate though sometimes additive at very low doses appeared to be essentially antagonistic at higher doses.
In particular, the weak oestrogens coumestrol and genistein, found in certain plants, markedly inhibited the UV action of potent oestrogens, e.g. oestradiol-17β, oestrone and diethylstilboestrol and this effect may account in part for the anti-oestrogenic activity of extracts of these plants.
Some differences in the ability of different oestrogens to promote uterine growth relative to vaginal growth were observed.
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SUMMARY
Loss of uptake during 24 hr. after administration of [3H]oestradiol showed approximately linear relationships between log uptake and time for uterus and vagina but not for skeletal muscle; these relationships were similar for mice pretreated with oestradiol. Uptake by uterus and vagina was less by about 50% when [3H]oestradiol was given to mice whose uteri and vaginae had reached maximum weight after pretreatment with oestradiol but cessation of growth of these organs was apparently not due to failure of their ability to take up oestradiol.
The relationship of uptake levels maintained in the uterus and vagina during 3 days and their consequent growth rate was studied.
When a second dose of [3H]oestradiol was given at various times after the first, new uptake, measured 1 hr. later, by uterus and vagina (but not skeletal muscle) was greatest when uptake remaining from the first dose was also greatest.
When a single dose of [3H]oestradiol (0·0039–2·5 μg.) was given to previously untreated mice or to mice with considerable oestradiol-induced uterine and vaginal growth, the only indications of any reduction of normal uptake ability were for the uterus when uptake was measured 1 hr. after doses greater than 0·11 μg.
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SUMMARY
Both norethisterone acetate and coumestrol enhanced uptake of [3H]oestradiol by the uterus and vagina measured 1 hr. after injection of the two compounds; the effect was, however, transient. Otherwise all the weak utero-vaginotrophic compounds markedly inhibited uptake of [3H]oestradiol by the uterus and vagina. This inhibition and the accompanying growth responses give further support to the conclusion that the interaction in uterine and vaginal tissue between oestradiol and the weaker utero-vaginotrophic compounds studied involves competition for retention at receptor sites followed by expression of the activity characteristic of the compounds retained.
