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Our purposes in this study were to ascertain the effects of oestrogen on the accessory reproductive organs of male mice and rats, and to determine the capacity of androgen to counteract these effects.
Methods
The oestrogen, Amniotin, was furnished by Dr. J. A. Morrell of E. R. Squibb and Sons; and the androgen, testosterone, was supplied by Dr. Erwin Schwenk of the Schering Corporation.
Seventy-two rats and 71 mice have been used in this study. Thirty-one rats were given injections of oestrogen. The other 41 rats, litter-mates to the treated animals, received no injections. In the case of mice, 36 received only oestrogen, 13 were given oestrogen and testosterone, and 22 controls received no injections. The control mice in most cases were not litter-mates of injected animals.
Both testes were surgically removed from some of the animals. The immature rats were castrated on the 17th–24th day of life. The adult
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ABSTRACT
Inhibition of microsomal prostaglandin (PG) biosynthesis by allantoic fluid, obtained from ewes at 80–120 days of gestation, was examined. Inhibition of cotyledonary microsomal PGE2 and PGF2α biosynthesis by lyophilized allantoic fluid occurred in a dosedependent manner. The concentration of allantoic fluid required to inhibit PGE2 and PGF2α production by 50% averaged 17·9 ± 3·2 (s.e.m.) mg dry weight/ml (n = 5). Microsomal PG biosynthesis was markedly enhanced by the addition of arachidonic acid (30 μmol/l). Synthesis of PGE2 and PGF2α was increased to 245 ± 65% and 184±14% of control (P<0·05, n = 5) respectively. Treatment of cotyledonary microsomes with porcine phospholipase A2 (PLA2; 0·125 units/ml) also stimulated PG synthesis, PGE2 increasing to 216 ± 27% and PGF2α to 172 ± 14% of control (P<0·05, n=5) respectively. Allantoic fluid (20 mg dry weight/ml) inhibited arachidonic acid-stimulated PG synthesis (PGE2 by 48·6 ± 13·8% and PGF2α by 44·2 ± 7·7%) and PLA2-stimulated PG synthesis (PGE2 by 60·6±11·6% and PGF2α by 74·8 ± 8·5%). Allantoic fluid, however, did not affect PLA2-stimulated release of arachidonic acid from microsomes, thus negating the possibility that allantoic fluid suppresses PG synthesis by inhibiting PLA2 activity. These data indicate that allantoic fluid inhibits PG production at the level of PG synthase enzymes. Prostaglandin inhibitor(s) in allantoic fluid may play a role in maintaining uterine quiescence throughout gestation and its withdrawal, at term, may be involved in the initiation of labour.
J. Endocr. (1987) 114, 295–300
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ABSTRACT
The effect of RU486, a synthetic progesterone receptor antagonist, on basal uterine prostaglandin (PG) release and release in response to oxytocin injection has been investigated in late-pregnant sheep (days 135–140 of gestation). Fifteen hours after i.m. injection of RU486 (50 mg; n = 5) or vehicle alone (n = 4), bolus injections of oxytocin (50, 500 and 5000 mU) were administered via a uterine artery ipsilateral to the pregnant uterine horn at 2-hourly intervals. Uteroovarian vein concentrations of 13,14-dihydro-15-keto PGF2α (PGFM) and PGE2 were determined before and during oxytocin stimulation. Basal concentrations of both PGFM and PGE2 were significantly (P < 0·001) increased in ewes 15 h after RU486 administration compared with ewes receiving vehicle alone. Concentrations of PGFM, but not PGE2, increased significantly (P < 0·001) following injection of each dose of oxytocin in both treated and untreated animals. The response to oxytocin, measured both as the area under the curve and as the peak height of PGFM release, was significantly (P <0·05) greater in RU486-treated ewes. There was no significant effect of oxytocin on the area or peak height of PGE2 response in either RU486-treated or control animals. These results demonstrate that treatment of late-pregnant ewes with RU486 results in an increase in basal uterine PGFM and PGE2 as well as oxytocin-stimulated PGFM release.
Journal of Endocrinology (1992) 134, 353–360
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ABSTRACT
Castrated prepubertal lambs were hypophysectomized and then treated with GH and testosterone either alone or in combination over a series of 3-week treatment periods. Hypophysectomy resulted in a rapid reduction in skeletal growth rate which could be reversed by the administration of either GH (4IU three times a week for 3 weeks) or testosterone propionate (10 mg daily for 3 weeks). When GH or testosterone treatment was withdrawn, skeletal growth fell to the post-operative rate. Combined treatment with both GH and testosterone was no more or less effective than either hormone given singly. The order of administration did not have any effect on the growth rate. Circulating concentrations of insulin-like growth factor-I (IGF-I) were reduced by hypophysectomy, but neither GH nor testosterone treatment, alone or in combination, had any effect on IGF-I concentrations. Concentrations of IGF-II rose following hypophysectomy, and again were not affected by any of the hormonal replacement treatments.
In conclusion, both GH and testosterone could stimulate skeletal growth in the hypophysectomized lamb without any alteration of circulating IGF concentrations, and testosterone can clearly stimulate skeletal growth in the complete absence of GH.
Journal of Endocrinology (1989) 121, 563–570
