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Search for other papers by I. CHESTER JONES in
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SUMMARY
The ovaries of the lungfish (Protopterus annectens Owen) were examined for sex steroids.
Extracts produced a positive response in the mouse uterine weight test. Processing by paper chromatographic methods indicated the presence of oestriol, oestrone, a trace of oestradiol-17β and progesterone, but not enough material was available for their definitive chemical demonstration. The possible significance of these results is discussed.
Search for other papers by Matti Poutanen in
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estriol. E 2 is the most active estrogen and the predominant female sex steroid during the reproductive years. In addition to these classical estrogens, there are various other steroidal and non-steroidal compounds that are able to interact with estrogen
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Sex steroid concentrations in plasma collected from the canine deferential vein were measured, after separation, by radioimmunoassay. The concentrations found were compared with those in the peripheral plasma. The mean concentrations of androstenedione, testosterone, 5α-dihydrotestosterone, 5α-androstane-3α,17β-diol, 5α-androstane-3β,17β-diol and oestradiol-17β were 13·2, 14·7, 8·9, 4·6, 8·0 and 7·5 fold higher respectively in plasma from the deferential vein than in peripheral plasma. A close anatomical relationship was found between the vasa deferentia, the deferential vein and the peripheral plasma as well as between the deferential vein and the prostate gland. These findings emphasize and extend earlier conclusions that high levels of sex steroids present in the deferential vein could have a local influence on the growth of the prostate.
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Abstract
Cellular receptors for sex steroids (SSRs) were studied in an unselected series of 55 human pituitary tumors. Cytosolic receptors for estrogen (ERcs) and progesterone (PgRcs) were determined in all cases and cytosolic androgen receptors (ARcs) in 47 cases. Nuclear receptors (ERns, PgRns, ARns) were also studied in 33 cases. ERs and PgRs were determined by an ELISA and ARs by [3H]methyltrienolone binding. Where both cytosolic and nuclear receptors were studied (n=33), ERs, PgRs and ARs were found in at least one subcellular fraction in 66·7, 60·6 and 81·8% of cases respectively, ERs and ARs being mainly recovered from the cytosol and PgRs from the nucleus. No linear correlation was found between preoperative plasma steroid hormones and their specific cellular receptors. Nonetheless, the differential expression of SSRs according to sex and gonadal status at the time of surgery strongly supports their regulation by the steroid environment in vivo: PgRcs were more frequent in tumors found in women (41·4 vs 15·4%, P<0·05), whereas a high expression of ERcs and ARcs (>15 fmol/mg protein) was more common in tumors found in men (34·5 vs 10·3%, P<0·05 and 54·5 vs 24·0% respectively). PgRs were positively correlated with ERns, indicating the possibility of estrogen priming of their expression, and negatively correlated with ARs in nuclear fractions. SSRs appeared to be widely distributed among pituitary tumors, although, compared with other hormone-secreting groups, prolactinomas displayed a higher ERc expression (34·8 ± 11·3 vs 4·8 ± 5·1 fmol/mg protein, P=0·007) and gonadotroph cell adenomas lower ARc values (1·3 ± 0·8 vs 38·2 ± 10·6 fmol/mg protein, P=0·048). Microadenomas were characterized by a higher PgR expression than macroadenomas, whereas hemorrhagic (macro)adenomas were characterized by a high ER expression (>90%). The present results indicate that most pituitary tumors are targets for sex steroids, SSR expression being partially triggered by the steroid environment itself. Possible physiopathological and therapeutic implications of these findings are discussed.
Journal of Endocrinology (1996) 151, 175–184
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Histamine is synthesized in cells by histidine decarboxylase (HDC). HDC-deficient knockout (KO) mice lack functional HDC and histamine in the tissues. In the present study we used this in vivo model for studying the role of HDC deficiency in the regulation of male steroid hormone metabolism. In agreement with earlier studies showing the lack of effects of central histamine on the basal secretion of gonadotrope hormones, we found no difference with in situ hybridization in the expression of GnRH in the hypothalamus of wild type and KO mice. The tissue concentrations of testosterone and several androgenic steroids were significantly elevated in the testes but not in the adrenal glands of HDC-KO mice. In contrast, serum estradiol levels failed to show a significant difference between the two groups. The weight of the testes was significantly smaller in both 7-day-old and adult KO mice. The ultrastructure of the adult testis indicated elevated steroid synthesis with more tightly coiled membranous whorls in Leydig cells. The present results suggest that changes in reproductive functions and sex steroid secretion in male HDC-KO mice are not due to altered hypothalamic GnRH expression but are probably related to definite modifications during fetal development of KO mice reinforced later by the lack of the effect of peripheral histamine. This may provide in vivo evidence that peripheral histamine is an important regulatory factor of male gonadal development during embryogenesis and of sex steroid metabolism later in adulthood.
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A study of the respiration of rat ventral prostate has been carried out with special reference to the effect of added carbohydrate and certain sex steroids.
The average Q o2 value for rat ventral prostate was 9·1. When this tissue was examined 48 hr after castration, there was a significant decrease in the average Q o2 value to 7·1. The rate of respiration remained the same in the absence and in the presence of added glucose or fructose.
A high concentration of testosterone, 50 μg/ml., inhibited the oxygen consumption of ventral prostate; oestradiol had a less pronounced effect. With lower concentrations of testosterone, such as 0·5 μg/ml. or 0·005 μg/ml., variable results were obtained, but the average Q o2 value did not differ significantly from that established for the ventral prostate alone. The addition of testosterone to the ventral prostate from castrate rats did not increase the respiration.
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SUMMARY
Modifications of chromatin activity, induced by sex steroids, were studied in rat endometrial tissues by the following semi-quantitative cytochemical methods: 'staining' of fixed uteri by [3H]actinomycin-D followed by radioautography and cytophotometric evaluation of Feulgen reaction kinetics in isolated endometrial nuclei. The following hormonal treatments were applied to groups of animals: oestradiol-17β (10 μg); progesterone (2 mg); progesterone (2 mg daily for 4 days) with oestradiol-17β (0·05 μg on the 4th day). With both cytochemical methods, different hormonal treatments were found to induce different patterns of response in endometrial cell types. In luminal epithelium and endometrial stroma, hormonal treatment increased the binding of actinomycin-D in a variable manner as judged from autoradiographic grain counts. Sex steroids also induced an overall increased DNA acid-lability as estimated by cytophotometric evaluation of Feulgen staining intensity. Hormonal treatments induced different hydrolysis curve patterns in both endometrial nuclear types.
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The effects of in vivo treatment with estrogen and progesterone on isoproterenol-induced uterine relaxation and beta(2)-adrenoceptor (beta(2)AR) mRNA production in non-pregnant rat myometrium were investigated. Whether homologous myometrial desensitization of beta(2)AR function was dependent on or modulated by the two steroids was also examined. Estrogen treatment alone or in combination with progesterone reduced maximal relaxation (E(max)) of isolated uterine strips subsequently challenged with isoproterenol whereas progesterone alone had no effect on this parameter. The reduction was accompanied by an enhanced beta(2)AR mRNA concentration. The concentration of isoproterenol giving half-maximal relaxing response (EC(50)) increased following estrogen treatment and this effect was curbed by progesterone. Isoproterenol had no effect on beta(2)AR transcription irrespective of the steroid regimes employed. E(max) of isolated uterine strips was reduced following prolonged in vivo treatment with isoproterenol but the effect was found only when estrogen alone was administered concomitantly. Finally, in vivo treatment with isoproterenol increased EC(50) of uterine strips subsequently stimulated with isoproterenol in vitro. This effect was independent of steroid treatment. We conclude that homologous desensitization of beta(2)AR function in non-pregnant rat myometrium in terms of sensitivity (EC(50)) is independent of sex steroids but in terms of maximal response (E(max)) occurs only in the presence of estrogen. We speculate whether progesterone withdrawal in connection with the well-known estrogen dominance at rat parturition may strengthen the desensitization induced by beta(2)AR activation and thus contribute to the transformation of the uterus from a quiescent to a highly contractile organ.
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ABSTRACT
The influence of gender and sex hormones upon both the hypothalamic-pituitary-adrenal (HPA) axis and the immune and inflammatory responses is well recognized, but it is not clear to what extent the two effects are interdependent. We have investigated this interaction using a chronic inflammation model. Corticosterone levels were measured in mature BALB/c male and female mice, which were intact, sham-operated or gonadectomized. No significant differences were found between groups in baseline corticosterone, but systemic inflammation (cotton-induced granulomas) resulted in stimulation of the HPA axis in a reproducible pattern. Corticosterone levels were higher in sham-operated females than in males, but gonadectomy had opposing effects in the two genders, resulting in reduced levels in females but significantly increased levels in males. A similar pattern emerged after stimulation by ether exposure or injection of interleukin-1β. In the chronic inflammatory model, replacement of ovariectomized females with physiological levels of progesterone restored a response similar to that of intact females. Physiological levels of 5α-dihydrotestosterone prevented the increase in corticosterone levels caused by castration in males and also resulted in reduced corticosterone levels in sham-operated females. Oestradiol treatment did not affect corticosterone levels. Release of interleukin-1 by peritoneal macrophages from intact and gonadectomized mice with chronic inflammation followed a similar pattern, females releasing more than males. These data suggest a complex inter-relationship between sex steroids, inflammatory stimuli and the HPA axis, such that females have a greater tendency than males to generate activating signals and in addition have a greater sensitivity to such factors.
Journal of Endocrinology (1993) 136, 389–397
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Estrogens are essential for bone mass accrual but their role before sexual maturation has remained elusive. Using in situ hybridization and immunohistochemistry, we investigated the expression of both estrogen receptor (ER) alpha and beta mRNA and protein as well as several mRNAs coding for enzymes involved in sex steroid metabolism (aromatase, type I and II 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD), steroid sulfatase (STS) and type I 5 alpha-reductase) on sections of tibial metaphyses before (1- and 4-week-old), during (7-week-old) and after (16-week-old) sexual maturation in female and male rats. ER alpha and ER beta mRNA and protein were detected in metaphyseal bone in lining cells, osteoblasts, osteoclasts and some osteocytes with no apparent differences in expression during development or between the sexes. In contrast, aromatase, type I and II 17 beta-HSD and type I 5 alpha-reductase mRNAs were first detected in osteoblasts, osteoclasts and occasionally in osteocytes from sexual maturation (7-week-old rat) and onwards. Only STS was present before sexual maturation. To study the significance of ER alpha and beta expression in bone before sexual maturation when circulating sex steroid levels are low, 26-day-old female and male rats underwent gonadectomy or 17 beta-estradiol (E(2)) supplementation (0.5 mg/21 days) during 3 weeks. Following gonadectomy, trabecular bone volume (TBV) was lower in males (P=0.03) and there was a trend towards reduction in females (P=0.057). E(2) supplementation increased tibial TBV compared with controls in both genders as assessed by Masson-Goldner staining. These data suggest that the presence of ERs in bone cells before sex maturation might be of significance for bone mass accrual. Furthermore, based on the mRNA expression of the crucial enzymes aromatase and type I 17 beta-HSD, we suggest that bone cells in the tibial metaphysis acquire the intrinsic capacity to metabolize sex steroids from sexual maturation onwards. This process may contribute to the beneficial effects of estrogen on bone mass accrual, possibly by intracrinology.
