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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

Prostaglandins Leukot Essent Fatty Acids. 2002 Apr;66(4):403-11.
Investigations into the mechanisms controlling prostaglandin production by the guinea-pig placenta: roles of calcium and gonadotrophin-releasing hormone.

Aitken H, Poyser NL.

Division of Biomedical and Clinical Laboratory Sciences, The University of Edinburgh, Edinburgh, UK.

The outputs of PGF(2 alpha), PGE(2) and 6-keto-PGF(1 alpha) were higher from the day 29 guinea-pig placenta than from the sub-placenta in culture, with PGF(2 alpha)being the major prostaglandin produced by the placenta. Lack of extracellular calcium reduced the production of all three prostaglandins by the sub-placenta and 6-keto-PGF(1 alpha) production by the placenta, but had no effect on the production of PGF(2 alpha) and PGE(2) by the placenta. EGTA (a calcium chelator) and a low concentration (30 microM) of TMB-8 (an intracellular calcium antagonist) generally inhibited prostaglandin output from the placenta and sub-placenta at various time points during culture, although EGTA had no effect on PGE(2) output from the placenta. Trifluoperazine and W-7 (calmodulin inhibitors) had no inhibitory effect on the outputs of PGF(2 alpha) and PGE(2) from the placenta, nor on the outputs of any prostaglandin from the sub-placenta. However, these two compounds inhibited the output of 6-keto-PGF(1 alpha) from the placenta. Nifedipine and verapamil (calcium channel blocking drugs) generally reduced the outputs of prostaglandins from the placenta and sub-placenta, except verapamil had no inhibitory effect on PGF(2 alpha) output from the sub-placenta. Gonadotrophin-releasing hormone (GnRH) did not stimulate the output of prostaglandins from the placenta, and tended to have a weak inhibitory action on this tissue. On the sub-placenta, GnRH had an initial inhibitory action on the outputs of PGF(2alpha) and 6-keto-PGF(1 alpha), which was then followed by a stimulation of the outputs of PGF(2 alpha) and, to a lesser extent, of PGE(2). 2002 Elsevier Science Ltd. All rights reserved.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12054910&dopt=Abstract

Prostaglandins Leukot Essent Fatty Acids. 2002 Apr;66(4):419-25.
Effect of fatty acids on estradiol and testosterone binding to whole DU-145 prostate cells.

Prinsloo SE, van Aswegen CH.

Wolmarans Research Laboratory, Department of Urology, University of Pretoria, Pretoria, South Africa. smulleoshllion.up.ac.za

Cancer of the prostate is one of the leading causes of cancer related deaths in men. An important role in the development of prostate cancer is played by androgens and androgen ablation is therefore currently used in cancer treatment. In the past, estrogens were widely used in treatment of prostate cancer, but there are indications that estrogens could also be involved in carcinogenesis. Lately, much research has been done on the modulation of the binding of steroid hormones to their receptors by polyunsaturated fatty acids (PUFAs), which could interfere with the steroid hormone's message. Therefore, the aim of this study was to determine in whole DU-145 human prostate cells the effect of EFAs and their metabolites on the binding and affinity of the estrogen receptor (ER) and androgen receptor (AR) to estradiol (E(2)) and testosterone (T), respectively. Fatty acids were dissolved in ethanol and added to the cell culture in a final ethanol concentration of 0.2% on the fourth day of incubation. The results showed that the PUFAs under investigation inhibited the AR's capacity, in contrast to the ER's capacity which was stimulated. However, the dissociation constants (K(d)) of the AR and ER complexes in the presence of the PUFAs, were as follows. Except for eicosapentaenoic acid (EPA) which decreased the AR dissociation constant and EPA and alpha-linolenic acid (ALA) which increased the ER dissociation constant, the remaining FAs had no significant effect on the K(d) values of both the AR and ER complexes. According to these priliminary results it is postulated that men should benefit with a diet rich in certain essential polyunsaturated fatty acids although its function remains to be clarified. 2002 Elsevier Science Ltd. All rights reserved.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12054912&dopt=Abstract

Int J Toxicol. 2002 May-Jun;21(3):191-9.
The blockade of mineralocorticoid hormone signaling provokes dramatic teratogenesis in cultured rat embryos.

Mirshahi M, Ayani E, Nicolas C, Golestaneh N, Ferrari P, Valamanesh F, Agarwal MK.

INSERM, Faculte de Medecine Paris VI, Paris, France. massoud.mirshanhdc.jussieu.fr

Although the administration of adrenocortical hormones to pregnant rats provokes only limited effect on the growth and development of the fetus, the direct influence of these steroids on cultured embryos has never been studied. The disruption of cell signaling by ZK 91587, which specifically occupies the mineralocorticoid receptor, resulted within 2 days in significant and pronounced adverse effects on the total length, the somite number, the embryo curvature, the communication between vitelline and umbilical blood vessels in the allantoid, and the vascularization of the vitelline sac, in 244-hour Wistar rat embryos in culture. The average score of 16 organs declined in a dose-dependent manner, following exposure to ZK 91587, and this was totally reversed by 10 microM aldosterone which, by itself, did not at all influence the embryonic development. The organogenesis was inhibited in the order: hind limb > fore limb > optic stalk > brain > olfactory pit > otic vesicle. ZK 91587 was completely ineffective in embryos that had attained the age of 260 hours. Similar, but less dramatic, results were obtained with the mineralocorticoid antagonist RU 26752, and with the antiglucocorticoid RU 38486. Sprague-Dawley rat embryos responded in a manner similar to the Wistar conceptuses. Thus, steroid receptor-mediated cell signaling is of critical importance to the growth and development of cultured rat embryos, which form a new model system to unravel adrenocortical hormone action.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12055020&dopt=Abstract

Biochem Biophys Res Commun. 2003 Jan 31;301(1):102-7.
Agouti-related protein has an inhibitory paracrine role in the rat adrenal gland.

Dhillo WS, Small CJ, Gardiner JV, Bewick GA, Whitworth EJ, Jethwa PH, Seal LJ, Ghatei MA, Hinson JP, Bloom SR.

Endocrine Unit, Faculty of Medicine, Imperial College, 6th Floor Commonwealth Building, Hammersmith Hospital, Du Cane Road, London W12 ONN, UK.

alpha-Melanocyte-stimulating-hormone (alpha-MSH) is an agonist at the melanocortin 3 receptor (MC3-R) and melanocortin 4 receptor (MC4-R). alpha-MSH stimulates corticosterone release from rat adrenal glomerulosa cells in vitro. Agouti-related protein (AgRP) an endogenous antagonist at the MC3-R and MC4-R, is expressed in the adrenal gland. We investigated the expression of the MC3-R and MC4-R and the role of AgRP in the adrenal gland. MC3-R and MC4-R expression was detected in rat adrenal gland using RT-PCR. The effect of AgRP on alpha-MSH-induced corticosterone release was investigated using dispersed rat adrenal glomerulosa cells. AgRP administered alone did not affect corticosterone release, but co-administration of AgRP and alpha-MSH attenuated alpha-MSH-induced corticosterone release. To investigate glucocorticoid feedback, adrenal AgRP expression was compared in rats treated with dexamethasone to controls. AgRP mRNA was increased in rats treated with dexamethasone treatment compared to controls. Our findings demonstrate that adrenal AgRP mRNA is regulated by glucocorticoids. AgRP acting via the MC3-R or MC4-R may have an inhibitory paracrine role, blocking alpha-MSH-induced corticosterone secretion.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12535647&dopt=Abstract

Eur J Clin Invest. 2002 Sep;32(9):669-73.
Rate-dependency of calcitonin secretion in response to increased plasma Ca2+.

Wang W, Lewin E, Olgaard K.

Nephrological Department P, Rigshospitalet, University of Copenhagen, Denmark.

BACKGROUND: Calcitonin (CT) is a polypeptide hormone secreted from C-cells of the thyroid gland in response to hypercalcemia. The physiological contribution of CT to calcium homeostasis has not been completely clarified. The present study therefore further characterized the sigmoidal relationship between plasma ionized calcium (P-Ca2+) and CT in normal rats, and examined the possibility of rate-dependency of CT secretion in response to changes in P-Ca2+. DESIGN: Hypercalcaemia was induced by an infusion of calcium gluconate at rate of 4.5 x 10(-2) mmol h-1 rat-1 i.v. (n = 8) and hypocalcaemia was induced by an EGTA infusion at a rate of 4.5 x 10(-2) mmol h-1 rat-1 (n = 7) in one protocol: the 'slow' protocol. In another protocol an increased rate of infusion of calcium gluconate or EGTA was used to induce a more rapid change in P-Ca2+. Calcium gluconate was infused at a rate of 6.0 x 10(-2) mmol h-1 rat-1 (n = 6) and EGTA infused at a rate of 7.5 x 10(-2) mmol h-1 rat-1 (n = 7): the 'rapid' protocol. RESULTS: The infusions of both the 'slow' and 'rapid' protocols resulted in linear changes in P-Ca2+, but with significantly different slopes (P < 0.01). The Ca2+/CT curves of both protocols were represented by sigmoidal curves. The 'rapid' increase of P-Ca2+ resulted in a higher maximal CT secretion (2032 +/- 215 pg mL-1) than the 'slow' increase of P-Ca2+ (1213 +/- 85 pg mL-1; P < 0.001), despite similar minimal and maximal levels being obtained in P-Ca2+ in the two protocols. Thus, a significantly greater CT response was obtained with a more rapid increment in P-Ca2+. CONCLUSION: The relationship between P-Ca2+ and CT is represented by a sigmoidal curve, as previously shown. The CT response depended, however, not only upon the concentration of P-Ca2+ obtained but also upon the rate of increase in P-Ca2+, demonstrating rate-dependency as another significant physiological relation between Ca2+ and CT.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12486866&dopt=Abstract

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