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Biomedical subjects

F Dray

Publications and source records attributed to F Dray.

At least 37 records · Page 2Linked to original sources
PubMed1989

Hypothalamic prostaglandin E2 receptors coupled to an adenylyl cyclase.

We show that the effect of prostaglandin (PG) E2 on luteinizing hormone-releasing hormone (LHRH) release involves a receptor-mediated process coupled to an adenylyl cyclase system. The adenylyl cyclase activity in rat hypothalamus synaptic membrane preparations was stimulated by PGE2 and this stimulation was directly related to the presence of guanine nucleotide (GTP). PGE2 specifically bound to P2 membranes from rat and porcine hypothalami with similar characteristics. Computer-fitted saturation curves provided evidence for two binding components which may be two states of the same receptor (RH and RL). Experiments with Gpp(NH)p, a non-metabolizable analogue of GTP, suggested the interconversion of RH and RL. These results may reflect different states of the ternary complex (hormone-receptor-guanine binding protein). Magnesium (Mg2+) can modify the RH and RL binding parameters, but seems to act directly on the PGE2 receptor site.

Adenylyl Cyclases↗
PubMed1989

Distinct localization of prostaglandin D2, E2 and F2 alpha binding sites in monkey brain.

Autoradiographic localization of binding sites for [3H]prostaglandin D2, E2 and F2 alpha in the monkey brain was investigated by using in vitro labeling and an image processing system. Specific binding sites were distinctly localized in various nuclei in the hypothalamus, thalamus, and limbic system and their localization well correlated to the known functions of PGs in the brain by pharmacological and neurophysiological experiments. Furthermore, no direct relation was observed between the localization of PG binding sites and that of muscarinic cholinergic, alpha 1-adrenergic, and mu-opioid receptors in the preoptic area and hypothalamus.

Animals↗
PubMed1988

Structural identification of prostaglandin A1 biotransformation products from tumor cells.

Rat B104 neuroblastoma and C6 glioma cells are able to metabolize prostaglandin A1 (PGA1). Four metabolites were isolated by high performance liquid chromatography. Their structure was elucidated by fast atom bombardment mass spectrometry and 1H nuclear magnetic resonance. It appears that these biotransformation products are two sets of stereoisomers: the two isomers that eluted first are 9 alpha- and 9 beta-hydroxy-11 alpha-cysteinylglycyl adducts whereas the other two are 9 alpha- and 9 beta-hydroxy-11 alpha-cysteinyl derivatives. These compounds were compared with authentic samples prepared by Michael addition of the corresponding thiol onto PGA1, then by reduction with sodium borohydride.

Animals↗
PubMed1988

12-Hydroperoxyeicosatetraenoic acid (12-HPETE) and 15-HPETE stimulate melatonin synthesis in rat pineals.

The role of arachidonic acid metabolites in norepinephrine (NE)-induced N-acetyltransferase (NAT) activity and melatonin release was examined from 6 h-incubations of rat pineal glands. A cyclooxygenase inhibitor, indomethacin (5 x 10(-8) - 5 x 10(-6) M) was ineffective on melatonin release, in the presence of absence of NE (5 x 10(-6) M) while a lipoxygenase inhibitor, nordihydroguaiaretic acid (5 x 10(-7) -5 x 10(-5) M) had an inhibitory effect. Among the lipoxygenase metabolites, 12-hydroperoxyeicosatetraenoic acid (12-HPETE) and 15-HPETE stimulated both NAT activity and melatonin release in a dose-dependent manner, with a maximal effect occurring at 10(-6) M, while 5-HPETE or hydroxy derivatives of these compounds (12-HETE, 15-HETE and 5-HETE) were ineffective. These results indicate that 12-HPETE and 15-HPETE can be involved in NE-induced melatonin release.

Animals↗
PubMed1988

Inhibitory effect of platelet-activating factor (PAF) on luteinizing hormone-releasing hormone and somatostatin release from rat median eminence in vitro correlated with the characterization of specific PAF receptor sites in rat hypothalamus.

Platelet-activating factor (PAF) exhibits a wide range of biological activities, including the stimulation of secretory processes in various cell types. However, little is known regarding its possible influence on the release of brain neuropeptides. In the present study we have examined the effect of PAF on the release of three hypothalamic releasing hormones in adult male rats, and have characterized the presence of specific PAF binding sites in rat hypothalamic membranes. PAF decreased LHRH and somatostatin (SRIF) release from the median eminence with a maximal inhibition at 10(-14) M for both neuropeptides, whereas GRF release was not significantly altered. Moreover, PAF strongly counteracted the Ca2+ ionophore A 23187-stimulated release of LHRH and SRIF from median eminence and medial basal hypothalamus (greater than 50% inhibition). These results suggest an involvement of Ca2+ dependent events in PAF action. This inhibitory effect was specifically exerted at a hypothalamic site because PAF failed to depress LH and GH release from the anterior pituitary. A specific, reversible and saturable binding of [3H]PAF to membrane preparations of rat hypothalamus was demonstrated and two classes of binding sites were characterized. The affinity (KD) of each binding class was 2.14 +/- 0.32 nM and 61.63 +/- 16.4 nM, respectively, and the corresponding maximal number of each binding class was 25.41 +/- 3.2 fmol/mg protein and 146.2 +/- 47.5 fmol/mg protein. In the same conditions no specific binding was observed using rat pituitary membranes. The specificity of PAF analogs for these binding sites was well correlated to their relative effectiveness in altering LHRH and SRIF release (order of potency: L-652,731, kadsurenone greater than BN 52021 greater than Lyso-PAF). These data suggest that the binding sites identified in the hypothalamus have the characteristics expected of a specific PAF receptor and that PAF effect on neuropeptides release is a receptor-mediated process.

Animals↗
PubMed1988

Identification of 6-keto-prostaglandin E1 obtained from isolated perfused kidney of the rabbit.

We studied the release of 6-keto-prostaglandin (PG) E1-like material into urinary and venous effluents of the isolated perfused kidney of the rabbit. After high performance liquid chromatographic (HPLC) separation, material coeluting with authentic 6-keto-PGE1 was measured by radioimmunoassay, platelet antiaggregation bioassay and characterized further by gas chromatography/mass spectrometry-single ion monitoring (GC/MS-SIM). Injection of either arachidonic acid or ATP into the renal artery stimulated the release of prostacyclin [measured as immunoreactive (i)-6-keto-PGF1 alpha] and i-6-keto-PGF1. HPLC fractions containing i-6-keto-PGE1, and coeluting with 6-keto-PGE1 standard, exhibited potent inhibition of platelet aggregation. The presence of authentic 6-keto-PGE1 was verified by the GC/MS-SIM spectra in HPLC zones from which radioimmunoassayable and bioassayable 6-keto-PGE1-like material was recovered.

Adenosine Triphosphate↗
PubMed1987

Leukotrienes C4 and D4 stimulate the release of luteinizing hormone-releasing hormone from rat median eminence in vitro.

The release of luteinizing hormone-releasing hormone (LH-RH), somatostatin (SRIF) and growth releasing factor (GRF) by male rat median eminences (MEs) incubated in vitro for 30 min, in the presence of leukotrienes (LT) C4, D4, E4 and B4 was estimated by radioimmunoassay (RIA). Leukotrienes, with the exception of LTE4 stimulated the release of LH-RH. The dose-response curve was bimodal for LTC4 with two maxima at 10(-8) and 10(-16) M (X2.2 and 1.9, respectively), biphasic for LTD4 with a maximum (X2) at 10(-8) M; LTB4 was active only at 10(-6) M (X1.9). These different curves suggest a specific effect on the release of LH-RH. Moreover, these effects were selective since no alteration of SRIF and GRF secretions was observed. No additive effect on LH-RH release was observed when LTC4 and LTD4 were added simultaneously at 10(-8) M. FPL-55712, a drug supposed to be an antagonist of LTC4, showed an unexpected stimulatory effect (X4.2 and 1.7-fold) on LH-RH release at 3.10(-5) and 10(-6) M, respectively. However, FPL-55712 did not alter the release of LH-RH induced with 10(-8) or 10(-16) M LTC4. These results extend our previous observations on the stimulatory action of LTC4 and are the first evidence of the stimulatory effect of LTD4 and LTB4 on the LH-RH release.

Animals↗
PubMed1987

Pulsatile secretion of growth hormone and insulin in relation to feeding in rats.

In unrestrained male Wistar rats chronically implanted with intracardiac catheters, blood samples were taken every 20 min throughout the 24 h of the diurnal cycle. Plasma concentrations of growth hormone (GH), insulin, and glucose were measured. The pattern of food intake was continuously monitored. The existence of 3-h pulsatile cycles of GH secretion was confirmed. In addition, short bursts of insulin secretion were observed in the middle of every second GH peak-to-peak interval. Food intake appeared to be enhanced during short periods that corresponded with GH release into the blood and was reduced during the GH peak-to-peak periods in which the bursts of insulin secretion were observed. From these observations this study draws a schematic relationship between the rhythmicity of the secretion of GH and insulin and the probability of occurrence of feeding. We speculate that the rhythmic endocrine activity may be causally related to feeding.

Animals↗
PubMed1986

Tumor cell biotransformation products of prostaglandin A1 with growth inhibitory activity.

The growth inhibitory effect and the fate of prostaglandin A1 (10(-6) M) were followed in cultures of rat B104 neuroblastoma and C6 glioma cells. More than 40% and 85% of the drug were neither recognized by a prostaglandin A1 antiserum nor extracted from the acidified medium with ethyl acetate, after 6 h and 24 h-incubation, respectively. When the supernatant of cells cultured in the presence of prostaglandin A1 during 24 hours was transferred to other cells and used as culture medium, the same growth inhibitory effect as with prostaglandin A1 was observed even when no prostaglandin A1 was added. After extensive purification and reverse phase HPLC of supernatant, four peaks more polar than prostaglandin A1 were shown; two of them were still active as growth inhibitors. This biotransformation was not observed with normal cells like L 929 or chick embryo fibroblasts, for which prostaglandin A1 had no inhibitory effect. The identification of these metabolites will allow the study of the structure-activity relationship.

Animals↗
PubMed1986

ELISA for detection of human antibodies to Chlamydiae.

An enzyme-linked immunosorbent assay for the detection of human antibodies to Chlamydiae is described which exploits the cross-react properties between the genus-specific antigen of Chlamydiae and the ReLPS constituent of the outer membrane of a Salmonella minnesota mutant. Of 100 random sera tested by ELISA-ReLPS and immunofluorescence 78% showed an absolute correlation, 15% were positive in immunofluorescence and negative in ELISA and 7% were positive in ELISA and negative in immunofluorescence. Furthermore results obtained by the ELISA-ReLPS on 55 sera from patients with clinical evidence of Chlamydiae infection correlated well with the values obtained by an ELISA using Chlamydia-coated microtitration plates and by two immunofluorescence tests using Chlamydia trachomatis and Chlamydia psittaci as antigens. The method described here is sensitive, simple, reproducible and may be employed for epidemiological and pathogenetic studies of chlamydial infections.

Antibodies, Bacterial↗