Antiaggregatory effect of selenium incorporated into algae with no effect on the microsomal enzymes in rats.
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Biomedical subjects
Publications and source records attributed to G Blaskó.
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The ethnobotany, ethnopharmacology and phytochemistry of the Thymelaeaceae are reviewed. Some members of this family find wide use commercially whilst others are used as deadly poisons or possess extreme irritant properties. The phytochemical evidence thus far available indicates that the daphnane and tigliane diterpene esters are clearly responsible for the toxic reactions observed, but chemotaxonomically it is not possible to predict which additional genera are likely to contain these toxins. Caution should therefore be exercised when studying members of this plant family.
Octahydroindolo[2,3-a]quinolizines and 3,4-dihydro-beta-carbolines proved to be powerful inhibitors of human platelet aggregation. They exhibited IC50 values two magnitudes lower than those of the commonly used cyclo-oxygenase inhibitors and no influence upon the routine parameters of blood coagulation was observed in vitro. Some of the compounds increased the vascular production of prostacyclin.
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Protopine, cryptopine and allocryptopine were demonstrated to enhance 3H-gamma-aminobutyric acid (3H-GABA) binding to rat brain synaptic membrane receptors. The above finding might be indicative of benzodiazepine-like activity of these alkaloids.
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Effects of a 72-h prostacyclin (PGI2) infusion (5 ng/kg/min) on hormone levels were studied in 11 patients (5 males, 6 females) suffering from obliterative arterial disease of the lower extremities. ACTH, cortisol, TSH, prolactin (Prl), GH, LH, FSH, T3, T4, calcitonin, parathyroid hormone (PTH), insulin, plasma renin activity (PRA), aldosterone and testosterone levels were measured at -15, 0, 30, 120, 240 min and 24, 48, 72 and 96 h after the infusion. During the first 240 min Prl and GH levels showed an increase that was thought to be either an effect of release of hormones or a consequence of stress. At the same time the thyroid hormones, T3, T4 and calcitonin decreased, presumably owing to an alteration in the blood flow to the thyroid gland. All these hormone levels returned to normal at 24 h in spite of the infusion continuing. PRA increased only during the second half of the infusion. No changes were found in the levels of ACTH, cortisol, TSH, LH, FSH, PTH, insulin, aldosterone and testosterone during the infusion. Five diabetics showed the same hormonal changes as the non-diabetics and their blood sugar levels remained unaffected during and after the procedure.
The binding of 45 bicuculline related phthalideisoquinoline alkaloids to the GABAA receptor was studied using rat brain synaptic membranes prepared both in Tris-HCl and in Tyrode buffers. The IC50 values determined in Tyrode for phthalideisoquinolines are lower (by about one order of magnitude) than and correlate well (r2 = 0.95) with the IC50 data obtained by [3H]GABA displacement in Tris-HCl. Applying Tyrode, the activities of GABA agonists relative to Tris-HCl are decreased. It can be recognized that activities in receptor binding are dependent on the conformations phthalideisoquinolines prefer in solution. On the basis of systematic alterations in the phthalideisoquinoline molecule the main structural elements involved in the binding of phthalideisoquinoline alkaloids appear to be identical with those of GABA agonists, suggesting that the same binding conformation of the GABAA receptor may be implicated for both agonists and antagonists. The opposite shift in relative potencies of agonists and antagonists may be the consequence of an alteration in the "ionic status" rather than that in the conformation of the GABAA receptor.
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The alkaloid 5,6,8,14-tetradehydro-4-hydroxy-3, 6-dimethoxy-17-methyl-morphinan-7-one[+/-)-salutaridine) was found to possess 3H-gamma-aminobutyric acid (3H-GABA) displacing activity (IC50 less than 1 mumol/l) in rat brain synaptic membranes. The enhancement of specific 3H-diazepam binding by increasing concentration of (+/-)-salutaridine follows a maximum curve indicating (+/-)-salutaridine to be a partial agonist at the GABA/benzodiazepine receptor complex.
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