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At least 937 records · Page 52Linked to original sources
PubMed1987

Lipoxin A augments release of thromboxane from human polymorphonuclear leukocyte suspensions.

Lipoxin A (LXA) is a novel eicosanoid, generated by the interactions of lipoxygenases, which has a variety of biological actions. When added to human polymorphonuclear leukocytes, LXA stimulated thromboxane formation which was monitored as TxB2 by radioimmunoassay. The compound augmented the formation of TxA2 stimulated by the ionophore of divalent cations (A23187). Formation of thromboxane was inhibited by two non-steroidal anti-inflammatory drugs (i.e. indomethacin and proglumetacin). Results of the present study indicate that LXA can provoke the release and transformation of endogenous arachidonic acid to thromboxane. Moreover, they suggest a relationship between lipoxin A and the formation of cyclooxygenase pathway products.

Calcimycin↗
PubMedDate not supplied

Monoamine metabolism in senile dementia of Alzheimer type.

Monoamine metabolism in senile dementia of the Alzheimer-type (SDAT) was assessed by measuring the concentrations of the dopamine metabolite HVA, the noradrenaline metabolite MHPG and serotonin metabolite 5-hydroxy-3-indoleacetic acid (5-HIAA) in post-mortem brains of SDAT patients, a group of control subjects and a group of chronically depressed patients. Concentrations of MHPG and 5-HIAA were significantly reduced in hippocampus and cortical regions of the SDAT group. These changes did not correlate with clinical assessments of the degree of dementia or neuropathological assessment of the degree of Alzheimer-type changes in the SDAT group. It is suggested that changes in monoamine metabolite concentrations are not primarily involved in the pathogenesis of SDAT, and may be secondary to the well established cholinergic deficits.

Aged↗
PubMed1990

Serotonin synthesis inhibition or receptor antagonism reduces pregnancy-induced nocturnal prolactin secretion.

During early pregnancy, two surges of prolactin (PRL) designated as nocturnal (N) and diurnal (D) are displayed by the rat. We previously reported the positive influence of serotonin (5-HT) in regulating the D surge. Its role in the N surge remained inconclusive due to the contradictory results obtained with the 5-HT synthesis inhibitor parachlorophenylalanine (PCPA) and 5-HT2 receptor antagonists. This study further characterizes the involvement of 5-HT in regulating the N surge. The effectiveness of different doses of ketanserin (KET), a 5-HT2 receptor antagonist, to reduce plasma PRL levels during the surge was established. Sub-threshold (1 mg/kg BW) or just maximally effective (10 mg/kg BW) doses of KET were administered to rats that had been pre-treated with PCPA (250 mg/kg BW) for 24h. The lower dose of KET was ineffective in reducing the N surge even though less 5-HT was available due to PCPA treatment 24h earlier. The higher dose was effective in blocking the surge. Subsequently, the effect of one compared to two injections of PCPA 24 hours apart on plasma PRL levels and concentrations of 5-HT, dopamine (DA) and their respective metabolites 5-hydroxy-indoleacetic acid (5-HIAA) and dihydroxyphenylacetic acid (DOPAC) in the medial basal hypothalamus (MBH) and the medial dorsal hypothalamus (MDH) was studied. Two injections of PCPA but not one abolished the N PRL surge. Levels of 5-HT and 5-HIAA were significantly (p less than .005) reduced following either one or two injections of PCPA. Nevertheless, there was a greater (50 fold) decrease in 5-HIAA following 2 injections compared to one injection (10 fold), resulting in lower 5-HT turnover as indicated by lower 5-HIAA/5-HT ratios. Levels of DA in the MBH were reduced significantly only following two injections of PCPA, suggesting that the lack of effect of PCPA after one injection on the N surge was not due to a decrease in DA.

Analysis of Variance↗
PubMed1995

Effects of fluoxetine on basal and K(+)-induced tritium release from synaptosomes preloaded with [3H]serotonin.

Synaptosomes from rat brain cortex and spinal cord were preloaded with [3H]serotonin ([3H]5-HT), superfused and exposed to fluoxetine and/or 15 mM K+. In both regions 10 microM, but not 1 microM fluoxetine evoked a marked tritium overflow, about 2 min later than the immediate [3H]5-HT release induced by K+, and mainly (73%) due to the efflux of a tritiated metabolite of 5-HT, possibly [3H]5-hydroxy-indoleacetic acid. These findings confirm previous data in the rat hippocampus and are probably due to fluoxetine interacting with the 5-HT storage vesicles. One microM fluoxetine significantly reduced the d-fenfluramine-induced [3H]5-HT overflow, in accordance with its action as 5-HT uptake blocker, but did not affect the K(+)-induced [3H]5-HT overflow. This latter finding does not confirm that fluoxetine inhibits the depolarization-induced Ca(2+)-influx, suggested to involve a drug interaction with the L-type Ca(2+)-channels. Thus, the overflow induced by 10 microM fluoxetine was additive with the depolarization-induced overflow, when the two stimuli were applied together. When 10 microM fluoxetine was added 7 min before 15 mM K+, there was no depolarization-induced overflow. Such inhibition might be only apparent and due either to the fluoxetine-induced loss of vesicular 5-HT or to a fluoxetine-induced alterations of synaptic vesicles. The in vivo relevance of the fluoxetine releasing effect remains to be assessed.

Animals↗
PubMed1996

Regionally specific effects of diazepam on brain serotonin metabolism in rats: sustained effects following repeated administration.

The effects of single (1mg/kg) and repeated (1mg/kg 2* daily for 4 days) diazepam administration are investigated on brain regional 5-hydroxytryptamine (5-HT; serotonin) and 5-hydroxy indoleacetic acid (5-HIAA) concentration in rats. Daily treatment decreased food intakes but body weights did not decrease. Administration of diazepam (1mg/kg) to 4 day saline injected rats on the 5th day decreased 5-HT levels in the hippocampus and increased it in the hypothalamus. 5-HIAA levels were increased in the striatum and decreased in the hypothalamus 4 day diazepam injected rats injected with saline on the 5th day also exhibited similar changes of 5-HT and 5-HIAA. Cortical levels of 5-HIAA were also smaller in these rats. Administration of diazepam to 4 day diazepam injected rats again decreased 5-HT in the hippocampus and 5-HIAA in the hypothalamus. 5-HT and 5-HIAA were both decreased in the striatum. Regionally specific effects of diazepam on brain serotonin metabolism are discussed in relation to their possible functions.

Animals↗
PubMed1977

Effect of hyper- and hypothyroidism on platelet monoamine oxidase activity and serotonin metabolism.

We evaluated platelet monoamine oxidase (MAO) activity in 13 hyperthyroid and 9 hypothyroid patients. The platelet MAO activity of these patients did not differ from that of age- and sex-matched euthyroid control subjects. Nineteen hyperthyroid and twelve hypothyroid subjects had serum serotonin concentrations similar to those of age- and sex-matched euthyroid control subjects. We also determined the urinary excretion of 5-hydroxy-indoleacetic acid (5-HlAA), serotonin, tryptamine, and tyramine in five hyperthyroid and four hypothyroid subjects. Two hyperthyroid patients had increased tyramine excretion; one of these patients also had increased tryptamine excretion. Three hypothyroid patients and one hyperthyroid patients had slightly decreased serotonin excretion. Both the hyper- and the hypothyroid subjects had normal urinary 5-HIAA excretion. There was no relationship between platelet MAO activity and monoamine excretion in the patients with thyroid dysfunction. We conclude that there is no systematic change in platelet MAO activity or serum serotonin concentration in patients with hyper- or hypothyroidism.

Adult↗
PubMed1989

Hypothalamic monoamines measured by microdialysis in rats treated with 2-deoxy-glucose or d-fenfluramine.

The effects on brain monoamines (norepinephrine, serotonin and the metabolite of dopamine) following administration of d-fenfluramine (10 mg/kg IP) and 2-deoxy-d-glucose (500 mg/kg IP) have been measured by microdialysis from the ventromedial hypothalamus, lateral hypothalamic area and dorsomedial hypothalamus of conscious, unrestrained rats. Following administration of d-fenfluramine there was a significant increase in the concentration of serotonin in the ventromedial hypothalamus and lateral hypothalamic area, but no significant increase in the DMH. 5-HIAA (5-hydroxy-3-indoleacetic acid), the metabolite of serotonin, was increased in the DMH, but not in the other two regions. DOPAC (3,4-dihydroxyphenylacetic acid) was increased following fenfluramine treatment in all three regions examined. An increase in norepinephrine was observed in the VMH, but not in the other two regions, while the concentration of the 3-methoxy-4-hydroxyphenylglycol (MHPG) was increased in both areas. Treatment with 2-deoxy-D-glucose (2DG) was associated with fewer changes. In the lateral hypothalamic area there was a decrease in 5-HIAA and an increase in DOPAC. In the VMH there was an increase in norepinephrine and a decrease in MHPG in the DMH, but otherwise no significant alterations were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effects of individual housing on circadian rhythms of adult rats.

Circadian rhythms of hypothalamic serotonin (5HT), its precursor tryptophan (TP) and its metabolite 5-hydroxy-indoleacetic acid (5HIAA), and of prolactin and corticosterone circulating hormones were determined in group-housed and in individually-housed male rats, adapted to a 12:12 light/dark cycle. After 5 weeks of individual housing, 5HT peaked later, TP and 5HIAA peaked earlier, and the mesor level of TP and 5HIAA decreased with respect to group-housed animals. Individual housing caused an increase in the corticosterone mesor level, but did not affect amplitude or acrophase. The circadian rhythm of prolactin was unchanged by individual housing.

Animals↗
PubMed1990

Chronic administration of imipramine antagonizes deranged circadian rhythm phases in individually housed rats.

The circadian rhythms of hypothalamic serotonin (5HT), tryptophan (TP) and 5-hydroxy-indoleacetic acid (5HIAA), and serum corticosterone were determined in male Wistar rats. The animals underwent a five-week 12:12-hr light/dark cycle conditioning period and were divided into three groups: rats housed four to a cage (group C, control), rats housed individually (group I), and rats housed individually and treated for two weeks with 10 mg/kg/day of imipramine continuously administered by osmotic pumps implanted under the skin (group T). Significant differences were found in the acrophases of 5HT, TP and 5HIAA between group I and group C, and corticosterone mesor was higher in group I than in group C. On the contrary, no differences were observed between group T (individually housed, but given imipramine) and group C. Therefore, chronically administered imipramine antagonizes the circadian changes induced by individual housing.

Animals↗
PubMed1993

Relationship of neuroendocrine cells of prostate and serotonin to benign prostatic hyperplasia.

Neuroendocrine (NE) cells containing neurosecretory granules, rich in various peptide hormones and biogenic amines such as serotonin (5-HT), are components of the human prostate epithelium. The NE cells probably subserve a paracrine or local regulatory role in both prostatic growth and differentiation as well as the exocrine secretory process. Neuroendocrine cells may be involved in the etiology of benign prostatic hyperplasia (BPH). In this study the number of NE cells in areas of BPH was compared with normal tissue using 5-HT immunocytochemistry. In addition, using high-performance liquid chromatography with electrochemical detection (HPLC-ECD), tissue levels of 5-HT and its metabolite 5-hydroxy-indoleacetic acid (5-HIAA) were analyzed in prostatic tissue extracts including 25 cases of BPH and 16 cases of normal tissue verified by adjacent histologic sections. Compared with normal prostate our results demonstrated a marked decrease in 5-HT immunoreactive NE cells in the vast majority of larger hyperplastic nodules of BPH. These findings were corroborated by quantitative analysis where a significant reduction in the tissue 5-HT levels in BPH (0.539 +/- 0.09 SE) compared with normal (1.75 +/- 0.22 SE) (p < 0.05) was found. When smaller nodules of BPH were studied, abundant NE cells, equal or increased in number compared with those in adjacent normal prostatic tissue, were seen. The small apparently developing BPH nodules and ductal-like structures contained NE cells which may be growth foci near the periphery of some hyperplastic nodules. These findings particularly in small hyperplastic nodules suggest that NE cells and their products involved in controlling cell proliferation through a paracrine hormonal mechanism and may be involved in the pathogenesis of BPH. Serotonin (5-HT) and NE peptides may represent that elusive local "missing link" often alluded to in various theories relating to the development of early nodular hyperplasia in BPH.

Aged↗
PubMed1976

Biosynthesis of thromboxane B2: assay, isolation, and properties of the enzyme system in human platelets.

The microsomal fraction of human platelets catalyzed the conversion of arachidonic acid to an unstable platelet-aggregating factor and a hydrolyzed product on the thin-layer chromatography (TLC). This product was isolated on TLC, purified by silica gel column chromatography and identified by combined gas chromatography-mass spectrometry as the hemiacetal derivative of 8-(1-hydroxy-3-oxopropyl)-9, 12L-dihydroxy-5, 10-heptadecatrienoic acid (thromboxane B2). The enzymatic activity was dependent upon methemoglobin and tryptophan as cofactors. Reduced glutathione had no effect either alone or in combination with other cofactors. Methemoglobin could be replaced by hematin or hemin; and tryptophan by 3-indolacetic acid or catecholamines. The apparent requirement for methemoglobin is due to the reductive activity of ferriprotoporphyrin IX. The reaction, however, catalyzed by the ferriprotoporphyrin IX in the thromboxane synthesizing system is different from that described for the decomposition of lipid peroxides. Certain transition metals and hydrogen donors, such as hydroquinone and ascorbate, which have been shown to stimulate the catalytic activity of ferriproroporphyrin IX in the decomposition of 15-hydroperoxy-prostaglandin E1 are inhibitors of thromboxane B2 formation. This enzyme preparation also transformed eicosa-8. 11, 14-trienoic acid to an unknown product on TLC. The enzyme system was rapidly inactivated upon incubation in the reaction mixture.

8,11,14-Eicosatrienoic Acid↗