Serotonergic characteristics of rainbow trout divergent in stress responsiveness.

Juvenile rainbow trout divergent in their cortisol response to confinement stress (HR: high responsive or LR: low responsive fish) were exposed to either 1 or 3 h of confinement stress. Untreated fish served as control. After the exposure blood and brain samples were collected.

Elevated dietary intake of L-tryptophan counteracts the stress-induced elevation of plasma cortisol in rainbow trout (Oncorhynchus mykiss).

Juvenile rainbow trout were isolated in individual compartments and allowed to acclimate for 1 week, during which they were fed commercial trout pellets. The feed was then replaced by pelleted feed supplemented with L-tryptophan (TRP) at two, four or eight times the concentration in the commercial feed. Fish were fed these supplemented feeds daily to satiety for 1 week, after which half of the fish were stressed, by lowering the water level for 2 h, while the remaining fish were left undisturbed.

Cytoprotection by deprenyl and tolcapone in a cell culture model of cerebral ischaemia.

Foetal rat brain aggregation cultures were exposed to a single episode of anoxia and hypoglycaemia for 30 min. Lactate dehydrogenase specific activity was estimated in the culture medium after ischaemia as a marker of lost cell integrity. Release of lactate dehydrogenase was most prominent during the first 24 hr period after the ischaemic damage, then it gradually declined.

A cell culture model of cerebral ischemia as a convenient system to screen for neuroprotective drugs.

Aggregation cultures of rat brain were exposed to a combination of anoxia and hypoglycaemia for 30 minutes. Thereafter, the release of lactate dehydrogenase into the cell culture medium was monitored up to 4 days as a measure of cell damage after the ischemic insult. Some cultures were treated with different concentrations of deprenyl or tolcapone, selective inhibitors of monoamine oxidase B and catechol-O-methyltransferase, respectively.

Oxidative stress decreases antioxidant enzyme activities in reaggregation cultures of rat brain cells.

The brain has been suggested to be especially sensitive to damage by reactive oxygen species. In this study, we examined the effects of hyperoxic conditions on the activities and mRNA levels of antioxidant enzymes in reaggregation cultures of rat forebrain cells. Cultures were exposed to 80% oxygen for 12-60 h starting on Days 17 and 33 in culture.

Ethanol-induced increase in catalase activity in reaggregation cultures of rat brain cells is due to increased oligodendrocyte differentiation.

Recent studies have shown that ethanol exposure of reaggregation cultures of fetal rat brain cells causes an increased activity and amount of catalase, and also an increased activity of the oligodendrocyte marker enzyme 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP). In the present study, reaggregation cultures were grown in the presence of 40 mM ethanol during 17 days, corresponding to a period in vivo from gestational day 17 to postnatal day 12. The activities of catalase, the peroxisomal marker enzyme acyl-coenzyme A oxidase and CNP were increased in ethanol-treated cultures.

Inhibition of aldehyde dehydrogenases by methylene blue.

The effect of the redox dye methylene blue on the stability of NADH and on the activity of the enzyme aldehyde dehydrogenase (ALDH; EC 1.2.1.

Effects of nerve growth factor on X-irradiated reaggregation cultures of rat brain cells.

The effects of exogenously added nerve growth factor (NGF) on reaggregation cultures of foetal rat brain cells after X-irradiation with 2 Gy were studied. Irradiation caused decreased protein and DNA levels, which was not prevented by NGF. The activities of the cholinergic marker enzymes choline acetyl transferase and acetylcholine esterase were increased in irradiated cultures.

Increase in catalase activity in developing rat brain cell reaggregation cultures in the presence of ethanol.

The aim of this investigation was to study the effects of ethanol on antioxidant enzymes in the developing brain, using reaggregation cultures of fetal rat brain cells as a model. The cultures were grown in the presence of 20 and 40 mM ethanol from day 2 until day 44 of the culture period, corresponding to a period in vivo from gestational day 17 to postnatal day 37. The catalase (EC 1.

Development of antioxidant enzymes in rat brain and in reaggregation culture of fetal brain cells.

The development of antioxidant enzymes in rat brain and reaggregation cultures of fetal brain cells was studied from embryonic day 15 to postnatal day 45. Both in vivo and in culture, the copper-zinc superoxide dismutase activity first increased and then decreased with age, whereas the manganese superoxide dismutase activity increased throughout the period. Catalase showed a maximum activity at day 5 after birth, thereafter decreasing to adult level around day 30, both in vivo and in culture.

Effects of low-dose X-irradiation on mouse-brain aggregation cultures.

Biochemical and morphological differentiation in reaggregating mouse-brain cell cultures after low-dose radiation (0.5 Gy) in vitro was studied. Cells were irradiated on culture day 2, corresponding to embryonic day 15-16, and different glial and neuronal markers were followed through development to postnatal day 40.

Effects of disulfiram and coprine on rat brain tryptophan hydroxylation in vivo.

The effects of disulfiram and coprine on brain tryptophan hydroxylation, and on the brain-levels of serotonin and 5-hydroxyindole-3-acetic acid, were studied in 45 and 235 days old rats. Both drugs were found to affect the parameters measured. Disulfiram increased the rate of tryptophan hydroxylation and the serotonin level in young rats, while these parameters appeared to be unaffected in old disulfiram-treated rats.

Neurons in primary cultures from five defined rat brain regions--cellular composition and morphological appearance.

Primary cultures from 15-17 days old fetal rat cerebral cortex, striatum, hippocampus, substantia nigra and brain stem were grown for ten days. Cell aggregates were formed one to two days after seeding. The cell bodies migrated peripherally from the clusters during development and networks of processes were formed.

Reactions of biogenic aldehydes with hemoglobin.

The aldehyde derivatives of dopamine and serotonin, 3,4-dihydroxyphenylacetaldehyde (DOPAL) and 5-hydroxyindole-3-acetaldehyde (5-HIAL), respectively, were incubated with human hemoglobin under physiological conditions. Both DOPAL and 5-HIAL, as well as dopamine, showed a time-dependent disappearance during the incubations, whereas this was not observed with serotonin. The amounts of free aldehydes recovered after incubation with hemoglobin, as analysed by high-performance liquid chromatography with electrochemical detection, corresponded to the amounts of acid metabolites formed in enzymatic assays, when the samples instead were incubated with aldehyde dehydrogenase.

Effect of acute ethanol administration on human blood aldehyde dehydrogenase activity.

The aldehyde dehydrogenase (EC 1.2.1.

Effects of disulfiram, cyanamide and 1-aminocyclopropanol on the aldehyde dehydrogenase activity in human erythrocytes and leukocytes.

The effects of the aldehyde dehydrogenase (ALDH; EC 1.2.1.

Effects of ethanol, acetaldehyde and disulfiram on the metabolism of biogenic aldehydes in isolated human blood cells and platelets.

The effects of ethanol, acetaldehyde and disulfiram on the metabolism of biogenic aldehydes were measured in different human blood fractions. Intact erythrocytes, leukocytes and platelets were incubated in phosphate-buffered saline with 3,4-dihydroxyphenylacetaldehyde (DOPAL) or 5-hydroxy-indole-3-acetaldehyde (5-HIAL), the aldehydes derived from dopamine and serotonin, respectively. The disappearance of the aldehyde and the formation of acid and alcohol metabolites were analysed in the presence of different concentrations of ethanol, acetaldehyde or disulfiram using high-performance liquid chromatography with electrochemical detection.

Aldehyde dehydrogenase activity and vascular disease in type II diabetes--a comparison between 2 different assays for activity.

We have recently reported that type II diabetic subjects with macroangiopathy have a higher activity of aldehyde dehydrogenase (ALDH) in blood than those without clinical vascular disease. ALDH activity was measured as the elimination of acetaldehyde added to a blood homogenate in vitro. We have re-examined our clinical material with another assay of ALDH which uses indole-3-acetaldehyde as substrate and measures the formation of indole-3-acetic acid.

Biogenic aldehydes in brain: on their preparation and reactions with rat brain tissue.

When 1 mM serotonin, dopamine, or norepinephrine was incubated with a monoamine oxidase preparation (mitochondrial membranes) in the presence of 4 mM sodium bisulfite, 85-95% of the amines were oxidized to the corresponding aldehydes. In the absence of bisulfite, the recoveries were only approximately 30%, and dark colored products were formed during the incubations. The aldehydes derived from tyramine, octopamine, methoxytyramine, and normetanephrine were also prepared by the use of this method.

Effects of biogenic aldehydes and aldehyde dehydrogenase inhibitors on rat brain tryptophan hydroxylase activity in vitro.

The effect of indole-3-acetaldehyde, 5-hydroxyindole-3-acetaldehyde, disulfiram, diethyldithiocarbamate, coprine, and 1-amino-cyclopropanol on tryptophan hydroxylase activity was studied in vitro using high performance liquid chromatography with electro-chemical detection. With the analytical method developed, 5-hydroxytryptophan, serotonin, and 5-hydroxyindole-3-acetic acid could be measured simultaneously. Indole-3-acetaldehyde (12-1200 microM) was found to cause a 6-33% inhibition of the enzyme.

Effects of aldehyde dehydrogenase inhibitors on hexobarbital sensitivity and neuroamine metabolism in rat brain.

Several authors have found that the aldehyde dehydrogenase (ALDH) inhibitor, disulfiram, prolongs hexobarbital-induced anaesthesia. It was suggested that this effect was caused by an alteration of the serotonergic system in brain, mediated by elevated levels of biogenic aldehydes. In the present study, disulfiram (300 mg/kg) was found to cause a 4-fold prolongation of hexobarbital-induced anaesthesia, while coprine (another potent ALDH-inhibitor) had no effect.

Metabolism of biogenic aldehydes in isolated human blood cells, platelets and in plasma.

The metabolism of biogenic aldehydes was measured in different human blood fractions. Isolated erythrocytes, leukocytes, platelets and plasma were incubated with 3,4-dihydroxyphenyl-acetaldehyde (DOPAL) or 5-hydroxyindole-3-acetaldehyde (5-HIAL), the aldehydes derived from dopamine and 5-hydroxytryptamine, respectively. The disappearance of the aldehydes and the formation of acid and alcohol metabolites were analysed using high-performance liquid chromatography with electrochemical detection.

Assay of human blood aldehyde dehydrogenase activity by high-performance liquid chromatography.

A simple and sensitive method for routine analysis of aldehyde dehydrogenase (ALDH, EC 1.2.1.

Metabolism of biogenic aldehydes in human blood: effects of ethanol, acetaldehyde and disulfiram.

The metabolism of biogenic aldehydes was measured in different fractions of human blood. Isolated erythrocytes, leukocytes, platelets and plasma were incubated with the aldehydes derived from dopamine and serotonin (DOPAL and 5-HIAL, respectively). The disappearance of the aldehydes and the formation of the acid and alcohol metabolites were analysed using HPLC with electrochemical detection.