The effect of tamoxifen on opening ATP-sensitive K channels enhances hydroxyl radical generation in rat striatum.

The present study was examined the antioxidant effect of tamoxifen, a synthetic non-steroidal antiestrogen, on cromakalim or nicorandil (ATP-sensitive K (K) channels opener)-enhanced hydroxyl radical (OH) generation induced by 1-methyl-4-phenylpyridinium ion (MPP) in extracellular fluid of rat striatum. Rats were anesthetized, and sodium salicylate in Ringer's solution (0.5 mM or 0.

Glutaminergic tonic action potentiate MPP-induced hydroxyl radical production in rat striatum.

The effect of glycine on 1-methyl-4-phenylpyridinium ion (MPP)-induced hydroxyl radical (OH) formation in the extracellular fluid of rat striatum were investigated. Rats were anesthetized and sodium salicylate in Ringer's solution (0.5 nmol/μl/min) was infused through a microdialysis probe to detect the generation of OH as reflected by the non-enzymatic formation of 2,3-dihydroxybenzoic acid (2,3-DHBA) in rat striatum.

Oxidative stress inactivates ecto-5'-nucleotidase by inhibiting protein kinase C in rat hearts in vivo.

Examined in the present study, allopurinol are xanthine oxidase inhibitors for use in rat hearts in vivo dialysis technology and ventricular myocardial intersitial adenosine production can increase. The microdialysis probe was implanted in the left ventricular myocardium of anesthetized rat hearts and the tissue in the vicinity of the dialysis was perfused with Tyrode's solution containing adenosine 5'-monophosphate (AMP) through the dialysis probe at a rate of 1.0ml/min to assess the activity of ecto-5'-nucleotidase.

Opening of ATP-sensitive K(+) (KATP) channels enhance hydroxyl radical generation induced by MPP(+) in rat striatum.

The present study examined whether opening of adenosine triphosphate (ATP) sensitive K(+) (KATP) channels can enhance 1-methyl-4-phenylpyridinium (MPP(+))-induced hydroxyl radical (OH) generation in rat striatum. Rats were anesthetized, and sodium salicylate in Ringer's solution (0.5nmol/ml per min) was infused through a microdialysis probe to detect the generation of OH as reflected by the non-enzymatic formation of 2.

Evidence for existence of thyroid hormone inducible semicarbazide-sensitive amine oxidase (SSAO) in rat heart cytosol.

Background: Semicarbazide-sensitive amine oxidase (SSAO; EC; 1.4.3.

Fluvastatin, an HMG-CoA reductase inhibitor, facilitate adenosine production in the rat hearts via activation of ecto-5'-nucleotidase.

Objective: The present study was examined whether fluvastatin, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, can increase the production of interstitial adenosine via activation of ecto-5'-nucleotidase in the ventricular myocardium, with use of microdialysis techniques in in situ rat hearts.

Methods: Adenosine in the dialysate collected during perfusion with Tyrode's solution containing 100μM AMP (through the probe) originated from the hydrolysis of AMP catalyzed by endogenous ecto-5'-nucleotidase, so that the level of adenosine reflected the activity of ecto-5'-nucleotidase in this tissue.

Results: Fluvastatin (100μM), an inhibitor of low-density lipoprotein (LDL) oxidation, significantly increased the concentration of adenosine measured in the presence of 100μM AMP (i.

Phytic acid suppresses ischemia-induced hydroxyl radical generation in rat myocardium.

The present study examined whether ischemia-reperfusion-induced hydroxyl radical (·OH) generation was attenuated by myo-inositol hexaphosphoric acid (phytic acid). A flexibly mounted microdialysis technique was used to detect the generation of ·OH in in vivo rat hearts. To measure the level of ·OH, sodium salicylate in Ringer's solution (0.

Effect of tyramine on the production of interstitial adenosine during perfusion with adenosine 5'-monophosphate in rat hearts in vivo.

The present study was examined whether tyramine-released norepinephrine enhances the production of interstitial adenosine via stimulation of ecto-5'-nucleotidase (a key enzyme responsible for adenosine production) using microdialysis techniques in in situ rat hearts. The microdialysis probe was implanted in the left ventricular myocardium of anesthetized rats and perfused in the presence of adenosine 5'-monophosphate. Tyramine (1mM) increased the adenosine concentration measured in the presence of 100 μM adenosine 5'-monophosphate, an increase which was inhibited by antagonist of the α(1)-adrenoceptors (prazosin, 50 μM) or of a protein kinase C inhibitor (chlerythrine, 10 μM), and in reserpinized rats, tyramine failed to increase the adenosine 5'-monophosphate-primed dialysate adenosine concentration.

Protective effect of diltiazem, a L-type calcium channel antagonist, on lysophosphatidylcholine-enhanced hydroxyl radical generation by MPP(+) in rat striatum.

Background: The interaction between the PKC and oxygen free radicals.

Objective And Methods: The present study examined the effects of lysophosphatidylcholine (LPC), an endogenous amphophilic lipid metabolite, on 1-methyl-4-phenylpyridinium ion (MPP(+))-induced hydroxyl radical (()OH) generation in rat striatum. LPC (50 μM) increased ()OH formation by MPP(+).

Diabetes modulates ethanol-induced increase in serotonin release from rat hippocampus: an in vivo microdialysis study.

We examined whether diabetes mellitus (DM) affects the acute ethanol (EtOH)-induced increase in serotonin (5-HT) release from the rat hippocampus, and compared the findings with those obtained from non-DM rats. Hippocampal 5-HT was measured by using in vivo microdialysis. Rats were rendered diabetic by an injection of streptozotocin (STZ).

Protective effect of tamoxifen, a synthetic non-steroidal antiestrogen, on phenelzine and 1-methyl-4-phenylpyridinium ion (MPP+)-induced hydroxyl radical generation in rat striatum.

The present study examined whether tamoxifen could suppress antidepressant drug phenelzine can increase an active dopaminergic neurotoxin, 1-methyl-4-phenylpyridinium ion (MPP+)-induced hydroxyl radical (*OH) generation in the extracellular fluid of rat striatum, using in vivo microdialysis system. Rats were anesthetized, and sodium salicylate (0.5 nmol/microl/min) was infused through a microdialysis probe to detect the generation of *OH as reflected by the non-enzymatic formation of 2,3-dihydroxybenzoic acid (DHBA) in the striatum.

Changes in monoamine oxidase activity in hepatic injury: a review.

This review focuses on multiplicity of monoamine oxidase (MAO) activity in rat hepatic injury. MAO play a major role in the metabolism of biogenic amines. Stress such as immobilization stress (IMMO) or cold stress changes the multiple forms of MAO activity in rat liver.

The properties of B-form monoamine oxidase in mitochondria from monkey platelet.

The present study was examined the effect of the properties of monkey platelet monoamine oxidase (MAO) based on inhibitor sensitivity. Monkey platelet showed a high MAO activity with beta-phenylethylamine (beta-PEA) as substrate and a very low A-form MAO activity with 5 hydroxytryptamine (5-HT) as substrate. Moreover, monkey platelet MAO was sensitive to the drugs deprenyl as B-form MAO inhibitor and less sensitive to clorgyline and harmaline as A form MAO inhibitor with beta-PEA as the B-form MAO substrate.

Effect of antidepressant drug on semicarbazide-sensitive amine oxidase (SSAO) in dog brain.

The present study examined whether or not other cyclic antidepressants, such as the dicyclic drug zimeldine, the tricyclic drug imipramine, and tetracyclic drug maprotiline, and the noncyclic drug nomifensine, inhibit semicarbazide-sensitive amine oxidase (SSAO) activity in dog brain. After treatment with 100 nM clorgyline and 100 nM deprenyl, all four antidepressant drugs inhibit SSAO activity in dog brain. The most potent of inhibition was observed by imipramine, followed by maprotiline, zimeldine and nomifensine.

Protective effect of tamoxifen, a synthetic non-steroidal antiestrogen, on phenelzine and 1-methyl-4-phenylpyridinium ion (MPP+)-induced hydroxyl radical generation in rat striatum.

The present study examined whether tamoxifen could suppress antidepressant drug phenelzine can increase an active dopaminergic neurotoxin, 1-methyl-4-phenylpyridinium ion (MPP+)-induced hydroxyl radical (*OH) generation in the extracellular fluid of rat striatum, using in vivo microdialysis system. Rats were anesthetized, and sodium salicylate (0.5 nmol/microl/min) was infused through a microdialysis probe to detect the generation of *OH as reflected by the non-enzymatic formation of 2,3-dihydroxybenzoic acid (DHBA) in the striatum.

Changes in monoamine oxidase activity in hepatic injury: a review.

This review focuses on multiplicity of monoamine oxidase (MAO) activity in rat hepatic injury. MAO play a major role in the metabolism of biogenic amines. Stress such as immobilization stress (IMMO) or cold stress changes the multiple forms of MAO activity in rat liver.

The properties of B-form monoamine oxidase in mitochondria from monkey platelet.

The present study was examined the effect of the properties of monkey platelet monoamine oxidase (MAO) based on inhibitor sensitivity. Monkey platelet showed a high MAO activity with beta-phenylethylamine (beta-PEA) as substrate and a very low A-form MAO activity with 5 hydroxytryptamine (5-HT) as substrate. Moreover, monkey platelet MAO was sensitive to the drugs deprenyl as B-form MAO inhibitor and less sensitive to clorgyline and harmaline as A form MAO inhibitor with beta-PEA as the B-form MAO substrate.

Effect of antidepressant drug on semicarbazide-sensitive amine oxidase (SSAO) in dog brain.

The present study examined whether or not other cyclic antidepressants, such as the dicyclic drug zimeldine, the tricyclic drug imipramine, and tetracyclic drug maprotiline, and the noncyclic drug nomifensine, inhibit semicarbazide-sensitive amine oxidase (SSAO) activity in dog brain. After treatment with 100 nM clorgyline and 100 nM deprenyl, all four antidepressant drugs inhibit SSAO activity in dog brain. The most potent of inhibition was observed by imipramine, followed by maprotiline, zimeldine and nomifensine.

The protective effect of fluvastatin on hydroxyl radical generation by inhibiting low-density lipoprotein (LDL) oxidation in the rat myocardium.

The present study examined the effect of fluvastatin on Cu(2+)-induced hydroxyl radical generation (*OH) in the extracellular fluid of rat myocardium using microdialysis technique (O system). Fluvastatin, an inhibitor of low-density lipoprotein (LDL) oxidation, was administered at a dose of 5.0 mg/kg/day i.

Protective effect of captopril and enalaprilat, angiotensin-converting enzyme inhibitors, on para-nonylphenol-induced *OH generation and dopamine efflux in rat striatum.

We recently reported that para-nonylphenol, an environmental chemical, induced hydroxyl radical (*OH) formation in rat striatum. In this study we examined the antioxidant effects of angiotensin-converting enzyme inhibitors (captopril or enalaprilat) on para-nonylphenol (nonylphenol) and 1-methyl-4-phenylpyridinium ion (MPP(+))-induced hydroxyl radical (*OH) formation and dopamine (DA) efflux in extracellular fluid of rat striatum, using a microdialysis technique. para-Nonylphenol clearly enhanced *OH formation and DA efflux induced by MPP(+).

Effects of ion channel blockers on basal hippocampal monoamine levels in freely moving diabetic and non-diabetic rats.

This study characterized the ion channel activities in the hippocampus of diabetic rats by monitoring the levels of monoamines. Extracellular levels of serotonin and dopamine were measured in the hippocampus of awake, freely moving streptozotocin-induced diabetic rats, spontaneously diabetic rats, and non-diabetic rats, using in vivo microdialysis. Sodium, calcium, and potassium ion channel blockers were used to assess the ion channel activities.

Absence of tissue-bound semicarbazide-sensitive amine oxidase activity in carp tissues.

We have previously reported that carp (Cyprinus carpio) tissue mitochondria contain a novel form of monoamine oxidase (MAO), which belongs neither to MAO-A nor to MAO-B of the mammalian enzyme. This conclusion results from the findings that the carp MAO was equally sensitive to a selective MAO-A inhibitor clorgyline and to the MAO-B selective inhibitor l-deprenyl, when tyramine, a substrate for both forms, serotonin or beta-phenylethylamine, a substrate for either A or B-form of mammalian MAO, was used. In the present study, we tried to detect another amine oxidase, termed tissue-bound semicarbazide-sensitive amine oxidase (SSAO), activity in carp tissues.

Blocking cardiac ATP-sensitive K+ channels reduces hydroxyl radicals caused by potassium chloride-induced depolarization in the rat myocardium.

The current study examined whether opening of the ATP-sensitive K(+) (K(ATP)) channel can induce hydroxyl free radical (OH) generation, as detected by increases in nonenzymatic formation of 2,3-dihydroxybenzoic acid (DHBA) levels in the rat myocardium. When KCl (4-140mM) was administered to rat myocardium through microdialysis probe, the level of 2,3-DHBA increased gradually in a potassium ion concentration ([K(+)](o))-dependent manner. The [K(+)](o) for half-maximal effect of the level of 2,3-DHBA production (ED(50)) was 67.

Immobilization stress increases endogenous monoamine oxidase (MAO) inhibitor in rat liver.

Although the physiological role of endogenous monoamine oxidase (MAO) inhibitor still remains unclear, the present study examined whether or not immobilization stress (IMMO) induce MAO inhibitor. An endogenous inhibitor of MAO was separated by gel filtration from 105,000 g supernate in rat liver cytosol following IMMO. The molecular weight of this inhibitor was estimated to be 500-600 by gel filtration.

Endogenous semicarbazide-sensitive amine oxidase (SSAO) inhibitor increases 1-methyl-4-phenylpyridinium ion (MPP+)-induced dopamine efflux by immobilization stress in rat striatum.

The present study examined whether or not immobilization stress (IMMO)-inducible semicarbazide-sensitive amine oxidase (SSAO) inhibitor by separated gel filtration from 105,000 g supernate in rat brain cytosol contribute to the dopamine (DA) efflux by 1-methyl-4-phenylpyridinium ion (MPP(+)) in the rat striatum. The isoelectric point (pI) value of this inhibitor was determined by isoelectric focusing (IEF)-gel electrophoresis to about 3.8.