Inhibition of monoamine oxidase activity by antidepressants and mood stabilizers
Jazyk angličtina Země Švédsko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
21200377
PII: NEL310510A19
Knihovny.cz E-zdroje
- MeSH
- afekt účinky léků MeSH
- amitriptylin farmakologie MeSH
- antidepresiva farmakologie MeSH
- antimanika farmakologie MeSH
- benzodiazepiny farmakologie MeSH
- citalopram farmakologie MeSH
- cyklohexanoly farmakologie MeSH
- desipramin farmakologie MeSH
- fluoxetin farmakologie MeSH
- imipramin farmakologie MeSH
- inhibitory MAO farmakologie MeSH
- iproniazid farmakologie MeSH
- klorgylin farmakologie MeSH
- kokain farmakologie MeSH
- kyselina valproová farmakologie MeSH
- lithium farmakologie MeSH
- mianserin analogy a deriváty farmakologie MeSH
- mirtazapin MeSH
- mitochondrie účinky léků enzymologie MeSH
- moklobemid farmakologie MeSH
- monoaminoxidasa účinky léků metabolismus MeSH
- morfoliny farmakologie MeSH
- mozková kůra cytologie MeSH
- olanzapin MeSH
- pargylin farmakologie MeSH
- prasata MeSH
- reboxetin MeSH
- techniky in vitro MeSH
- thiazepiny farmakologie MeSH
- venlafaxin hydrochlorid MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- amitriptylin MeSH
- antidepresiva MeSH
- antimanika MeSH
- benzodiazepiny MeSH
- citalopram MeSH
- cyklohexanoly MeSH
- desipramin MeSH
- fluoxetin MeSH
- imipramin MeSH
- inhibitory MAO MeSH
- iproniazid MeSH
- klorgylin MeSH
- kokain MeSH
- kyselina valproová MeSH
- lithium MeSH
- mianserin MeSH
- mirtazapin MeSH
- moklobemid MeSH
- monoaminoxidasa MeSH
- morfoliny MeSH
- olanzapin MeSH
- pargylin MeSH
- reboxetin MeSH
- thiazepiny MeSH
- tianeptine MeSH Prohlížeč
- venlafaxin hydrochlorid MeSH
OBJECTIVE: Monoamine oxidase (MAO), the enzyme responsible for metabolism of monoamine neurotransmitters, has an important role in the brain development and function, and MAO inhibitors have a range of potential therapeutic uses. We investigated systematically in vitro effects of pharmacologically different antidepressants and mood stabilizers on MAO activity. METHODS: Effects of drugs on the activity of MAO were measured in crude mitochondrial fraction isolated from cortex of pig brain, when radiolabeled serotonin (for MAO-A) or phenylethylamine (for MAO-B) was used as substrate. The several antidepressants and mood stabilizers were compared with effects of well known MAO inhibitors such as moclobemide, iproniazid, pargyline, and clorgyline. RESULTS: In general, the effect of tested drugs was found to be inhibitory. The half maximal inhibitory concentration, parameters of enzyme kinetic, and mechanism of inhibition were determined. MAO-A was inhibited by the following drugs: pargyline > clorgyline > iproniazid > fluoxetine > desipramine > amitriptyline > imipramine > citalopram > venlafaxine > reboxetine > olanzapine > mirtazapine > tianeptine > moclobemide, cocaine >> lithium, valproate. MAO-B was inhibited by the following drugs: pargyline > clorgyline > iproniazid > fluoxetine > venlafaxine > amitriptyline > olanzapine > citalopram > desipramine > reboxetine > imipramine > tianeptine > mirtazapine, cocaine >> moclobemide, lithium, valproate. The mechanism of inhibition of MAOs by several antidepressants was found various. CONCLUSIONS: It was concluded that MAO activity is acutely affected by pharmacologically different antidepressants at relatively high drug concentrations; this effect is inhibitory. There are differences both in inhibitory potency and in mechanism of inhibition between both several drugs and the two MAO isoforms. While MAO inhibition is not primary biochemical effect related to their therapeutic action, it can be supposed that decrease of MAO activity may be concerned in some effects of these drugs on serotonergic, noradrenergic, and dopaminergic neurotransmission.
In vitro effects of antidepressants and mood-stabilizing drugs on cell energy metabolism
In vitro effects of antipsychotics on mitochondrial respiration
