Inhibition of monoamine oxidase activity by antidepressants and mood stabilizers
Language English Country Sweden Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
21200377
PII: NEL310510A19
Knihovny.cz E-resources
- MeSH
- Affect drug effects MeSH
- Amitriptyline pharmacology MeSH
- Antidepressive Agents pharmacology MeSH
- Antimanic Agents pharmacology MeSH
- Benzodiazepines pharmacology MeSH
- Citalopram pharmacology MeSH
- Cyclohexanols pharmacology MeSH
- Desipramine pharmacology MeSH
- Fluoxetine pharmacology MeSH
- Imipramine pharmacology MeSH
- Monoamine Oxidase Inhibitors pharmacology MeSH
- Iproniazid pharmacology MeSH
- Clorgyline pharmacology MeSH
- Cocaine pharmacology MeSH
- Valproic Acid pharmacology MeSH
- Lithium pharmacology MeSH
- Mianserin analogs & derivatives pharmacology MeSH
- Mirtazapine MeSH
- Mitochondria drug effects enzymology MeSH
- Moclobemide pharmacology MeSH
- Monoamine Oxidase drug effects metabolism MeSH
- Morpholines pharmacology MeSH
- Cerebral Cortex cytology MeSH
- Olanzapine MeSH
- Pargyline pharmacology MeSH
- Swine MeSH
- Reboxetine MeSH
- In Vitro Techniques MeSH
- Thiazepines pharmacology MeSH
- Venlafaxine Hydrochloride MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Amitriptyline MeSH
- Antidepressive Agents MeSH
- Antimanic Agents MeSH
- Benzodiazepines MeSH
- Citalopram MeSH
- Cyclohexanols MeSH
- Desipramine MeSH
- Fluoxetine MeSH
- Imipramine MeSH
- Monoamine Oxidase Inhibitors MeSH
- Iproniazid MeSH
- Clorgyline MeSH
- Cocaine MeSH
- Valproic Acid MeSH
- Lithium MeSH
- Mianserin MeSH
- Mirtazapine MeSH
- Moclobemide MeSH
- Monoamine Oxidase MeSH
- Morpholines MeSH
- Olanzapine MeSH
- Pargyline MeSH
- Reboxetine MeSH
- Thiazepines MeSH
- tianeptine MeSH Browser
- Venlafaxine Hydrochloride 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
