R-(-)-deprenyl inhibits monocytic THP-1 cell neurotoxicity independently of monoamine oxidase inhibition
Identifieur interne : 000C51 ( PascalFrancis/Corpus ); précédent : 000C50; suivant : 000C52R-(-)-deprenyl inhibits monocytic THP-1 cell neurotoxicity independently of monoamine oxidase inhibition
Auteurs : Andis Klegeris ; Patrick L. McgeerSource :
- Experimental neurology : (Print) [ 0014-4886 ] ; 2000.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson's disease. This action could be mediated by inhibition of MAO-B but there may also be unrelated mechanisms. Direct neuroprotective and antiapoptotic actions of deprenyl have previously been observed in vitro. Here we describe an antineurotoxic action of deprenyl which is independent of direct neuronal effects. We employed a previously described assay in which human neuroblastoma SH-SY5Y cells are exposed to cell-free supernatants of stimulated human monocytic THP-1 cells. Deprenyl reduced the secretion of neurotoxic products by such stimulated cells in a concentration-dependent manner, while the MAO inhibitors iproniazid, isocarboxazid, nialamide, tranylcypromine, phenelzine, and clorgyline were without effect. No antineurotoxic action was observed when deprenyl was added directly to SH-SY5Y cells. Messenger RNAs for MAO-A and MAO-B were not detected in THP-1 cells by reverse transcriptase-polymerase chain reaction analysis of total RNA extracts. Such mRNAs were easily detected in extracts of SH-SY5Y cells under comparable conditions. MAO enzymatic activity was also undetectable in THP-1 cell lysates, while it was readily observed in SH-SY5Y cells. It was concluded that the effect of deprenyl on THP-1 cells was not mediated by MAO and that deprenyl itself was not protecting neurons. These data suggest that deprenyl may have utility in neurodegenerative diseases due to its antineurotoxic actions.
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pA |
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Format Inist (serveur)
NO : | PASCAL 01-0095078 INIST |
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ET : | R-(-)-deprenyl inhibits monocytic THP-1 cell neurotoxicity independently of monoamine oxidase inhibition |
AU : | KLEGERIS (Andis); MCGEER (Patrick L.) |
AF : | Kinsmen Laboratory of Neurological Research, University of British Columbia/Vancouver, British Columbia V6T 1Z3/Canada (1 aut., 2 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Experimental neurology : (Print); ISSN 0014-4886; Coden EXNEAC; Etats-Unis; Da. 2000; Vol. 166; No. 2; Pp. 458-464; Bibl. 46 ref. |
LA : | Anglais |
EA : | R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson's disease. This action could be mediated by inhibition of MAO-B but there may also be unrelated mechanisms. Direct neuroprotective and antiapoptotic actions of deprenyl have previously been observed in vitro. Here we describe an antineurotoxic action of deprenyl which is independent of direct neuronal effects. We employed a previously described assay in which human neuroblastoma SH-SY5Y cells are exposed to cell-free supernatants of stimulated human monocytic THP-1 cells. Deprenyl reduced the secretion of neurotoxic products by such stimulated cells in a concentration-dependent manner, while the MAO inhibitors iproniazid, isocarboxazid, nialamide, tranylcypromine, phenelzine, and clorgyline were without effect. No antineurotoxic action was observed when deprenyl was added directly to SH-SY5Y cells. Messenger RNAs for MAO-A and MAO-B were not detected in THP-1 cells by reverse transcriptase-polymerase chain reaction analysis of total RNA extracts. Such mRNAs were easily detected in extracts of SH-SY5Y cells under comparable conditions. MAO enzymatic activity was also undetectable in THP-1 cell lysates, while it was readily observed in SH-SY5Y cells. It was concluded that the effect of deprenyl on THP-1 cells was not mediated by MAO and that deprenyl itself was not protecting neurons. These data suggest that deprenyl may have utility in neurodegenerative diseases due to its antineurotoxic actions. |
CC : | 002B02B06 |
FD : | Parkinson maladie; Sélégiline; Phénelzine; IMAO B; Neuroprotecteur; Mécanisme action; Homme; RNA-directed DNA polymerase; Antiparkinsonien; Antidépresseur |
FG : | Nucleotidyltransferases; Transferases; Enzyme; Système nerveux pathologie; Système nerveux central pathologie; Maladie dégénérative; Extrapyramidal syndrome; Encéphale pathologie; Tumeur maligne; Système nerveux sympathique pathologie |
ED : | Parkinson disease; Selegiline; Phenelzine; MAO B inhibitor; Neuroprotective agent; Mechanism of action; Human; RNA-directed DNA polymerase; Antiparkinson agent; Antidepressant agent |
EG : | Nucleotidyltransferases; Transferases; Enzyme; Nervous system diseases; Central nervous system disease; Degenerative disease; Extrapyramidal syndrome; Cerebral disorder; Malignant tumor; Autonomic neuropathy |
SD : | Parkinson enfermedad; Selegilina; Fenelzina; IMOA B; Neuroprotector; Mecanismo acción; Hombre; RNA-directed DNA polymerase; Antiparkinsoniano; Antidepresor |
LO : | INIST-9181.354000093425030260 |
ID : | 01-0095078 |
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Pascal:01-0095078Le document en format XML
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<front><div type="abstract" xml:lang="en">R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson's disease. This action could be mediated by inhibition of MAO-B but there may also be unrelated mechanisms. Direct neuroprotective and antiapoptotic actions of deprenyl have previously been observed in vitro. Here we describe an antineurotoxic action of deprenyl which is independent of direct neuronal effects. We employed a previously described assay in which human neuroblastoma SH-SY5Y cells are exposed to cell-free supernatants of stimulated human monocytic THP-1 cells. Deprenyl reduced the secretion of neurotoxic products by such stimulated cells in a concentration-dependent manner, while the MAO inhibitors iproniazid, isocarboxazid, nialamide, tranylcypromine, phenelzine, and clorgyline were without effect. No antineurotoxic action was observed when deprenyl was added directly to SH-SY5Y cells. Messenger RNAs for MAO-A and MAO-B were not detected in THP-1 cells by reverse transcriptase-polymerase chain reaction analysis of total RNA extracts. Such mRNAs were easily detected in extracts of SH-SY5Y cells under comparable conditions. MAO enzymatic activity was also undetectable in THP-1 cell lysates, while it was readily observed in SH-SY5Y cells. It was concluded that the effect of deprenyl on THP-1 cells was not mediated by MAO and that deprenyl itself was not protecting neurons. These data suggest that deprenyl may have utility in neurodegenerative diseases due to its antineurotoxic actions.</div>
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<ET>R-(-)-deprenyl inhibits monocytic THP-1 cell neurotoxicity independently of monoamine oxidase inhibition</ET>
<AU>KLEGERIS (Andis); MCGEER (Patrick L.)</AU>
<AF>Kinsmen Laboratory of Neurological Research, University of British Columbia/Vancouver, British Columbia V6T 1Z3/Canada (1 aut., 2 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
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<EA>R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson's disease. This action could be mediated by inhibition of MAO-B but there may also be unrelated mechanisms. Direct neuroprotective and antiapoptotic actions of deprenyl have previously been observed in vitro. Here we describe an antineurotoxic action of deprenyl which is independent of direct neuronal effects. We employed a previously described assay in which human neuroblastoma SH-SY5Y cells are exposed to cell-free supernatants of stimulated human monocytic THP-1 cells. Deprenyl reduced the secretion of neurotoxic products by such stimulated cells in a concentration-dependent manner, while the MAO inhibitors iproniazid, isocarboxazid, nialamide, tranylcypromine, phenelzine, and clorgyline were without effect. No antineurotoxic action was observed when deprenyl was added directly to SH-SY5Y cells. Messenger RNAs for MAO-A and MAO-B were not detected in THP-1 cells by reverse transcriptase-polymerase chain reaction analysis of total RNA extracts. Such mRNAs were easily detected in extracts of SH-SY5Y cells under comparable conditions. MAO enzymatic activity was also undetectable in THP-1 cell lysates, while it was readily observed in SH-SY5Y cells. It was concluded that the effect of deprenyl on THP-1 cells was not mediated by MAO and that deprenyl itself was not protecting neurons. These data suggest that deprenyl may have utility in neurodegenerative diseases due to its antineurotoxic actions.</EA>
<CC>002B02B06</CC>
<FD>Parkinson maladie; Sélégiline; Phénelzine; IMAO B; Neuroprotecteur; Mécanisme action; Homme; RNA-directed DNA polymerase; Antiparkinsonien; Antidépresseur</FD>
<FG>Nucleotidyltransferases; Transferases; Enzyme; Système nerveux pathologie; Système nerveux central pathologie; Maladie dégénérative; Extrapyramidal syndrome; Encéphale pathologie; Tumeur maligne; Système nerveux sympathique pathologie</FG>
<ED>Parkinson disease; Selegiline; Phenelzine; MAO B inhibitor; Neuroprotective agent; Mechanism of action; Human; RNA-directed DNA polymerase; Antiparkinson agent; Antidepressant agent</ED>
<EG>Nucleotidyltransferases; Transferases; Enzyme; Nervous system diseases; Central nervous system disease; Degenerative disease; Extrapyramidal syndrome; Cerebral disorder; Malignant tumor; Autonomic neuropathy</EG>
<SD>Parkinson enfermedad; Selegilina; Fenelzina; IMOA B; Neuroprotector; Mecanismo acción; Hombre; RNA-directed DNA polymerase; Antiparkinsoniano; Antidepresor</SD>
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