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Article: A novel effect of an opioid receptor antagonist, naloxone, on the production of reactive oxygen species by microglia: A study by electron paramagnetic resonance spectroscopy

TitleA novel effect of an opioid receptor antagonist, naloxone, on the production of reactive oxygen species by microglia: A study by electron paramagnetic resonance spectroscopy
Authors
Issue Date2000
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainres
Citation
Brain Research, 2000, v. 854 n. 1-2, p. 224-229 How to Cite?
AbstractMicroglia as the first line of defensive cells in the brain produce free radicals including superoxide and nitric oxide (NO), contributing to neurodegeneration. An opioid receptor antagonist, naloxone, has been considered pharmacologically beneficial to endotoxin shock, experimental cerebral ischemia, and spinal cord injury. However, the mechanisms underlying these beneficial effects of naloxone are still not clear. This study explores the effects of naloxone on the production of superoxide and NO by the murine microglial cell line, BV2, stimulated with lipopolysaccharide (LPS) as measured by electron paramagnetic resonance (EPR). The production of superoxide triggered by phobol-12-myristate-13-acetate (PMA) resulted in superoxide dismutase (SOD)-inhibitable, catalase-uninhibitable 5,5-dimethyl- 1-pyrroline N-oxide (DMPO) hydroxyl radical adduct formation. LPS enhanced the production of superoxide and triggered the formation of non-heme iron- nitrosyl complex. Cells pre-treated with naloxone showed significant reduction of superoxide production by 35%. However, it could not significantly reduce the formation of non-heme iron-nitrosyl complex and nitrite. Taken together, the results expand our understanding of the neuroprotective effects of naloxone as it decreases superoxide production by microglia. (C) 2000 Elsevier Science B.V.
Persistent Identifierhttp://hdl.handle.net/10722/149586
ISSN
2015 Impact Factor: 2.561
2015 SCImago Journal Rankings: 1.351
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChang, RCCen_US
dc.contributor.authorRota, Cen_US
dc.contributor.authorGlover, REen_US
dc.contributor.authorMason, RPen_US
dc.contributor.authorHong, JSen_US
dc.date.accessioned2012-06-26T05:55:35Z-
dc.date.available2012-06-26T05:55:35Z-
dc.date.issued2000en_US
dc.identifier.citationBrain Research, 2000, v. 854 n. 1-2, p. 224-229en_US
dc.identifier.issn0006-8993en_US
dc.identifier.urihttp://hdl.handle.net/10722/149586-
dc.description.abstractMicroglia as the first line of defensive cells in the brain produce free radicals including superoxide and nitric oxide (NO), contributing to neurodegeneration. An opioid receptor antagonist, naloxone, has been considered pharmacologically beneficial to endotoxin shock, experimental cerebral ischemia, and spinal cord injury. However, the mechanisms underlying these beneficial effects of naloxone are still not clear. This study explores the effects of naloxone on the production of superoxide and NO by the murine microglial cell line, BV2, stimulated with lipopolysaccharide (LPS) as measured by electron paramagnetic resonance (EPR). The production of superoxide triggered by phobol-12-myristate-13-acetate (PMA) resulted in superoxide dismutase (SOD)-inhibitable, catalase-uninhibitable 5,5-dimethyl- 1-pyrroline N-oxide (DMPO) hydroxyl radical adduct formation. LPS enhanced the production of superoxide and triggered the formation of non-heme iron- nitrosyl complex. Cells pre-treated with naloxone showed significant reduction of superoxide production by 35%. However, it could not significantly reduce the formation of non-heme iron-nitrosyl complex and nitrite. Taken together, the results expand our understanding of the neuroprotective effects of naloxone as it decreases superoxide production by microglia. (C) 2000 Elsevier Science B.V.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainresen_US
dc.relation.ispartofBrain Researchen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCyclic N-Oxides - Metabolismen_US
dc.subject.meshElectron Spin Resonance Spectroscopyen_US
dc.subject.meshHydroxyl Radical - Metabolismen_US
dc.subject.meshIron - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshLipopolysaccharides - Pharmacologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMicroglia - Metabolismen_US
dc.subject.meshNaloxone - Pharmacologyen_US
dc.subject.meshNarcotic Antagonists - Pharmacologyen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshNitrogen Oxides - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshReactive Oxygen Species - Metabolismen_US
dc.subject.meshReceptors, Opioid - Antagonists & Inhibitorsen_US
dc.subject.meshSuperoxides - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshTetradecanoylphorbol Acetate - Pharmacologyen_US
dc.titleA novel effect of an opioid receptor antagonist, naloxone, on the production of reactive oxygen species by microglia: A study by electron paramagnetic resonance spectroscopyen_US
dc.typeArticleen_US
dc.identifier.emailChang, RCC:rccchang@hkucc.hku.hken_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0006-8993(99)02267-2en_US
dc.identifier.pmid10784126-
dc.identifier.scopuseid_2-s2.0-0033978959en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033978959&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume854en_US
dc.identifier.issue1-2en_US
dc.identifier.spage224en_US
dc.identifier.epage229en_US
dc.identifier.isiWOS:000085122300028-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridChang, RCC=7403713410en_US
dc.identifier.scopusauthoridRota, C=7004049630en_US
dc.identifier.scopusauthoridGlover, RE=7005630933en_US
dc.identifier.scopusauthoridMason, RP=35372107900en_US
dc.identifier.scopusauthoridHong, JS=34770185100en_US

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