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Article: Neuroprotective and neurorescuing effects of isoform-specific nitric oxide synthase inhibitors, nitric oxide scavenger, and antioxidant against beta-amyloid toxicity

TitleNeuroprotective and neurorescuing effects of isoform-specific nitric oxide synthase inhibitors, nitric oxide scavenger, and antioxidant against beta-amyloid toxicity
Authors
Issue Date2001
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 2001, v. 133 n. 7, p. 1114-1124 How to Cite?
Abstract1. Beta amyloid (Aβ) is implicated in Alzheimer's disease (AD). Aβ 1-42 (5, 10, or 20 μM) was able to increase NO release and decrease cellular viability in primary rat cortical mixed cultures. 2. L-NOARG and SMTC (both at 10 or 100 μM) - type I NOS inhibitors - reduced cellular NO release in the absence of Aβ 1-42. At 100 μM, both drugs decreased cell viability. 3. L-NIL (10 or 100 μM), and 1400W (1 or 5 μM) - type II NOS inhibitors - reduced NO release and improved viability when either drug was administered up to 4 h post Aβ 1-42 (10 μM) treatment. L-NOARG and SMTC (both at 10 or 100 μM) were only able to decrease NO release. Carboxy-PTIO or Trolox (both at 10 or 100 μM) - a NO scavenger and an antioxidant, respectively-increased viability when administered up to 1 h post Aβ 1-42 treatment. Either L-NIL (50 μM) or 1400W (3 μM) and Trolox (50 μM) showed synergistic actions. 4. Peroxynitrite (100 or 200 μM) reduced cell viability. Viabilities were improved by L-NIL (100 μM), 1400W (5 μM), carboxy-PTIO (10 or 100 μM), and Trolox (10 or 100 μM). 5. Hence, the data show that Aβ 1-42 induced NO release in neurons and glial cells, and that Aβ neurotoxicity is, at least in part, mediated by NO. NO concentration modulating compounds and antioxidant may have therapeutic importance in neurological disorders where oxidative stress is likely involved such as in AD.
Persistent Identifierhttp://hdl.handle.net/10722/171902
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLaw, Aen_US
dc.contributor.authorGauthier, Sen_US
dc.contributor.authorQuirion, Ren_US
dc.date.accessioned2012-10-30T06:18:19Z-
dc.date.available2012-10-30T06:18:19Z-
dc.date.issued2001en_US
dc.identifier.citationBritish Journal Of Pharmacology, 2001, v. 133 n. 7, p. 1114-1124en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/171902-
dc.description.abstract1. Beta amyloid (Aβ) is implicated in Alzheimer's disease (AD). Aβ 1-42 (5, 10, or 20 μM) was able to increase NO release and decrease cellular viability in primary rat cortical mixed cultures. 2. L-NOARG and SMTC (both at 10 or 100 μM) - type I NOS inhibitors - reduced cellular NO release in the absence of Aβ 1-42. At 100 μM, both drugs decreased cell viability. 3. L-NIL (10 or 100 μM), and 1400W (1 or 5 μM) - type II NOS inhibitors - reduced NO release and improved viability when either drug was administered up to 4 h post Aβ 1-42 (10 μM) treatment. L-NOARG and SMTC (both at 10 or 100 μM) were only able to decrease NO release. Carboxy-PTIO or Trolox (both at 10 or 100 μM) - a NO scavenger and an antioxidant, respectively-increased viability when administered up to 1 h post Aβ 1-42 treatment. Either L-NIL (50 μM) or 1400W (3 μM) and Trolox (50 μM) showed synergistic actions. 4. Peroxynitrite (100 or 200 μM) reduced cell viability. Viabilities were improved by L-NIL (100 μM), 1400W (5 μM), carboxy-PTIO (10 or 100 μM), and Trolox (10 or 100 μM). 5. Hence, the data show that Aβ 1-42 induced NO release in neurons and glial cells, and that Aβ neurotoxicity is, at least in part, mediated by NO. NO concentration modulating compounds and antioxidant may have therapeutic importance in neurological disorders where oxidative stress is likely involved such as in AD.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_US
dc.relation.ispartofBritish Journal of Pharmacologyen_US
dc.subject.meshAmyloid Beta-Peptides - Toxicityen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntioxidants - Pharmacologyen_US
dc.subject.meshBenzoates - Pharmacologyen_US
dc.subject.meshCell Survival - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCerebral Cortex - Cytology - Drug Effects - Metabolismen_US
dc.subject.meshChromans - Pharmacologyen_US
dc.subject.meshCitrulline - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshImidazoles - Pharmacologyen_US
dc.subject.meshIsoenzymes - Antagonists & Inhibitorsen_US
dc.subject.meshLysine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshNeuroprotective Agents - Pharmacologyen_US
dc.subject.meshNitrates - Pharmacologyen_US
dc.subject.meshNitric Oxide - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshNitric Oxide Synthase - Antagonists & Inhibitorsen_US
dc.subject.meshNitroarginine - Pharmacologyen_US
dc.subject.meshOxidants - Pharmacologyen_US
dc.subject.meshPeptide Fragments - Toxicityen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshThiourea - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshTime Factorsen_US
dc.titleNeuroprotective and neurorescuing effects of isoform-specific nitric oxide synthase inhibitors, nitric oxide scavenger, and antioxidant against beta-amyloid toxicityen_US
dc.typeArticleen_US
dc.identifier.emailLaw, A:acklaw@hku.hken_US
dc.identifier.authorityLaw, A=rp00262en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.bjp.0704179-
dc.identifier.pmid11487523-
dc.identifier.scopuseid_2-s2.0-0034883504en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034883504&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume133en_US
dc.identifier.issue7en_US
dc.identifier.spage1114en_US
dc.identifier.epage1124en_US
dc.identifier.isiWOS:000170427900022-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLaw, A=26323772800en_US
dc.identifier.scopusauthoridGauthier, S=7102604782en_US
dc.identifier.scopusauthoridQuirion, R=7202416940en_US

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