Please use this identifier to cite or link to this item: https://doi.org/10.1016/0304-3940(91)90804-3
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dc.title1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity: Partial protection against striato-nigral dopamine depletion in C57BL/6J mice by cigarette smoke exposure and by β-naphthoflavone-pretreatment
dc.contributor.authorShahi, G.S.
dc.contributor.authorDas, N.P.
dc.contributor.authorMoochhala, S.M.
dc.date.accessioned2011-12-07T08:16:52Z
dc.date.available2011-12-07T08:16:52Z
dc.date.issued1991
dc.identifier.citationShahi, G.S., Das, N.P., Moochhala, S.M. (1991). 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity: Partial protection against striato-nigral dopamine depletion in C57BL/6J mice by cigarette smoke exposure and by β-naphthoflavone-pretreatment. Neuroscience Letters 127 (2) : 247-250. ScholarBank@NUS Repository. https://doi.org/10.1016/0304-3940(91)90804-3
dc.identifier.issn03043940
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/29723
dc.description.abstractThis study aimed to find a possible biochemical basis for the frequent epidemiological observation of a negative correlation between smoking and Parkinson's disease. The effects of cigarette smoke exposure and of β-naphthoflavone(BNF)-pretreatment on corpus striatal dopamine depletion by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were studied using the mouse MPTP model. Brain and hepatic monoamine oxidase (MAO) activity, hepatic cytochrome P450 content, BNF-inducible ethoxyresorufin O-dealkylase (EROD) activity and corpus striatal dopamine levels were measured. Cigarette smoke exposure partially protected against corpus striatal dopamine depletion by MPTP. This protection was associated with monoamine oxidase (MAO) inhibition in brain and liver, as well as with cytochrome P450 induction. BNF pretreatment also partially protected against MPTP-induced depletion of striatal dopamine. This was associated with a strong induction of cytochrome P450 but no inhibition of MAO activity. Our findings suggest that both MAO inhibition and cytochrome P450 induction may play a role in any biochemical protection afforded by cigarette smoke exposure against the development of Parkinson's disease.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/0304-3940(91)90804-3
dc.sourceScopus
dc.subject1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)
dc.subjectcigarette smoke
dc.subjectcytochrome P450
dc.subjectdopamine
dc.subjectmonoamine oxidase (MAO)
dc.typeArticle
dc.contributor.departmentPHARMACOLOGY
dc.contributor.departmentBIOCHEMISTRY
dc.contributor.departmentPHYSIOLOGY
dc.description.doi10.1016/0304-3940(91)90804-3
dc.description.sourcetitleNeuroscience Letters
dc.description.volume127
dc.description.issue2
dc.description.page247-250
dc.description.codenNELED
dc.identifier.isiutA1991FV37000024
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