Linked Life Data

17689566

Source:http://linkedlifedata.com/resource/pubmed/id/17689566

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2007-8-24
pubmed:abstractText
To examine the interaction between nicotine and MPTP/MPP+ in the blood-brain barrier, cellular uptake of MPTP and MPP+ was studied in the presence of nicotine and several compounds, including MPTP/MPP+ analogs and a specific inhibitor of organic cation transporter (OCT) in an adult rat brain microvascular endothelial cell line (ARBEC). The kinetic properties of the uptake of MPTP, MPP+, and nicotine were also examined. In addition, a microdialysis study was performed to evaluate the in vivo effect of nicotine (i.p.) on extracellular levels of MPTP and MPP+ in the brain after intravenous administration of MPTP. The results showed that uptake of MPTP, MPP+, and nicotine was partly mediated by a carrier system that was sensitive to decynium22, a specific OCT inhibitor. RT-PCR showed the presence of OCT1 mRNA in ARBEC. Capacity for uptake of MPTP and nicotine was much higher than that for MPP+ (Km and Vm values of 10.94+/-1.44 microM and 0.049+/-0.007 pmol/mg s, respectively, for MPP+, compared to values of 35.75+/-0.85 microM and 40.95+/-3.56 pmol/mg s for MPTP and 25.29+/-6.44 microM and 51.15+/-14.18 pmol/mg s for nicotine). In addition, nicotine competitively inhibited the uptake of both MPTP and MPP+, with inhibition constants (Ki) of 328 microM and 210 microM, respectively. In vivo microdialysis results showed that nicotine significantly reduced brain extracellular levels of MPTP in the first 30 min (507.4+/-8.5 ng/ml vs. 637.9+/-30.8 ng/ml with and without nicotine pre-treatment, respectively), but did not have significant effect on those of MPP+. In conclusion, nicotine can inhibit in vitro cellular uptake and in vivo transfer of MPTP across the blood-brain barrier, which can be mediated by multiple pathways including OCT1.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
81
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
664-72
pubmed:meshHeading
pubmed-meshheading:17689566-1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, pubmed-meshheading:17689566-Algorithms, pubmed-meshheading:17689566-Animals, pubmed-meshheading:17689566-Blood-Brain Barrier, pubmed-meshheading:17689566-Brain, pubmed-meshheading:17689566-Cells, Cultured, pubmed-meshheading:17689566-Cotinine, pubmed-meshheading:17689566-Data Interpretation, Statistical, pubmed-meshheading:17689566-Dopamine Agents, pubmed-meshheading:17689566-Dopamine Antagonists, pubmed-meshheading:17689566-Endothelial Cells, pubmed-meshheading:17689566-Extracellular Space, pubmed-meshheading:17689566-MPTP Poisoning, pubmed-meshheading:17689566-Male, pubmed-meshheading:17689566-Microdialysis, pubmed-meshheading:17689566-Nicotine, pubmed-meshheading:17689566-Nicotinic Agonists, pubmed-meshheading:17689566-Nonlinear Dynamics, pubmed-meshheading:17689566-Rats, pubmed-meshheading:17689566-Rats, Wistar, pubmed-meshheading:17689566-Reverse Transcriptase Polymerase Chain Reaction
pubmed:year
2007
pubmed:articleTitle
Interaction between nicotine and MPTP/MPP+ in rat brain endothelial cells.
pubmed:affiliation
Department of Pharmacology, College of Medicine, National Taiwan University, and Department of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't