Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1996-3-5
pubmed:abstractText
The effect of the parkinsonian neurotoxin, 1-methyl-4-phenylpyridinium (MPP+) together with nitric oxide donors on mitochondrial calcium homeostasis and membrane potential was investigated. Simultaneous exposure of calcium-loaded mitochondria to MPP+ and nitric oxide donors led to Cyclosporin A-sensitive mitochondrial calcium efflux and depolarisation. When MPP+ was replaced with the respiratory inhibitor rotenone, mitochondrial calcium efflux and depolarisation also occurred. As both MPP+ and rotenone induce mitochondrial superoxide formation, the possibility that calcium efflux and depolarisation were due to peroxynitrite formation from reaction of superoxide with nitric oxide was investigated. It was shown that simultaneous exposure of mitochondrial membranes to nitric oxide donors and rotenone led to peroxynitrite formation. The possible roles of nitric oxide, peroxynitrite, mitochondrial depolarisation, and calcium efflux in MPP+ toxicity are discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0006-2952
pubmed:author
pubmed:issnType
Print
pubmed:day
9
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
267-73
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Exposure to the parkinsonian neurotoxin 1-methyl-4-phenylpyridinium (MPP+) and nitric oxide simultaneously causes cyclosporin A-sensitive mitochondrial calcium efflux and depolarisation.
pubmed:affiliation
Department of Biochemistry, University of Otago, Dunedin, New Zealand.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't