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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1-3
|
| pubmed:dateCreated |
1993-4-12
|
| pubmed:abstractText |
Hydrogen peroxide, a physiological metabolite, and a variety of other potentially toxic prooxidants, cause oxidation of the pyridine nucleotides NAD(P)H to NAD(P)+ in mitochondria. In Ca(2+)-loaded mitochondria NAD+ thus formed is hydrolyzed to ADP-ribose and nicotinamide. Subsequent to NAD+ hydrolysis, Ca2+ is released from the organelles via a specific pathway which is sensitive to several inhibitors, among them cyclosporine A and some of its derivatives. The release is probably regulated by peptidyl-prolyl cis-trans isomerase. Prolonged stimulation of the release pathway by certain prooxidants followed by re-uptake and release of Ca2+ (Ca2+ 'cycling') leads to collapse of the mitochondrial membrane potential, and is detrimental to the organelles. Excessive Ca2+ 'cycling' is likely to be a basis for the cell toxicity of some prooxidants. On the other hand, the toxicity of inhibitors of the prooxidant-induced Ca2+ release pathway may be due to long-term Ca2+ overloading of mitochondria.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Apr
|
| pubmed:issn |
0378-4274
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
67
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
119-27
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading | |
| pubmed:year |
1993
|
| pubmed:articleTitle |
Mitochondrial calcium release induced by prooxidants.
|
| pubmed:affiliation |
Laboratorium für BIochemie I, ETH Zürich Schweiz.
|
| pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
|