Tetraphenylphosphonium-selective electrode as a tool for evaluating mitochondrial permeability transition pore function in isolated rat hepatocytes
Language English Country Slovakia Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
17197730
Knihovny.cz E-resources
- MeSH
- Electrodes MeSH
- Hepatocytes drug effects metabolism MeSH
- Indicators and Reagents MeSH
- Rats MeSH
- Membrane Potential, Mitochondrial MeSH
- Onium Compounds MeSH
- Organophosphorus Compounds MeSH
- Mitochondrial Permeability Transition Pore MeSH
- Oxygen Consumption MeSH
- In Vitro Techniques MeSH
- tert-Butylhydroperoxide pharmacology MeSH
- Mitochondrial Membrane Transport Proteins metabolism MeSH
- Calcium pharmacology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Indicators and Reagents MeSH
- Onium Compounds MeSH
- Organophosphorus Compounds MeSH
- Mitochondrial Permeability Transition Pore MeSH
- tert-Butylhydroperoxide MeSH
- tetraphenylphosphonium MeSH Browser
- Mitochondrial Membrane Transport Proteins MeSH
- Calcium MeSH
The changes in mitochondrial membrane potential (Deltapsi(m)) were used as an indicator for evaluating the mitochondrial permeability transition pore (MPTP) function. We found that in situ mitochondria in digitonin-permeabilized hepatocytes were coupled and responded to the addition of substrates, inhibitors and uncouplers. Ca(2+)-induced Deltapsi(m) dissipation was caused by MPTP opening because this process was inhibited by cyclosporin A. MPTP opening was enhanced by the pro-oxidant tert-butyl hydroperoxide.
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