Peroxidative damage of mitochondrial respiration is substrate-dependent
Language English Country Czech Republic Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
19093725
DOI
10.33549/physiolres.931635
PII: 1635
Knihovny.cz E-resources
- MeSH
- Cell Respiration MeSH
- Mitochondria, Liver metabolism MeSH
- Rats MeSH
- Glutamic Acid metabolism MeSH
- Succinic Acid metabolism MeSH
- Pyruvic Acid metabolism MeSH
- Ketoglutaric Acids metabolism MeSH
- Membrane Potential, Mitochondrial MeSH
- Oxidative Stress * MeSH
- Palmitoylcarnitine metabolism MeSH
- Rats, Wistar MeSH
- Oxygen Consumption MeSH
- tert-Butylhydroperoxide pharmacology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Glutamic Acid MeSH
- Succinic Acid MeSH
- Pyruvic Acid MeSH
- Ketoglutaric Acids MeSH
- Palmitoylcarnitine MeSH
- tert-Butylhydroperoxide MeSH
The concentration-dependence of tert-butyl hydroperoxide (BHP) inhibitory effect on oxygen consumption in isolated rat liver mitochondria was measured in the presence of various respiratory substrates. Strong inhibitory effect at low concentrations of BHP (15-30 microM) was found for oxoglutarate and palmitoyl carnitine oxidation. Pyruvate and glutamate oxidation was inhibited at higher concentrations of BHP (100-200 microM). Succinate oxidation was not affected even at 3.3 mM BHP. Determination of mitochondrial membrane potential has shown that in the presence of NADH-dependent substrates the membrane potential was dissipated by BHP but was completely restored after addition of succinate. Our data thus indicate that beside peroxidative damage of complex I also various mitochondrial NADH-dependent dehydrogenases are inhibited, but to a different extent and with different kinetics. Our data also show that succinate could be an important nutritional substrate protecting hepatocytes during peroxidative damage.
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