Inhibition of palmityl carnitine oxidation in rat liver mitochondria by tert-butyl hydroperoxide
Language English Country Czech Republic Media print-electronic
Document type Comparative Study, Journal Article, Research Support, Non-U.S. Gov't
PubMed
17465699
DOI
10.33549/physiolres.931198
PII: 1198
Knihovny.cz E-resources
- MeSH
- Hepatocytes cytology drug effects metabolism MeSH
- Liver cytology metabolism MeSH
- Rats MeSH
- Succinic Acid metabolism MeSH
- Fatty Acids metabolism MeSH
- Mitochondria drug effects metabolism MeSH
- NADP drug effects metabolism MeSH
- Oxidative Stress physiology MeSH
- Oxidants pharmacology MeSH
- Palmitoylcarnitine metabolism MeSH
- Rats, Wistar 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
- Comparative Study MeSH
- Names of Substances
- Succinic Acid MeSH
- Fatty Acids MeSH
- NADP MeSH
- Oxidants MeSH
- Palmitoylcarnitine MeSH
- tert-Butylhydroperoxide MeSH
Mitochondria as an energy generating cell device are very sensitive to oxidative damage. Our previous findings obtained in hepatocytes demonstrated that Complex I of the respiratory chain is more sensitive to oxidative damage than other respiratory chain complexes. We present additional data on isolated mitochondria showing that palmityl carnitine oxidation is strongly depressed at a low (200 microM) tert-butyl hydroperoxide (tBHP) concentration, while oxidation of the flavoprotein-dependent substrate-succinate is not affected and neither is ATP synthesis inhibited by tBHP. In the presence of tBHP, the respiratory control index for palmityl carnitine oxidation is strongly depressed, but when succinate is oxidized the respiratory control index remains unaffected. Our findings thus indicate that flavoprotein-dependent substrates could be an important nutritional factor for the regeneration process in the necrotic liver damaged by oxidative stress.
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