Inhibition of palmityl carnitine oxidation in rat liver mitochondria by tert-butyl hydroperoxide
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
PubMed
17465699
DOI
10.33549/physiolres.931198
PII: 1198
Knihovny.cz E-zdroje
- MeSH
- hepatocyty cytologie účinky léků metabolismus MeSH
- játra cytologie metabolismus MeSH
- krysa rodu Rattus MeSH
- kyselina jantarová metabolismus MeSH
- mastné kyseliny metabolismus MeSH
- mitochondrie účinky léků metabolismus MeSH
- NADP účinky léků metabolismus MeSH
- oxidační stres fyziologie MeSH
- oxidancia farmakologie MeSH
- palmitoyl karnitin metabolismus MeSH
- potkani Wistar MeSH
- terc-butylhydroperoxid farmakologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- kyselina jantarová MeSH
- mastné kyseliny MeSH
- NADP MeSH
- oxidancia MeSH
- palmitoyl karnitin MeSH
- terc-butylhydroperoxid 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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