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Inhibition of glycerophosphate-dependent H2O2 generation in brown fat mitochondria by idebenone
Rauchová H, Vrbacký M, Bergamini C, Fato R, Lenaz G, Houstek J, Drahota Z.
Language English Country United States
- MeSH
- Antioxidants pharmacology MeSH
- Benzoquinones pharmacology MeSH
- Ferricyanides pharmacology MeSH
- Financing, Organized MeSH
- Glycerophosphates metabolism MeSH
- Adipose Tissue, Brown metabolism ultrastructure MeSH
- Cricetinae MeSH
- Mesocricetus MeSH
- Mitochondria metabolism drug effects MeSH
- Hydrogen Peroxide metabolism MeSH
- Reactive Oxygen Species MeSH
- Free Radical Scavengers MeSH
- Oxygen Consumption drug effects MeSH
- Succinates metabolism MeSH
- Ubiquinone metabolism MeSH
- Animals MeSH
- Check Tag
- Cricetinae MeSH
- Male MeSH
- Animals MeSH
The established protective effect of coenzyme Q (CoQ) analogs is dependent on the location of reactive oxygen species (ROS) generation. One of these analogs--idebenone (hydroxydecyl-ubiquinone) is used as an antioxidative therapeutic drug. We tested its scavenging effect on the glycerophosphate (GP)-dependent ROS production as this enzyme was shown as a new site in the mitochondrial respiratory chain where ROS can be generated. We observed that idebenone inhibits both GP- and succinate-dependent ROS production. Idebenone and CoQ1 were found to be more efficient in the scavenging activity (IC50: 0.052 and 0.075 microM, respectively) than CoQ3 (IC50: 45.8 microM). Idebenone also inhibited ferricyanide (FeCN)-activated, GP-dependent ROS production. Our data thus extend previous findings on the scavenging effect of idebenone and show that it can also eliminate GP-dependent ROS generation.
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- $a The established protective effect of coenzyme Q (CoQ) analogs is dependent on the location of reactive oxygen species (ROS) generation. One of these analogs--idebenone (hydroxydecyl-ubiquinone) is used as an antioxidative therapeutic drug. We tested its scavenging effect on the glycerophosphate (GP)-dependent ROS production as this enzyme was shown as a new site in the mitochondrial respiratory chain where ROS can be generated. We observed that idebenone inhibits both GP- and succinate-dependent ROS production. Idebenone and CoQ1 were found to be more efficient in the scavenging activity (IC50: 0.052 and 0.075 microM, respectively) than CoQ3 (IC50: 45.8 microM). Idebenone also inhibited ferricyanide (FeCN)-activated, GP-dependent ROS production. Our data thus extend previous findings on the scavenging effect of idebenone and show that it can also eliminate GP-dependent ROS generation.
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