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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.
Jazyk angličtina Země Spojené státy americké
NLK
ScienceDirect (archiv)
od 1993-01-01 do 2009-12-31
- MeSH
- antioxidancia farmakologie MeSH
- benzochinony farmakologie MeSH
- ferrikyanidy farmakologie MeSH
- financování organizované MeSH
- glycerolfosfáty metabolismus MeSH
- hnědá tuková tkáň metabolismus ultrastruktura MeSH
- křečci praví MeSH
- křeček rodu Mesocricetus MeSH
- mitochondrie metabolismus účinky léků MeSH
- peroxid vodíku metabolismus MeSH
- reaktivní formy kyslíku MeSH
- scavengery volných radikálů MeSH
- spotřeba kyslíku účinky léků MeSH
- sukcináty metabolismus MeSH
- ubichinon metabolismus MeSH
- zvířata MeSH
- Check Tag
- křečci praví MeSH
- mužské pohlaví MeSH
- zvířata 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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