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The impact of complex II (succinate:ubiquinone oxidoreductase) on the mitochondrial production of reactive oxygen species (ROS) has been underestimated for a long time. However, recent studies with intact mitochondria revealed that complex II can be a significant source of ROS. Using submitochondrial particles from bovine heart mitochondria as a system that allows the precise setting of substrate concentrations we could show that mammalian complex II produces ROS at subsaturating succinate concentrations in the presence of Q-site inhibitors like atpenin A5 or when a further downstream block of the respiratory chain occurred. Upon inhibition of the ubiquinone reductase activity, complex II produced about 75

作者:Ilka, Siebels;Stefan, Dr?se

来源:Biochimica et biophysica acta 2013 年 1827卷 10期

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作者:
Ilka, Siebels;Stefan, Dr?se
来源:
Biochimica et biophysica acta 2013 年 1827卷 10期
标签:
2-n-decyl-quinazolin-4-yl-amine 2-thenoyltrifluoroacetone Atpenin A5 Complex II DQA Dicarboxylates FAD HRP Mitochondria NAD(+)/NADH Q Q(o) site Q-site QFR RET ROS Reactive oxygen species (ROS) SMP SOD SQR Succinate:ubiquinone oxidoreductase TTFA flavin adenine dinucleotide horseradish peroxidase oxidized/reduced from of nicotinamide adenine dinucleotide quinol:fumarate oxidoreductases reactive oxygen species reverse electron transfer submitochondrial particles succinate:quinone oxidoreductases superoxide dismutase ubiquinol oxidation site of cytochrome bc(1) complex (complex III) ubiquinone ubiquinone reduction site of complex II
The impact of complex II (succinate:ubiquinone oxidoreductase) on the mitochondrial production of reactive oxygen species (ROS) has been underestimated for a long time. However, recent studies with intact mitochondria revealed that complex II can be a significant source of ROS. Using submitochondrial particles from bovine heart mitochondria as a system that allows the precise setting of substrate concentrations we could show that mammalian complex II produces ROS at subsaturating succinate concentrations in the presence of Q-site inhibitors like atpenin A5 or when a further downstream block of the respiratory chain occurred. Upon inhibition of the ubiquinone reductase activity, complex II produced about 75