2004
DOI: 10.1074/jbc.m310341200
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Abstract: Mitochondrial respiratory chain complexes I and III have been shown to produce superoxide but the exact contribution and localization of individual sites have remained unclear. We approached this question investigating the effects of oxygen, substrates, inhibitors, and of the NAD ؉ /NADH redox couple on H 2 O 2 and superoxide production of isolated mitochondria from rat and human brain. Although rat brain mitochondria in the presence of glutamate؉malate alone do generate only small amounts of H 2 O 2 (0.04 ؎ 0… Show more

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Cited by 460 publications
(339 citation statements)
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“…Elevated brain tissue O 2 tension could, however, directly increase the rate of existing redox protein-mediated production of both nitric oxide and superoxide. For example, several studies indicate that mitochondrial superoxide production is directly related to [O 2 ] (between normal pO 2 up to 100% O 2 saturation) [38,39]. Although reports indicate that severe hypoxia can also stimulate superoxide production [40][41][42], promotion of superoxide generation by high brain tissue pO 2 is a more likely explanation for the increased 3-nitrotyrosine immunoreactivity in the hyperoxic-resuscitated animals.…”
Section: Discussionmentioning
confidence: 99%
“…Elevated brain tissue O 2 tension could, however, directly increase the rate of existing redox protein-mediated production of both nitric oxide and superoxide. For example, several studies indicate that mitochondrial superoxide production is directly related to [O 2 ] (between normal pO 2 up to 100% O 2 saturation) [38,39]. Although reports indicate that severe hypoxia can also stimulate superoxide production [40][41][42], promotion of superoxide generation by high brain tissue pO 2 is a more likely explanation for the increased 3-nitrotyrosine immunoreactivity in the hyperoxic-resuscitated animals.…”
Section: Discussionmentioning
confidence: 99%
“…Under pathological conditions (e.g., in ischemia-reperfusion injury, in inflammation, etc. ), this is highly relevant, because interruption of electron flow through mitochondrial respiratory chain (e.g., by cytochrome c release, modification of electron transport proteins) would considerably increase superoxide generation by all relevant single electron donor sites of damaged mitochondria, given enough oxygen is available (32,40,53). Thus, pathological conditions strongly facilitating ROS-mediated oxidative damage of proteins, lipids, and DNA would require an effective elimination of damaged proteins but also damaged mitochondria by the quality control machinery discussed above (section ''Mitochondrial Quality Control''), in order to avoid further cellular damage.…”
Section: Mitochondrial Formation Of Ros and Neurodegenerationmentioning
confidence: 99%
“…Complex I impairment seems to be important for the pathogenesis of PD since exposure to inhibitors of this complex, such as MPP + or rotenone, reproduces the clinical symptoms of PD observed in human subjects [105,106].Complex I is the largest of the electron transport chain (ETC) complexes, consisting of 46 subunits, 7 of which are encoded by mitochondrial DNA (mtDNA) [107]and the major site of superoxide production in the ETC [108]. Complex I activity and expression are decreased in the SN[109Ͳ112] and cortex [113] of PD patients to a greater extent than would be expected from normal aging [107].…”
Section: Sources Of Oxidative Damage In Pdmentioning
confidence: 99%