Production of superoxide radicals and hydrogen peroxide by NADH-ubiquinone reductase and ubiquinol-cytochrome c reductase from beef-heart mitochondria

Cadenas, Enrique; Boveris, A; Ragan, C I; Stoppani, A. O. M.

doi:10.1016/0003-9861(77)90035-2

Cited by 793 publications

(381 citation statements)

References 30 publications

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“…In another study (17), water-soluble CoQ homologs used as electron acceptors from isolated Complex I stimulated H 2 O 2 production; the rate of H 2 O 2 production was partly inhibited by rotenone, indicating that water-soluble quinones react with oxygen when reduced at sites both upstream and downstream of the rotenone block. The one-electron donor to oxygen in Complex I is a nonphysiological hydrophilic site (11) that reduces several quinones to the corresponding semiquinone forms, which are unstable and reduce oxygen to superoxide.…”

Section: Complex Imentioning

confidence: 93%

The Mitochondrial Production of Reactive Oxygen Species: Mechanisms and Implications in Human Pathology

2001

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SummaryMitochondria are major sources of reactive oxygen species (ROS); the main sites of superoxide radical production in the respiratory chain are Complexes III and I; however, other mitochondrial enzymes, such as Complex II, glycerol-1-phosphate dehydrogenase, and dihydroorotate dehydrogenase, are also involved in production of ROS. ROS appear to be released both in the matrix and in the intermembrane space; however, their appearance outside the mitochondria may not be physiologically relevant. ROS production is increased in State 4 and in all conditions when the respiratory components are substantially in the reduced form. Accordingly, defects inducing decrease of electron transfer in the respiratory chain, as in many pathological conditions, are bound to enhance ROS production.

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Section: Complex Imentioning

confidence: 93%

The Mitochondrial Production of Reactive Oxygen Species: Mechanisms and Implications in Human Pathology

2001

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“…2 is considered the stoichiometric precursor of mitochondrial H 2 O 2 (24-27 ) during ubisemiquinone autoxidation (reaction 2) (13,20,26,27 ) and, secondarily, as a by-product of NADH-dehydrogenas e activity (28). O !…”

Section: Mitochondrial Generation Of H 2 Omentioning

confidence: 99%

Mitochondrial Production of Hydrogen Peroxide Regulation by Nitric Oxide and the Role of Ubisemiquinone

Boveris

Cadenas

2000

IUBMB Life

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“…Rotenone inhibition of hydrogen peroxide production diminishes in proportion to the extent of NADH available to reduce complex I in either isolated mitochondrial preparations or substrate-respiring cells (32)(33)(34). 2 Given that Bcl-2 expression limited the effect of rotenone on the production of hydrogen peroxide production (Fig.…”

Section: Bcl-2 Expression Increases Basal Levels Of Hydrogen Peroxidementioning

confidence: 99%

Bcl-2 and Mitochondrial Oxygen Radicals

Esposti

Hatzinisiriou

McLennan

et al. 1999

Journal of Biological Chemistry

161

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Investigations into the capacity of the Bcl-2 protein to prevent apoptosis have targeted mitochondria as key sites of the preventative action accorded by Bcl-2 to cells. Using novel approaches with fluorescence probes and autofluorescence detection of endogenous NAD(P)H, we have examined the effects of expressing Bcl-2 in the Bcl-2 negative Burkitt's lymphoma cell line Daudi. We evaluated for the first time the effect of Bcl-2 expression on the intracellular distribution and production of hydrogen peroxide, under basal conditions and after treatment with apoptosis inducing agents, ceramide analogs and tumor necrosis factor (TNF)-␣. Increased availability of mitochondrial NAD(P)H was detected in Bcl-2-expressing cells and was correlated with an increased constitutive mitochondrial production of hydrogen peroxide. Although production of hydrogen peroxide was increased by either C 6 -ceramide or TNF-␣ in Bcl-2 negative Daudi cells commensurate with the early phases of apoptosis, this increase did not occur in Bcl-2-expressing cells. Thus, Bcl-2 appears to allow cells to adapt to an increased state of oxidative stress, fortifying the cellular anti-oxidant defenses and counteracting the radical overproduction imposed by different cell death stimuli. Furthermore, we report altered cytological features of mitochondria during the early phases of apoptosis induced by C 6 -ceramide and TNF-␣. In particular, mitochondria changed in appearance, clustering in the perinuclear region and Bcl-2 expression prevented these changes from occurring.

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Production of superoxide radicals and hydrogen peroxide by NADH-ubiquinone reductase and ubiquinol-cytochrome c reductase from beef-heart mitochondria

Cited by 793 publications

References 30 publications

The Mitochondrial Production of Reactive Oxygen Species: Mechanisms and Implications in Human Pathology

The Mitochondrial Production of Reactive Oxygen Species: Mechanisms and Implications in Human Pathology

Mitochondrial Production of Hydrogen Peroxide Regulation by Nitric Oxide and the Role of Ubisemiquinone

Bcl-2 and Mitochondrial Oxygen Radicals

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