• Publications
  • Influence
Assessing mitochondrial dysfunction in cells
TLDR
Measurement of both respiration and potential during appropriate titrations enables the identification of the primary sites of effectors and the distribution of control, allowing deeper quantitative analyses, as discussed in the present review. Expand
Topology of Superoxide Production from Different Sites in the Mitochondrial Electron Transport Chain*
TLDR
The results do not support the idea that mitochondria produce considerable amounts of reactive oxygen species under physiological conditions and the proportion of electron flow giving rise to hydrogen peroxide with palmitoyl carnitine as substrate is more than an order of magnitude lower than commonly cited values. Expand
The sites and topology of mitochondrial superoxide production
  • M. Brand
  • Medicine, Biology
  • Experimental Gerontology
  • 1 August 2010
TLDR
The relative contribution of each site to mitochondrial reactive oxygen species generation in the absence of electron transport inhibitors is unknown in isolated mitochondria, in cells or in vivo, and may vary considerably with species, tissue, substrate, energy demand and oxygen tension. Expand
Superoxide activates mitochondrial uncoupling proteins
TLDR
It is shown that superoxide increases mitochondrial proton conductance through effects on UCP1, UCP2 and UCP3, indicating that the interaction of superoxide with UCPs may be a mechanism for decreasing the concentrations of reactive oxygen species inside mitochondria. Expand
Uncoupling to survive? The role of mitochondrial inefficiency in ageing
  • M. Brand
  • Medicine, Biology
  • Experimental Gerontology
  • 1 September 2000
TLDR
There is no direct evidence in cells or organisms that mitochondrial proton cycling lowers ROS production or oxidative damage or that it increases lifespan, but an attractive candidate for the function of the universal and expensive energy-dissipating proton cycle is to decrease the production of superoxide and other reactive oxygen species (ROS). Expand
Mitochondrial superoxide: production, biological effects, and activation of uncoupling proteins.
TLDR
Observations suggest a hypothesis for the main, ancestral function of uncoupling proteins: to cause mild uncoupled and so diminish mitochondrial superoxide production, hence protecting against disease and oxidative damage at the expense of a small loss of energy. Expand
The efficiency and plasticity of mitochondrial energy transduction.
  • M. Brand
  • Biology, Medicine
  • Biochemical Society transactions
  • 26 October 2005
TLDR
UCP1 (uncoupling protein 1) is used in specialized tissues to uncouple oxidative phosphorylation, causing adaptive thermogenesis and UCPs may also integrate inputs from different fuels in pancreatic beta-cells and modulate insulin secretion, creating exciting potential targets for treatment of obesity, cachexia, aging and diabetes. Expand
Mitochondrial generation of superoxide and hydrogen peroxide as the source of mitochondrial redox signaling.
  • M. Brand
  • Chemistry, Medicine
  • Free radical biology & medicine
  • 1 November 2016
TLDR
This review examines the generation of reactive oxygen species by mammalian mitochondria, and the status of different sites of production in redox signaling and pathology, and identifies specific suppressors of two sites that allow the cellular roles of mitochondrial superoxide/hydrogen peroxide production to be investigated without catastrophic confounding bioenergetic effects. Expand
Inhibitors of the Quinone-binding Site Allow Rapid Superoxide Production from Mitochondrial NADH:Ubiquinone Oxidoreductase (Complex I)*
TLDR
Observed rates of superoxide generation by rat skeletal muscle mitochondria under a variety of conditions suggest that quinone-binding site inhibitors can make complex I adopt the highly radical-producing state that occurs during reverse electron transport. Expand
Mitochondrial Complex II Can Generate Reactive Oxygen Species at High Rates in Both the Forward and Reverse Reactions*
TLDR
It is found that when complex I and complex III are inhibited and succinate concentration is low, complex II in rat skeletal muscle mitochondria can generate superoxide or H2O2 at high rates, which approach or exceed the maximum rates achieved by complex I or complex III. Expand
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