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How mitochondria produce reactive oxygen species
- M. Murphy
- BiologyThe Biochemical journal
- 12 December 2008
The description outlined here facilitates the understanding of factors that favour mitochondrial ROS production and develops better methods to measure mitochondrial O2•− and H2O2 formation in vivo, as uncertainty about these values hampers studies on the role of mitochondrial ROS in pathological oxidative damage and redox signalling.
Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS
It is shown that selective accumulation of the citric acid cycle intermediate succinate is a universal metabolic signature of ischaemia in a range of tissues and is responsible for mitochondrial ROS production during reperfusion, and a new pathway for metabolic control of ROS production in vivo is revealed.
Neurofibrillary tangles, amyotrophy and progressive motor disturbance in mice expressing mutant (P301L) tau protein
The phenotype of mice expressing P301L mutant tau mimics features of human tauopathies and provides a model for investigating the pathogenesis of diseases with NFT.
Succinate Dehydrogenase Supports Metabolic Repurposing of Mitochondria to Drive Inflammatory Macrophages
Selective fluorescent imaging of superoxide in vivo using ethidium-based probes
- Kristine M. Robinson, M. Janes, J. Beckman
- Biology, ChemistryProceedings of the National Academy of Sciences
- 10 October 2006
It is found that the superoxide product of both HE and Mito-HE could be selectively excited at 396 nm with minimal interference from other nonspecific oxidation products, indicating the more selective detection of superoxide in vivo.
Itaconate is an anti-inflammatory metabolite that activates Nrf2 via alkylation of KEAP1
It is shown that itaconate is required for the activation of the anti-inflammatory transcription factor Nrf2 by lipopolysaccharide in mouse and human macrophages and that type I interferons boost the expression of Irg1 (also known as Acod1) and itaconates production.
Selective Targeting of a Redox-active Ubiquinone to Mitochondria within Cells
- G. F. Kelso, C. M. Porteous, M. Murphy
- Biology, ChemistryThe Journal of Biological Chemistry
- 16 February 2001
It is shown that selectively manipulating mitochondrial antioxidant status with targeted and recyclable antioxidants is a feasible approach to investigate the role of mitochondrial oxidative damage in apoptotic cell death and will have further applications in investigating mitochondrial dysfunction in a range of experimental models.
DICER1 Loss and Alu RNA Induce Age-Related Macular Degeneration via the NLRP3 Inflammasome and MyD88
Targeting antioxidants to mitochondria by conjugation to lipophilic cations.
- M. Murphy, Robin A. J. Smith
- Biology, ChemistryAnnual review of pharmacology and toxicology
- 8 January 2007
The background and work to date on this class of mitochondria-targeted antioxidants, developed by conjugating the lipophilic triphenylphosphonium cation to an antioxidant moiety, such as ubiquinol or alpha-tocopherol, are reviewed.
The Qo site of the mitochondrial complex III is required for the transduction of hypoxic signaling via reactive oxygen species production
Genetic and pharmacologic evidence is provided that the Qo site of complex III is required for the transduction of hypoxic signal by releasing ROS to stabilize the HIF-1α protein.