Caito 2015 Antioxid Redox Signal: Difference between revisions
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{{Publication | {{Publication | ||
|title=Caito SW, Aschner M (2015) Mitochondrial redox dysfunction and environmental exposures. Antioxid Redox Signal [Epub ahead of print]. ย | |title=Caito SW, Aschner M (2015) Mitochondrial redox dysfunction and environmental exposures. Antioxid Redox Signal [Epub ahead of print]. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/25826672 PMID:25826672] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/25826672 PMID:25826672] | ||
|authors=Caito SW, Aschner M | |authors=Caito SW, Aschner M | ||
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Dysregulation of respiration has been linked to cell death and is a major contributor to acute neuronal trauma, peripheral diseases, as well as chronic neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease. | Dysregulation of respiration has been linked to cell death and is a major contributor to acute neuronal trauma, peripheral diseases, as well as chronic neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease. | ||
Here, we discuss the mechanisms underlying the sensitivity of the mitochondrial respiratory complexes to redox modulation, as well as examine the effects of environmental contaminants that have well-characterized mitochondrial toxicity. The contaminants discussed in this review are some of the most prevalent and potent environmental contaminants that have been linked to neurological dysfunction, altered cellular respiration, and oxidation. ย | Here, we discuss the mechanisms underlying the sensitivity of the mitochondrial respiratory complexes to redox modulation, as well as examine the effects of environmental contaminants that have well-characterized mitochondrial toxicity. The contaminants discussed in this review are some of the most prevalent and potent environmental contaminants that have been linked to neurological dysfunction, altered cellular respiration, and oxidation. | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=mt-Membrane, Comparative MiP;environmental MiP, Pharmacology;toxicology | |area=mt-Membrane, Comparative MiP;environmental MiP, mt-Medicine, Patients, Pharmacology;toxicology | ||
|organism=Human, Mouse, Rat, Bovines | |organism=Human, Mouse, Rat, Bovines, Drosophila | ||
|taxonomic group=Fishes, Hexapods | |taxonomic group=Fishes, Hexapods | ||
|tissues=Heart, Lung;gill | |tissues=Heart, Nervous system, Liver, Kidney, Lung;gill, Endothelial;epithelial;mesothelial cell | ||
|preparations=Isolated mitochondria | |||
|enzymes=Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase | |enzymes=Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase | ||
|injuries=Ischemia-reperfusion;preservation, Oxidative stress;RONS | |injuries=Cell death, Ischemia-reperfusion;preservation, Oxidative stress;RONS | ||
|diseases=COPD | |||
|topics=Calcium | |||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
|substratestates=CI, CII, CIII, CIV | |substratestates=CI, CII, CIII, CIV | ||
|additional=Labels, [Epub ahead of print] | |additional=Labels, [Epub ahead of print] | ||
}} | }} |
Revision as of 09:13, 11 May 2015
Caito SW, Aschner M (2015) Mitochondrial redox dysfunction and environmental exposures. Antioxid Redox Signal [Epub ahead of print]. |
Caito SW, Aschner M (2015) Antioxid Redox Signal
Abstract: Mitochondria are structurally and biochemically diverse, even within a single type of cell. Protein complexes localized to the inner mitochondrial membrane synthesize ATP by coupling electron transport and oxidative phosphorylation. The organelles produce reactive oxygen species (ROS) from mitochondrial oxygen and ROS can, in turn, alter the function and expression of proteins used for aerobic respiration by post-translational and transcriptional regulation. Recent Advances: New interest is emerging not only into the roles of mitochondria in disease development and progression but also as a target for environmental toxicants.
Dysregulation of respiration has been linked to cell death and is a major contributor to acute neuronal trauma, peripheral diseases, as well as chronic neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease.
Here, we discuss the mechanisms underlying the sensitivity of the mitochondrial respiratory complexes to redox modulation, as well as examine the effects of environmental contaminants that have well-characterized mitochondrial toxicity. The contaminants discussed in this review are some of the most prevalent and potent environmental contaminants that have been linked to neurological dysfunction, altered cellular respiration, and oxidation.
Labels: MiParea: mt-Membrane, Comparative MiP;environmental MiP, mt-Medicine, Patients, Pharmacology;toxicology
Pathology: COPD
Stress:Cell death, Ischemia-reperfusion;preservation"Ischemia-reperfusion;preservation" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property., Oxidative stress;RONS
Organism: Human, Mouse, Rat, Bovines, Drosophila
Tissue;cell: Heart, Nervous system, Liver, Kidney, Lung;gill, Endothelial;epithelial;mesothelial cell
Preparation: Isolated mitochondria
Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase
Regulation: Calcium
Coupling state: OXPHOS
Labels, [Epub ahead of print]