Jones 2010 Biochim Biophys Acta: Difference between revisions
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{{Publication | {{Publication | ||
|title=Jones TT, Brewer GJ (2010) Age-related deficiencies in | |title=Jones TT, Brewer GJ (2010) Age-related deficiencies in Complex I endogenous substrate availability and reserve capacity of Complex IV in cortical neuron electron transport. Biochim Biophys Acta 1797:167-76. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19799853 PMID: 19799853] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/19799853 PMID: 19799853 Open Access] | ||
|authors=Jones TT, Brewer GJ | |authors=Jones TT, Brewer GJ | ||
|year=2010 | |year=2010 | ||
|journal=Biochim | |journal=Biochim Biophys Acta | ||
|abstract=Respiratory enzyme complex dysfunction is mechanistically involved in mitochondrial failure leading to neurodegenerative disease, but the pathway is unclear. Here, age-related differences in mitochondrial respiration were measured in both whole and permeabilized neurons from 9-month and 24-month adult rat cortex cultured in common conditions. After permeabilization, respiration increased in both ages of neurons with excess substrates. To dissect specific deficiencies in the respiratory chain, inhibitors for each respiratory chain complex were used to isolate their contributions. Relative to neurons from 9-month rats, in neurons isolated from 24-month rats, | |abstract=Respiratory enzyme complex dysfunction is mechanistically involved in mitochondrial failure leading to neurodegenerative disease, but the pathway is unclear. Here, age-related differences in mitochondrial respiration were measured in both whole and permeabilized neurons from 9-month and 24-month adult rat cortex cultured in common conditions. After permeabilization, respiration increased in both ages of neurons with excess substrates. To dissect specific deficiencies in the respiratory chain, inhibitors for each respiratory chain complex were used to isolate their contributions. Relative to neurons from 9-month rats, in neurons isolated from 24-month rats, Complexes I, III, and IV were more sensitive to selective inhibition. Flux control point analysis identified Complex I in neurons isolated from 24-month rats as the most sensitive to endogenous substrate availability. The greatest age-related deficit in flux capacity occurred at Complex IV with a 29% decrease in neurons isolated from 24-month rats relative to those from 9-month rats. The deficits in Complexes I and III may contribute to a redox shift in the quinone pool within the electron transport chain, further extending these age-related deficits. Together these changes could lead to an age-related catastrophic decline in energy production and neuronal death. | ||
|keywords=Oxidative phosphorylation, Aging, Mitochondria, Coenzyme Q, NADH, Rotenone | |keywords=Oxidative phosphorylation, Aging, Mitochondria, Coenzyme Q, NADH, Rotenone | ||
|mipnetlab= | |mipnetlab=US IL Springfield Brewer GJ | ||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |||
|organism=Rat | |||
|tissues=Nervous system | |||
|preparations=Intact cells, Permeabilized cells | |||
|enzymes=Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Uncoupling protein | |||
|diseases=Aging;senescence, Neurodegenerative | |||
|topics=Inhibitor, Substrate | |||
|couplingstates=OXPHOS | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
}} | }} |
Latest revision as of 14:38, 20 March 2015
Jones TT, Brewer GJ (2010) Age-related deficiencies in Complex I endogenous substrate availability and reserve capacity of Complex IV in cortical neuron electron transport. Biochim Biophys Acta 1797:167-76. |
Jones TT, Brewer GJ (2010) Biochim Biophys Acta
Abstract: Respiratory enzyme complex dysfunction is mechanistically involved in mitochondrial failure leading to neurodegenerative disease, but the pathway is unclear. Here, age-related differences in mitochondrial respiration were measured in both whole and permeabilized neurons from 9-month and 24-month adult rat cortex cultured in common conditions. After permeabilization, respiration increased in both ages of neurons with excess substrates. To dissect specific deficiencies in the respiratory chain, inhibitors for each respiratory chain complex were used to isolate their contributions. Relative to neurons from 9-month rats, in neurons isolated from 24-month rats, Complexes I, III, and IV were more sensitive to selective inhibition. Flux control point analysis identified Complex I in neurons isolated from 24-month rats as the most sensitive to endogenous substrate availability. The greatest age-related deficit in flux capacity occurred at Complex IV with a 29% decrease in neurons isolated from 24-month rats relative to those from 9-month rats. The deficits in Complexes I and III may contribute to a redox shift in the quinone pool within the electron transport chain, further extending these age-related deficits. Together these changes could lead to an age-related catastrophic decline in energy production and neuronal death. โข Keywords: Oxidative phosphorylation, Aging, Mitochondria, Coenzyme Q, NADH, Rotenone
โข O2k-Network Lab: US IL Springfield Brewer GJ
Labels: MiParea: Respiration
Pathology: Aging;senescence, Neurodegenerative
Organism: Rat Tissue;cell: Nervous system Preparation: Intact cells, Permeabilized cells Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Uncoupling protein Regulation: Inhibitor, Substrate Coupling state: OXPHOS
HRR: Oxygraph-2k