Difference between revisions of "Lores-Arnaiz 2016 Neurochem Res"
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|abstract=Alterations in mitochondrial bioenergetics have been associated with brain aging. In order to evaluate the susceptibility of brain cortex synaptosomes and non-synaptic mitochondria to aging-dependent dysfunction, male Swiss mice of 3 or 17 months old were used. Mitochondrial function was evaluated by oxygen consumption, mitochondrial membrane potential and respiratory complexes activity, together with UCP-2 protein expression. Basal respiration and respiration driving proton LEAK were decreased by 26 and 33 % in synaptosomes from 17-months old mice, but spare respiratory capacity was not modified by aging. Succinate supported state 3 respiratory rate was decreased by 45 % in brain cortex non-synaptic mitochondria from 17-month-old mice, as compared with young animals, but respiratory control was not affected. Synaptosomal mitochondria would be susceptible to undergo calcium-induced depolarization in 17 months-old mice, while non-synaptic mitochondria would not be affected by calcium overload. UCP-2 was significantly up-regulated in both synaptosomal and submitochondrial membranes from 17-months old mice, compared to young animals. UCP-2 upregulation seems to be a possible mechanism by which mitochondria would be resistant to suffer oxidative damage during aging. | |abstract=Alterations in mitochondrial bioenergetics have been associated with brain aging. In order to evaluate the susceptibility of brain cortex synaptosomes and non-synaptic mitochondria to aging-dependent dysfunction, male Swiss mice of 3 or 17 months old were used. Mitochondrial function was evaluated by oxygen consumption, mitochondrial membrane potential and respiratory complexes activity, together with UCP-2 protein expression. Basal respiration and respiration driving proton LEAK were decreased by 26 and 33 % in synaptosomes from 17-months old mice, but spare respiratory capacity was not modified by aging. Succinate supported state 3 respiratory rate was decreased by 45 % in brain cortex non-synaptic mitochondria from 17-month-old mice, as compared with young animals, but respiratory control was not affected. Synaptosomal mitochondria would be susceptible to undergo calcium-induced depolarization in 17 months-old mice, while non-synaptic mitochondria would not be affected by calcium overload. UCP-2 was significantly up-regulated in both synaptosomal and submitochondrial membranes from 17-months old mice, compared to young animals. UCP-2 upregulation seems to be a possible mechanism by which mitochondria would be resistant to suffer oxidative damage during aging. | ||
|keywords=Synaptosomes, Non-synaptic mitochondria, Aging, Cerebral cortex, Respiration, Depolarization | |keywords=Synaptosomes, Non-synaptic mitochondria, Aging, Cerebral cortex, Respiration, Depolarization | ||
|mipnetlab=AR Buenos Aires Boveris A | |mipnetlab=AR Buenos Aires Boveris A | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration, mt-Biogenesis;mt-density, mt-Membrane | |area=Respiration, mt-Biogenesis;mt-density, mt-Membrane | ||
|diseases=Aging;senescence | |||
|organism=Mouse | |organism=Mouse | ||
|tissues=Nervous system | |tissues=Nervous system | ||
|preparations=Intact cells, Isolated mitochondria | |preparations=Intact cells, Isolated mitochondria | ||
|enzymes=Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase | |enzymes=Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase | ||
|couplingstates=LEAK, ROUTINE, OXPHOS, ETS | |couplingstates=LEAK, ROUTINE, OXPHOS, ETS | ||
|pathways=N, S | |pathways=N, S | ||
Revision as of 11:59, 11 July 2017
| Lores-Arnaiz S, Lombardi P, Karadayian AG, Orgambide F, Cicerchia D, Bustamante J (2016) Brain cortex mitochondrial bioenergetics in synaptosomes and non-synaptic mitochondria during aging. Neurochem Res 41:353-63. |
Lores-Arnaiz S, Lombardi P, Karadayian AG, Orgambide F, Cicerchia D, Bustamante J (2016) Neurochem Res
Abstract: Alterations in mitochondrial bioenergetics have been associated with brain aging. In order to evaluate the susceptibility of brain cortex synaptosomes and non-synaptic mitochondria to aging-dependent dysfunction, male Swiss mice of 3 or 17 months old were used. Mitochondrial function was evaluated by oxygen consumption, mitochondrial membrane potential and respiratory complexes activity, together with UCP-2 protein expression. Basal respiration and respiration driving proton LEAK were decreased by 26 and 33 % in synaptosomes from 17-months old mice, but spare respiratory capacity was not modified by aging. Succinate supported state 3 respiratory rate was decreased by 45 % in brain cortex non-synaptic mitochondria from 17-month-old mice, as compared with young animals, but respiratory control was not affected. Synaptosomal mitochondria would be susceptible to undergo calcium-induced depolarization in 17 months-old mice, while non-synaptic mitochondria would not be affected by calcium overload. UCP-2 was significantly up-regulated in both synaptosomal and submitochondrial membranes from 17-months old mice, compared to young animals. UCP-2 upregulation seems to be a possible mechanism by which mitochondria would be resistant to suffer oxidative damage during aging. • Keywords: Synaptosomes, Non-synaptic mitochondria, Aging, Cerebral cortex, Respiration, Depolarization
• O2k-Network Lab: AR Buenos Aires Boveris A
Labels: MiParea: Respiration, mt-Biogenesis;mt-density, mt-Membrane
Pathology: Aging;senescence
Organism: Mouse Tissue;cell: Nervous system Preparation: Intact cells, Isolated mitochondria Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase
Coupling state: LEAK, ROUTINE, OXPHOS, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property. Pathway: N, S HRR: Oxygraph-2k
2016-03
