Brain cortex mitochondrial bioenergetics in synaptosomes and non-synaptic mitochondria during aging

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• 作者：Silvia Lores-Arnaiz ; Paulina Lombardi ; Analía G. Karadayian…
• 关键词：Synaptosomes ; Non ; synaptic mitochondria ; Aging ; Cerebral cortex ; Respiration ; Depolarization
• 刊名：Neurochemical Research
• 出版年：2016
• 出版时间：February 2016
• 年：2016
• 卷：41
• 期：1-2
• 页码：353-363
• 全文大小：2,350 KB
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• 作者单位：Silvia Lores-Arnaiz (1)
  Paulina Lombardi (1)
  Analía G. Karadayian (1)
  Federico Orgambide (1)
  Daniela Cicerchia (1)
  Juanita Bustamante (2)
  
  1. Instituto de Bioquímica y Medicina Molecular, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Junín 956, C1113AAD, Buenos Aires, Argentina
  2. Centro de Altos Estudios en Ciencias de la Salud, Universidad Abierta Interamericana, Buenos Aires, Argentina
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Biochemistry
  Neurology
  
• 出版者：Springer Netherlands
• ISSN：1573-6903

文摘

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.