Mitochondrial dysfunction early after traumatic brain injury in immature rats

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Abstract

Mitochondria play central roles in acute brain injury; however, little is known about mitochondrial function following traumatic brain injury (TBI) to the immature brain. We hypothesized that TBI would cause mitochondrial dysfunction early (<4 h) after injury. Immature rats underwent controlled cortical impact (CCI) or sham injury to the left cortex, and mitochondria were isolated from both hemispheres at 1 and 4 h after TBI. Rates of phosphorylating (State 3) and resting (State 4) respiration were measured with and without bovine serum albumin. The respiratory control ratio was calculated (State 3/State 4). Rates of mitochondrial H2O2 production, pyruvate dehydrogenase complex enzyme activity, and cytochrome c content were measured. Mitochondrial State 4 rates (ipsilateral/contralateral ratios) were higher after TBI at 1 h, which was reversed with bovine serum albumin. Four hours after TBI, pyruvate dehydrogenase complex activity and cytochrome c content (ipsilateral/ contralateral ratios) were lower in TBI mitochondria. These data demonstrate abnormal mitochondrial function early (≤4 h) after TBI in the developing brain. Future studies directed at reversing mitochondrial abnormalities could guide neuroprotective interventions after pediatric TBI.

Original languageEnglish (US)
Pages (from-to)1248-1257
Number of pages10
JournalJournal of Neurochemistry
Volume101
Issue number5
DOIs
StatePublished - Jun 2007
Externally publishedYes

Keywords

  • Brain mitochondria
  • Cerebral metabolism
  • Cytochrome c
  • Development
  • Oxidative stress

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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