Journal
JOURNAL OF NEUROCHEMISTRY
Volume 101, Issue 5, Pages 1248-1257Publisher
WILEY
DOI: 10.1111/j.1471-4159.2007.04489.x
Keywords
brain mitochondria; cerebral metabolism; cytochrome c; development; oxidative stress
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Funding
- NINDS NIH HHS [K08 NS42805] Funding Source: Medline
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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.
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