Mitochondrial metabolism following traumatic brain injury in rats.
Although a number of studies of traumatic brain injury have implicated mitochondrial dysfunction as a cause of altered posttraumatic energy metabolism, no studies to date have isolated mitochondria and measured their respiratory capacity following trauma. The present study sought to determine whether mitochondrial capacity for oxidative phosphorylation is adversely affected by fluid-percussion-induced traumatic brain injury in rats. Prior to brain injury, the mitochondrial respiratory control ratio was 4.3 +/- 0.2 and the ratio of nmoles of ADP phosphorylated per natom oxygen consumed (ADP/O ratio) was 2.66 +/- 0.09. After injury (2.8 atm; t = 4 h), there were slight but not significant alterations in ADP/O ratio (2.41 +/- 0.07) and state 3 respiratory rate (ADP stimulated); however, there were no changes in the respiratory control ratio. These data suggest that traumatic brain injury, unlike ischemia, does not cause uncoupling of ATP synthesis from respiration, and that brain mitochondria are quite resistant to trauma-induced injury.
Vink
R
R
Department of Chemistry and Biochemistry, James Cook University, Townsville, Australia.
Head
V A
VA
Rogers
P J
PJ
McIntosh
T K
TK
Faden
A I
AI
D000244:Adenosine Diphosphate / Q000378:metabolism; D000818:Animals; D001930:Brain Injuries / Q000378:metabolism*; D004734:Energy Metabolism; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D000244:Adenosine Diphosphate