Electronic Thesis and Dissertation Repository


Master of Science




Staples, James F.


Hibernation protects mammalian tissues against ischemia-reperfusion injury, but the underlying biochemical mechanisms are unknown. I hypothesized that the mechanisms allowing for mitochondrial metabolic flexibility during hibernation permit anoxia tolerance and contribute to tissue ischemia-reperfusion tolerance. I assessed mitochondrial performance before and after five minutes of anoxia in liver mitochondria isolated from thirteen-lined ground squirrels. I compared this anoxia effect among animals that were summer active (SA), or during hibernation (in torpor or interbout euthermia; IBE). Anoxia decreased state 3 respiration in all groups, but mitochondria isolated from torpid squirrels were least affected; these decreases paralleled decreased activity of electron transport system complexes in IBE and SA. Leak respiration was more elevated in SA mitochondria following anoxia than in either IBE or torpor. These findings suggest that during hibernation (especially in torpor) mitochondrial respiration is maintained with a concurrent reduction in oxidative damage following anoxia, which may protect from ischemia-reperfusion injury.