Reactive oxygen species damage and consequences for mitochondrial function in the hibernating thirteen-lined ground squirrel, Ictidomys tridecemlineatus
Abstract
Hibernators experience changes in blood flow, similar to ischemia-reperfusion injury, which may lead to oxidative damage. I hypothesized that suppression of mitochondrial metabolism during hibernation protects against such damage. I compared oxidative damage and antioxidant capacity in tissues and isolated liver mitochondria among summer, torpid, and interbout euthermic thirteen-lined ground squirrels (TLGS). I found less oxidative tissue damage during summer than hibernation, but no mitochondrial differences. I also compared metabolic activity of isolated mitochondria before and after five minutes of anoxia, followed by reoxygenation, among hibernation states and rats. Anoxia-reoxygenation decreased state-three respiration (ST3) in all groups, with rat mitochondria affected the most, and torpor TLGS mitochondria affected the least. With rotenone inhibition, ST3 was less affected by anoxia-reoxygenation, suggesting ETS complex-I is a source of ROS production. An exogenous antioxidant (ascorbate) mitigated changes in ST3. My findings suggest that metabolic suppression offers some protection against oxidative damage during hibernation.