Hayward 2018 Thesis
| Hayward L (2018) The effect of anoxia on mitochondrial function in a hibernator (Ictidomys tridecemlineatus). Master's Thesis 57. |
Hayward L (2018) Master's Thesis
Abstract: 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. • Keywords: Ischemia, Reperfusion, Hibernation, Metabolism, Thirteen-lined ground squirrel, High-resolution respirometry • Bioblast editor: Plangger M • O2k-Network Lab: CA London Staples JF
Labels: MiParea: Respiration
Stress:Ischemia-reperfusion Organism: Other mammals Tissue;cell: Liver Preparation: Isolated mitochondria Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex V;ATP synthase Regulation: mt-Membrane potential Coupling state: LEAK, OXPHOS Pathway: N, NS HRR: Oxygraph-2k, TPP
Labels, 2019-02
