Larsen FJ 2013 Abstract MiP2013

Larsen FJ, Schiffer TA, Lundberg JO, Weitzberg E (2013) Human mitochondria has a unique response to ischemia reperfusion injury compared to mitochondria from rat, mouse and pig . Mitochondr Physiol Network 18.08.

Link:

Larsen FJ, Schiffer TA, Lundberg JO, Weitzberg E (2013)

Event: MiP2013

Mitochondrial function and respiratory dysfunction after short periods of ischemia has been implicated as major determinants of ischemic cell injury [1]. In vitro models of isolated mitochondria subjected to anoxia-reoxygenation are routinely used to study mitochondrial abnormalities and pharmacological approaches to attenuate ischemic injury [2]. Mice and rat mitochondria are by far the most common animal model in this area of research. We here show, in agreement with a plethora of other studies, that respiration of mice and rat mitochondria decreases after a brief period of in vitro anoxia-reoxygenation, an effect most often related to ROS injury of Complex I. Conversely, human mitochondria demonstrate a unique feature with increased respiration after anoxia-reoxygenation. This effect is increasing with longer anoxic periods, independent of uncoupling of the mitochondrial membrane potential or potassium channel activation and cannot be inhibited by in vitro application of antioxidants. The increase in respiration is also present regardless of the route of electron-entry into the ETS and cannot be inhibited by any known inhibitors of the mitochondrial complexes. Instead, the differing responses seem to be associated with interspecific differences in the function of cytochrome c oxidase.

• O2k-Network Lab: SE Stockholm Weitzberg E

Labels:

Stress:Ischemia-Reperfusion; Preservation"Ischemia-Reperfusion; Preservation" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property.  Organism: Human, Mouse, Rat 

Preparation: Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.  Enzyme: Complex IV; Cytochrome c Oxidase"Complex IV; Cytochrome c Oxidase" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" property. 

Coupling state: OXPHOS 

HRR: Oxygraph-2k 

Prep2 

Affiliations and author contributions

Karolinska Institutet, Dept of Physiology and Pharmacology, Stockholm, Sweden.

Email: [email protected]

References

1. Honda HM, Korge P, Weiss JN, Ann NY (2005) Mitochondria and ischemia/reperfusion injury. Acad Sci 1047: 248-58.
2. Navet R, Mouithys-Mickalad A, Douette P, Sluse-Goffart CM, Jarmuszkiewicz W, Sluse FE (2006) Proton leak induced by reactive oxygen species produced during in vitro anoxia/reoxygenation in rat skeletal muscle mitochondria. Bioenerg Biomembr 38: 23-32.