Difference between revisions of "Larsen FJ 2013 Abstract MiP2013"
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{{Abstract | {{Abstract | ||
|title=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. | |title=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. | ||
|info=[ | |info=[[File:LarsenF.jpg|150px|right|Filip Larsen]][[MiP2013]], [[Laner 2013 Mitochondr Physiol Network MiP2013|Book of Abstracts Open Access]] | ||
|authors=Larsen FJ, Schiffer TA, Lundberg JO, Weitzberg E | |authors=Larsen FJ, Schiffer TA, Lundberg JO, Weitzberg E | ||
|year=2013 | |year=2013 | ||
|event= | |event=MiPNet18.08_MiP2013 | ||
|abstract=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. | |abstract=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 | 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 ET-pathway 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. | ||
|mipnetlab=SE Stockholm Weitzberg E | |mipnetlab=SE Stockholm Weitzberg E, SE Stockholm Larsen FJ | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration, Comparative MiP;environmental MiP | |area=Respiration, Comparative MiP;environmental MiP | ||
|injuries=Ischemia-reperfusion, Oxidative stress;RONS | |||
|organism=Human, Pig, Mouse, Rat | |organism=Human, Pig, Mouse, Rat | ||
|preparations=Isolated | |preparations=Isolated mitochondria | ||
|enzymes=Complex IV; | |enzymes=Complex IV;cytochrome c oxidase | ||
|topics=Coupling efficiency;uncoupling, Ion;substrate transport, mt-Membrane potential | |topics=Coupling efficiency;uncoupling, Ion;substrate transport, mt-Membrane potential | ||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
| | |pathways=ROX | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=MiP2013 | |additional=MiP2013 | ||
Latest revision as of 16:23, 27 March 2018
| 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:
MiP2013, Book of Abstracts Open Access
Larsen FJ, Schiffer TA, Lundberg JO, Weitzberg E (2013)
Event: MiPNet18.08_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 ET-pathway 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, SE Stockholm Larsen FJ
Labels: MiParea: Respiration, Comparative MiP;environmental MiP
Stress:Ischemia-reperfusion, Oxidative stress;RONS Organism: Human, Pig, Mouse, Rat
Preparation: Isolated mitochondria Enzyme: Complex IV;cytochrome c oxidase Regulation: Coupling efficiency;uncoupling, Ion;substrate transport, mt-Membrane potential Coupling state: OXPHOS Pathway: ROX HRR: Oxygraph-2k
MiP2013
Affiliations and author contributions
Karolinska Institutet, Dept of Physiology and Pharmacology, Stockholm, Sweden. - Email: [email protected]
References
- Honda HM, Korge P, Weiss JN, Ann NY (2005) Mitochondria and ischemia/reperfusion injury. Acad Sci 1047: 248-58.
- 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.
