Starkov 2014 Abstract MiP2014: Difference between revisions
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{{Abstract | {{Abstract | ||
|title=Mitochondria as | |title=Mitochondria as H<sub>2</sub>O<sub>2</sub> buffering system. | ||
|info=[[File: | |info=[[File:Starkov_AA.jpg|150px|right|Starkov AA]] [[Laner 2014 Mitochondr Physiol Network MiP2014|Mitochondr Physiol Network 19.13]] - [http://www.mitophysiology.org/index.php?mip2014 MiP2014] | ||
|authors=Starkov AA | |authors=Starkov AA | ||
|year=2014 | |year=2014 | ||
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In this presentation, I will briefly summarize the state of knowledge on the sources and regulation of ROS production and scavenging in mitochondria and present experimental data on mitochondrial ROS-buffering properties. | In this presentation, I will briefly summarize the state of knowledge on the sources and regulation of ROS production and scavenging in mitochondria and present experimental data on mitochondrial ROS-buffering properties. | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|injuries=RONS | |injuries=Oxidative stress;RONS | ||
|event=B2, Oral | |||
|additional=MiP2014 | |additional=MiP2014 | ||
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Latest revision as of 16:51, 23 February 2015
| Mitochondria as H2O2 buffering system. |
Link:
Mitochondr Physiol Network 19.13 - MiP2014
Starkov AA (2014)
Event: MiP2014
For decades, mitochondria have been considered a major intracellular source of reactive oxygen species (ROS). Mitochondrial ROS have been viewed as a negative factor, contributing to the damage of cellular components. More recent data point to a more physiological role of mitochondrial-produced ROS in mitochondria-cell communication and intra- and extracellular signaling [1].
The eventual unraveling of the complex and powerful mitochondrial ROS detoxication system resulted in a concept that mitochondria are more a sink than a source of ROS [2,3]. However, our research indicates that mitochondria are a ROS buffering system that can maintain the intracellular level of ROS in relation to the metabolic circumstances.
In this presentation, I will briefly summarize the state of knowledge on the sources and regulation of ROS production and scavenging in mitochondria and present experimental data on mitochondrial ROS-buffering properties.
Labels:
Stress:Oxidative stress;RONS
Event: B2, Oral
MiP2014
Affiliation
Brain Mind Research Inst, Weill Cornell Medical College Cornell Univ, NY, USA. - [email protected]
References
- Lenaz G (2012) Mitochondria and reactive oxygen species. Which role in physiology and pathology? Adv Exp Med Biol 942: 93-136.
- Starkov AA (2008) The role of mitochondria in reactive oxygen species metabolism and signaling. Ann N Y Acad Sci 1147: 37-52.
- Andreyev AY, Kushnareva YE, Starkov AA (2005) Mitochondrial metabolism of reactive oxygen species. Biochemistry (Mosc) 70: 200-14.
