Starkov 2014 Abstract MiP2014

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Mitochondria as H2O2 buffering system.
Link:
Starkov AA
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. - ans2024@med.cornell.edu

References

  1. Lenaz G (2012) Mitochondria and reactive oxygen species. Which role in physiology and pathology? Adv Exp Med Biol 942: 93-136.
  2. Starkov AA (2008) The role of mitochondria in reactive oxygen species metabolism and signaling. Ann N Y Acad Sci 1147: 37-52.
  3. Andreyev AY, Kushnareva YE, Starkov AA (2005) Mitochondrial metabolism of reactive oxygen species. Biochemistry (Mosc) 70: 200-14.