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REVIEW: Reactive Oxygen and Nitrogen Species: Friends or Foes?

D. B. Zorov1*, S. Y. Bannikova1, V. V. Belousov2, M. Y. Vyssokikh1, L. D. Zorova1, N. K. Isaev1, B. F. Krasnikov1,3, and E. Y. Plotnikov1

1Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119992 Moscow, Russia; fax: (7-095) 939-3181; E-mail: zorov@genebee.msu.ru

2Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, ul. Miklukho-Maklaya 16/10, 117997 Moscow, Russia

3Burke Medical Research Institute, White Plains, New York, USA

* To whom correspondence should be addressed.

Received October 4, 2004
Chemical and physiological functions of molecular oxygen and reactive oxygen species (ROS) and existing equilibrium between pools of pro-oxidants and anti-oxidants providing steady state ROS level vital for normal mitochondrial and cell functioning are reviewed. The presence of intracellular oxygen and ROS sensors is postulated and few candidates for this role are suggested. Possible involvement of ROS in the process of fragmentation of mitochondrial reticulum made of long mitochondrial filaments serving in the cell as “electric cables”, as well as the role of ROS in apoptosis and programmed mitochondrial destruction (mitoptosis) are reviewed. The critical role of ROS in destructive processes under ischemia/reoxygenation and ischemic preconditioning is discussed. Mitochondrial permeability transition gets special consideration as a possible component of the apoptotic cascade, resulting in excessive “ROS-induced ROS release”.
KEY WORDS: reactive oxygen species, nitric oxide, mitochondria, apoptosis, ischemia/reoxygenation, ischemic preconditioning, fragmentation, electric cable