The mystery of reactive oxygen species derived from cell respiration.
Mitochondrial respiration is considered to provide reactive oxygen species (ROS) as byproduct of regular electron transfer. Objections were raised since results obtained with isolated mitochondria are commonly transferred to activities of mitochondria in the living cell. High electrogenic membrane potential was reported to trigger formation of mitochondrial ROS involving complex I and III. Suggested bioenergetic parameters, starting ROS formation, widely change with the isolation mode. ROS detection systems generally applied may be misleading due to possible interactions with membrane constituents or electron carriers. Avoiding these problems no conditions reported to transform mitochondrial respiration to a radical source were confirmed. However, changing the physical membrane state affected the highly susceptible interaction of the ubiquinol/bc(1) redox complex such that ROS formation became possible.
Nohl
Hans
H
Basic Research in Pharmacology and Toxicology, University of Veterinary Medicine Vienna, Vienna, Austria. hans.nohl@vu-wien.ac.at
Gille
Lars
L
Staniek
Katrin
K
D000818:Animals; D019069:Cell Respiration / Q000502:physiology*; D004734:Energy Metabolism; D015227:Lipid Peroxidation / Q000502:physiology; D008563:Membrane Lipids / Q000502:physiology; D008564:Membrane Potentials / Q000502:physiology; D008565:Membrane Proteins / Q000737:chemistry / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism*; D010101:Oxygen Consumption; D010743:Phospholipids / Q000502:physiology; D011487:Protein Conformation; D017382:Reactive Oxygen Species / Q000378:metabolism*
D008563:Membrane Lipids; D008565:Membrane Proteins; D010743:Phospholipids; D017382:Reactive Oxygen Species