The mystery of reactive oxygen species derived from cell respiration.
Author(s) -
Hans Nohl,
Lars Gille,
Katrin Staniek
Publication year - 2004
Publication title -
acta biochimica polonica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.452
H-Index - 78
eISSN - 1734-154X
pISSN - 0001-527X
DOI - 10.18388/abp.2004_3615
Subject(s) - reactive oxygen species , bioenergetics , mitochondrion , ubiquinol , respiration , redox , chemistry , electron transport chain , biophysics , cellular respiration , electron transfer , oxygen , membrane potential , mitochondrial ros , inner mitochondrial membrane , membrane , microbiology and biotechnology , biochemistry , biology , photochemistry , coenzyme q – cytochrome c reductase , botany , cytochrome c , organic chemistry
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.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom