Pathways of oxidative damage.
The phenomenon of oxygen toxicity is universal, but only recently have we begun to understand its basis in molecular terms. Redox enzymes are notoriously nonspecific, transferring electrons to any good acceptor with which they make electronic contact. This poses a problem for aerobic organisms, since molecular oxygen is small enough to penetrate all but the most shielded active sites of redox enzymes. Adventitious electron transfers to oxygen create superoxide and hydrogen peroxide, which are partially reduced species that can oxidize biomolecules with which oxygen itself reacts poorly. This review attempts to present our still-incomplete understanding of how reactive oxygen species are formed inside cells and the mechanisms by which they damage specific target molecules. The vulnerability of cells to oxidation lies at the root of obligate anaerobiosis, spontaneous mutagenesis, and the use of oxidative stress as a biological weapon.
Imlay
James A
JA
Department of Microbiology, University of Illinois, Urbana, Illinois 61801, USA. jimlay@uiuc.edu
D024322:Amino Acids, Aromatic / Q000378:metabolism; D000818:Animals; D002374:Catalase / Q000378:metabolism; D004926:Escherichia coli / Q000378:metabolism; D006801:Humans; D007506:Iron-Sulfur Proteins / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D010100:Oxygen / Q000009:adverse effects / Q000737:chemistry / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism
D024322:Amino Acids, Aromatic; D007506:Iron-Sulfur Proteins; D017382:Reactive Oxygen Species; D002374:Catalase; D013482:Superoxide Dismutase; D010100:Oxygen