Biochemistry of reoxygenation injury.
This paper summarizes current knowledge on the biochemistry of oxygen toxicity in general and the ischemia-reoxygenation tissue injury in particular. The superoxide radical, hydrogen peroxide, and the hydroxyl radical in cells can be formed enzymically or nonenzymically. Primary effects of oxygen radicals result in lipid peroxidation, which is believed to be initiated by a perferryl radical. Secondary effects are believed to be due to a disturbance in cellular calcium homeostasis. Reactions and treatment potentials are highly complex and their effects on cells, tissues, and organism are difficult to predict. Treatment potentials include superoxide dismutase, catalase, calcium entry blockers, iron chelators, xanthine oxidase inhibitors, and agents to prevent leukocyte adhesion. Reoxygenation injury mechanisms during resuscitation from clinical death can be studied in animals by evaluating the effects of antireoxygenation injury therapies and by monitoring free radical reactions.
Ernster
L
L
Department of Biochemistry, Arrhenius Laboratory, University of Stockholm, Sweden.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D006878:Hydroxides / Q000378:metabolism; D017665:Hydroxyl Radical; D015227:Lipid Peroxidation; D010100:Oxygen / Q000633:toxicity*; D012151:Resuscitation; D013482:Superoxide Dismutase / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism
D006878:Hydroxides; D013481:Superoxides; D017665:Hydroxyl Radical; D006861:Hydrogen Peroxide; D013482:Superoxide Dismutase; D010100:Oxygen; D002118:Calcium