Human disease, free radicals, and the oxidant/antioxidant balance.
The reduction of molecular oxygen by healthy cells is a finely tuned, tightly controlled process. When cells are sick or injured they make increased amounts of superoxide radical (O2.-) and hydrogen peroxide. A few recurring basic mechanisms appear to be responsible for the free radical-mediated components of a broad spectrum of disease states. Recent research indicates that the relationship between superoxide radical and the enzymes responsible for its removal (the superoxide dismutases, SOD) reflects a much more delicate balance than was first envisioned. When used therapeutically at high doses, SOD either loses its ability to protect ischemically injured isolated hearts, or actually exacerbates the injury. This concept of a "downside" due to too much superoxide dismutase is strongly supported by other studies in which SOD is genetically overexpressed, causing a variety of metabolic problems.
McCord
J M
JM
Webb-Waring Lung Institute, University of Colorado Health Sciences Center, Denver 80262.
D005609:Free Radicals / Q000378:metabolism*; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D007249:Inflammation / Q000378:metabolism*; D007501:Iron / Q000378:metabolism; D015227:Lipid Peroxidation; D010084:Oxidation-Reduction; D010100:Oxygen / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015427:Reperfusion Injury / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism
D005609:Free Radicals; D017382:Reactive Oxygen Species; D013481:Superoxides; D006861:Hydrogen Peroxide; D007501:Iron; D013482:Superoxide Dismutase; D010100:Oxygen