Free radicals and the heart.
Free radicals may arise from a number of sources as a result of a variety of cellular mechanisms; they are generated under both normal and pathological circumstances. The xanthine oxidase pathway, the arachidonic acid pathway, invading leucocytes, catecholamine oxidation, and mitochondrial activity can all lead to the production of a variety of reactive oxygen intermediates including superoxide, hydrogen peroxide, and the hydroxyl radical. Whatever their source, free radicals can be extremely toxic to the cell and they are capable of causing major membrane injury by initiating lipid peroxidation or by altering the activity of membrane-bound enzyme systems which control ionic movement. The cell possesses highly efficient protective mechanisms, including antioxidants such as vitamins C and E and the enzymes superoxide dismutase and catalase, all of which are designed to prevent the occurrence of free radical-induced injury under normal conditions. However, during ischaemia and reperfusion, these protective mechanisms may be overwhelmed and severe free radical-mediated injury may occur. Ischaemia may prime the myocardium for free radical-induced injury. The great majority of the evidence that manipulation of free radicals may protect against such injury is, however, circumstantial.
Hearse
D J
DJ
Cardiovascular Research, Rayne Institute, St. Thomas' Hospital, London, England.
D000818:Animals; D003327:Coronary Disease / Q000378:metabolism; D005609:Free Radicals; D006801:Humans; D015428:Myocardial Reperfusion Injury / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism
D005609:Free Radicals; D010100:Oxygen