Mechanism of production of toxic oxygen radicals by granulocytes and macrophages and their function in the inflammatory process.
The paper deals with 1) the features of the respiratory burst (increase of the respiration with production of O2 metabolites, O2-, H2O2, OH) of the inflammatory cells; 2) the factors responsible for its activation; 3) the methods for its measurement; 4) the molecular events which take place at the level of the plasma membrane following the interaction between the stimuli and the cell surface (the Ca++ changes, the modification of membrane potential, the activation of phospholipid turnover) and the hypothesis of the activation of the protein kinase C; 5) the nature of the NADPH oxidase whose activation is responsible for the respiratory burst and the production of O2 metabolites; 6) the defensive, toxic, proinflammatory and modulatory effects due to the reactivity of the oxygen metabolites.
D000818:Animals; D002462:Cell Membrane / Q000502:physiology; D004789:Enzyme Activation; D005609:Free Radicals; D006098:Granulocytes / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D007700:Kinetics; D008264:Macrophages / Q000502:physiology*; D009247:NADH, NADPH Oxidoreductases / Q000378:metabolism; D019255:NADPH Oxidases; D010100:Oxygen / Q000378:metabolism*; D010101:Oxygen Consumption; D010586:Phagocytes / Q000502:physiology; D010587:Phagocytosis
D005609:Free Radicals; D009247:NADH, NADPH Oxidoreductases; D019255:NADPH Oxidases; D010100:Oxygen