Nitric oxide and hydrogen peroxide production during apoptosis of human neutrophils.

BUSTAMANTE J, CARRERAS MC, RIOBÓ N, TOVAR A, MONTERO G, PODEROSO JJ, BOVERIS A

Oxidative stress, Cancer, AIDS, and Neurodegenerative Diseases

Año: 1998; p. 205 - 211

Polymorphonuclear Ieukocytes (PMN) play detcrminant roles in immunity and inflammation. These processes are mediated by the activation of the NADPH oxidase, which generates superoxidc anion (O2-), and by the activation of a cytoplasmic, constitutive and inducible nitric oxide synthase (NOS and iNOS), which produces nitric oxide (NO·) (1 – 5). Superoxide anion, H2O2, and NO· are not only efficient antimicrobial effector molecules, they are key mediators in inflammatory reactions in which they participate, altering the expression of endothelial adhesion molecules and inducing the production of different cytokines (6-8). Together with these molecules and proteolytic enzymes, PMN cells can mediate intra- and extracellular cytotoxicity and modulate different cellular functions in adjacent cells. Afer degradation of the ingested material, polymorphonuclear cells die. These terminally differentiated cells are not able to proliferate and in vitro they demise rapidly by an apoptotic mechanism; PMN senecent cells are then recognized by macrophages by a cell-surface mechanism mediated by vitronectin receptor (9). The molecular mechanisms by which spontaneous apoptosis of human PMN occurs are not known. The present study deals with the role of O2-, H2O2, and NO· as inducers of spontaneous apoptosis in human neutrophils and with the inhibition of this physiological process by the antioxidant compound lipoic acid.