Abstract
Activation of poly(ADP-ribose) polymerase plays an essential role in mediating the toxic effects of DNA damage in non-dividing lymphocytes. In cells with extensive DNA damage, excessive poly(ADP-ribose) polymerase activity can exhaust the available NAD pool, leading to a depletion of cellular ATP and to toxic perturbations of intermediary metabolism (1). Various agents known to damage DNA have been shown in vitro to elicit the biochemical sequelae of poly(ADP-ribose) polymerase activity in resting human lymphocytes (2). For example, exposure of lymphocytes to xanthine oxidase plus hypoxanthine causes massive DNA damage and a lethal fall in cellular NAD and ATP levels, attributable to excessive poly(ADP-ribose) polymerase activity (3). This model system suggests that poly(ADP-ribose) polymerase activation may contribute to immune dysfunction in certain chronic inflammatory states, in which stimulated neutrophils release toxic oxygen species.
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