ABSTRACT
A role for oxidative stress in the pathogenesis of AIDS is suggested by a large body of data from in vitro and biochemical-clinical studies (1-10).
Recent reports have implicated the intracellular excess of reactive oxygen species (ROS) in the induction of HIV expression (1-4) and in the initiation of apoptotic cell death (11-13). Proof of a metabolic alteration leading to decreased ability to counteract oxidative stress came from studies which showed that glutathione is decreased in peripheral blood mononuclear cells from symptom-free individuals (10). Other studies showed alterations of biochemical indicators of systemic oxidative damage (7-9), thus suggesting an increase in tissue degeneration with the progression of AIDS. These findings together give a rational basis for antioxidant treatments to reduce viral multiplication and apoptotic cell death (14,15). However, the origin of these cellular and systemic oxidative alterations and whether, and to what extent, they influence immune functions are still far from clear.
