Bacteria are killed by a variety of lethal stressors, some of which promote a cascade of reactive oxygen species (ROS). Perturbations expected to alter ROS accumulation affect the lethal action of diverse antibacterials, leading to the hypothesis that killing by these agents can involve ROS-mediated self-destruction. Recent challenges to the hypothesis are considered, particularly with respect to complexities in assays that distinguish primary damage from the cellular response to that damage. Also considered are bifunctional factors that are protective at low stress levels but destructive at high levels. These considerations, plus new data, support an involvement of ROS in the lethal action of some antimicrobials and raise important questions concerning consumption of antioxidant dietary supplements during antimicrobial chemotherapy.
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