Reactive oxygen species and the bacterial response to lethal stress

X Zhao, K Drlica - Current opinion in microbiology, 2014 - Elsevier
X Zhao, K Drlica
Current opinion in microbiology, 2014Elsevier
Highlights•Lethal antimicrobial stress triggers accumulation of reactive oxygen species
(ROS).•The stress-mediated ROS cascade and its effects are controlled in multiple ways.•At
moderate levels, ROS reduce stress by inducing protective regulons.•At high levels, ROS
can be destructive by creating a variety of secondary lesions.•Dietary consumption of
antioxidants may antagonize antimicrobial therapy.Bacteria are killed by a variety of lethal
stressors, some of which promote a cascade of reactive oxygen species (ROS) …
Highlights
  • Lethal antimicrobial stress triggers accumulation of reactive oxygen species (ROS).
  • The stress-mediated ROS cascade and its effects are controlled in multiple ways.
  • At moderate levels, ROS reduce stress by inducing protective regulons.
  • At high levels, ROS can be destructive by creating a variety of secondary lesions.
  • Dietary consumption of antioxidants may antagonize antimicrobial therapy.
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.
Elsevier