Where in the world do bacteria experience oxidative stress?

Abstract

Summary Reactive oxygen species – superoxide, hydrogen peroxide and hydroxyl radicals – have long been suspected of constraining bacterial growth in important microbial habitats and indeed of shaping microbial communities. Over recent decades, studies of paradigmatic organisms such as Escherichia coli, Salmonella typhimurium, Bacillus subtilis and Saccharomyces cerevisiae have pinpointed the biomolecules that oxidants can damage and the strategies by which microbes minimize their injuries. What is lacking is a good sense of the circumstances under which oxidative stress actually occurs. In this MiniReview several potential natural sources of oxidative stress are considered: endogenous ROS formation, chemical oxidation of reduced species at oxic–anoxic interfaces, H2O2 production by lactic acid bacteria, the oxidative burst of phagocytes and the redox‐cycling of secreted small molecules. While all of these phenomena can be reproduced and verified in the lab, the actual quantification of stress in natural habitats remains lacking – and, therefore, we have a fundamental hole in our understanding of the role that oxidative stress actually plays in the biosphere.

Phage-centric ecological interactions in aquatic ecosystems revealed through ultra-deep metagenomics

“…254 phage genomes) harbored genes involved in oxidative stress mitigation (Supplementary Table S5). Aquatic bacteria routinely experience the damaging effects of reactive oxygen species (ROS) (superoxide, hydrogen peroxide and hydroxyl radicals) produced by their own metabolic machineries, released by other community members or generated by UV-induced photochemical reactions [37]. In defense, bacteria employ several strategies to prevent ROS formation, deactivate ROS and repair the ROS-induced damage.…”

DNA double-strand breaks induced by reactive oxygen species promote DNA polymerase IV activity inEscherichia coli

“…2). In the presence of ROS, E. coli cells induce the peroxide and/or superoxide stress responses in which expression of superoxide dismutase, alkyl hydroperoxidase and Fe 3+ enterobactin transporter genes are upregulated (reviewed in (3,4,40–44)). Therefore, we developed an assay to monitor expression of gfp from ROS-regulated and iron-responsive promoters in cells treated with ciprofloxacin, trimethoprim or hydrogen peroxide (as a control).…”

“…For this purpose, we constructed three plasmids that express GFP (fast-folding GFP, sf-gfp (45)) from the ROS-regulated promoters of sodA (notably regulated by superoxides/redox active compound via SoxRS and by the iron (Fe 2+ ) concentration via Fur (4, 41), SI Appendix , Fig. 3 A ), ahpC (regulated by OxyR (4,42,43), SI Appendix , Fig. 4 A ) or fepD (regulated by Fur pathway; iron homeostasis (44), SI Appendix , Fig.…”

“…Three promoters of genes regulated by changes in ROS or iron levels were cloned and fused to the sf-gfp gene (45) into a pQBI63 plasmid (Qbiogene). Briefly, upstream regions of sodA gene (consisting of the 284 nt intergenic region of rhaT and sodA ) regulated by soxS and Fur (4, 41), or ahpC gene (−372 to −1 nt of ATG) regulated by OxyR (4,42,43), or fepD gene (−170 to −1 nt of ATG) regulated by Fur (44), were amplified and cloned into the pQBI63 plasmid using Bgl II/ Nhe I restriction enzyme to generate respectively pSTB- sodA-gfp , pCJH0008 and pCJH0009. All constructions were confirmed by sequencing.…”

“…Many antibiotics induce the accumulation of reactive oxygen species (ROS) within bacterial cells (1–4). These highly reactive molecules cause widespread damage to biomolecules.…”