Oxidative stress responses in Escherichia coli and Salmonella typhimurium

Abstract

Oxidative stress is strongly implicated in a number of diseases, such as rheumatoid arthritis, inflammatory bowel disorders, and atherosclerosis, and its emerging as one of the most important causative agents of mutagenesis, tumorigenesis, and aging. Recent progress on the genetics and molecular biology of the cellular responses to oxidative stress, primarily in Escherichia coli and Salmonella typhimurium, is summarized. Bacteria respond to oxidative stress by invoking two distinct stress responses, the peroxide stimulon and the superoxide stimulon, depending on whether the stress is mediated by peroxides or the superoxide anion. The two stimulons each contain a set of more than 30 genes. The expression of a subset of genes in each stimulon is under the control of a positive regulatory element; these genes constitute the OxyR and SoxRS regulons. The schemes of regulation of the two regulons by their respective regulators are reviewed in detail, and the overlaps of these regulons with other stress responses such as the heat shock and SOS responses are discussed. The products of Oxy-R- and SoxRS-regulated genes, such as catalases and superoxide dismutases, are involved in the prevention of oxidative damage, whereas others, such as endonuclease IV, play a role in the repair of oxidative damage. The potential roles of these and other gene products in the defense against oxidative damage in DNA, proteins, and membranes are discussed in detail. A brief discussion of the similarities and differences between oxidative stress responses in bacteria and eukaryotic organisms concludes this review.

Proteome of Geobacter sulfurreducens in the presence of U(VI)

“…This reduction could potentially be catalysed by two proteins encoding typical 2-Cys subfamily peroxiredoxins (GSU0352 and GSU3246) and glutaredoxin (GSU1155), which were more highly expressed in cells grown in the presence of U(VI) (Table 2). Homologues of rhodanese-like proteins (GSU0505 and GSU2516) that are involved in the oxidative stress response of E. coli (Farr & Kogoma, 1991) were also expressed in higher abundance when U(VI) was present (Table 2).…”

Marinobacter atlanticus electrode biofilms differentially regulate gene expression depending on electrode potential and lifestyle

“…A gene for the gamma-subunit of exodeoxyribonuclease V (ACP86_09165), also known as RecD, was also more highly expressed. In E. coli , RecBCD initiates recombinatorial repair of damaged double-stranded DNA, including that caused by oxidative stress [ 45 ]. The genes for the alpha- and beta-subunits, RecBC (ACP86_09155 and ACP86_09160) were not differentially expressed at the cutoff values.…”

Research progress on the injury mechanism and detection method of disinfectant-injured Escherichia coli in the drinking water system

“…These results all indicated that after exposure to NaClO, a strong oxidative stress reaction occurred in E. coli, which caused its oxidative injury and formed disinfectantinjured bacteria ( Jin et al 2020). Studies have shown that oxidative stress can lead to the peroxidation of lipids on bacterial cell membranes, which will destroy the structural integrity of the cell membrane and affect the related functions of the membrane (Farr & Kogoma 1991;Ibrahim et al 2000). Tandon et al (2007) found that chlorine-injured E. coli and Enterococcus faecalis become sensitive to ROS, giving higher counts under ROS-neutralized enumeration conditions than under conventional aerobic conditions.…”