Oxidative inactivation of <i>Escherichia coli</i> by hypochlorous acid

Albrich, J M; Hurst, James K.

doi:10.1016/0014-5793(82)80591-7

Cited by 94 publications

(41 citation statements)

References 20 publications

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“…Hypochlorous acid is generally considered to be a highly destructive, nonselective oxidant which reacts avidly with a variety of subcellular compounds and affects metabolic processes (2,3,41). It acts on membranes, changing their permeability (46,54), inhibits transport (7), fragments proteins (49), and reacts with nucleotides (10,17).…”

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confidence: 99%

Hypochlorous acid stress in Escherichia coli: resistance, DNA damage, and comparison with hydrogen peroxide stress

1996

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We have investigated the mechanisms of killing of Escherichia coli by HOCl by identifying protective functions. HOCl challenges were performed on cultures arrested in stationary phase and in exponential phase. Resistance to HOCl in both cases was largely mediated by genes involved in resistance to hydrogen peroxide (H 2 O 2 ). In stationary phase, a mutation in rpoS, which controls the expression of starvation genes including those which protect against oxidative stress, renders the cells hypersensitive to killing by HOCl. RpoSregulated genes responsible for this sensitivity were dps, which encodes a DNA-binding protein, and, to a lesser extent, katE and katG, encoding catalases; all three are involved in resistance to H 2 O 2 . In exponential phase, induction of the oxyR regulon, an adaptive response to H 2 O 2 , protected against HOCl exposure, and the oxyR2 constitutive mutant is more resistant than the wild-type strain. The genes involved in this oxyR-dependent resistance have not yet been identified, but they differ from those primarily involved in resistance to H 2 O 2 , including katG, ahp, and dps. Pretreatment with HOCl conferred resistance to H 2 O 2 in an OxyR-independent manner, suggesting a specific adaptive response to HOCl. fur mutants, which have an intracellular iron overload, were more sensitive to HOCl, supporting the generation of hydroxyl radicals upon HOCl exposure via a Fenton-type reaction. Mutations in recombinational repair genes (recA or recB) increased sensitivity to HOCl, indicative of DNA strand breaks. Sensitivity was visible in the wild type only at concentrations above 0.6 mg/liter, but it was observed at much lower concentrations in dps recA mutants.

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Hypochlorous acid stress in Escherichia coli: resistance, DNA damage, and comparison with hydrogen peroxide stress

1996

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“…This correlation between EC and viability has not been extensively tested, however, and several exceptions to the general behavior have been reported. Notably, the fermentative bacterium Streptococcus cremoris (16), the obligate intracellular bacterium Rickettsia typhi (19), and two microbial eucaryotes (4,13) inactivated cell suspensions, bacteria were flow-mixed with HOCI through a tangential 12-jet mixing chamber as previously described (2). Sodium thiosulfate was added 15 min after the bacteria were mixed to stop any residual chlorination reactions.…”

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Viability and metabolic capability are maintained by Escherichia coli, Pseudomonas aeruginosa, and Streptococcus lactis at very low adenylate energy charge

et al. 1988

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Metabolic regulation by nucleotides has been examined in several bacteria within the context of the adenylate energy charge (EC) concept. The ECs of bacteria capable of only fermentative metabolism (Streptococcus lactis and the ATPase-less mutant Escherichia coli AN718) fell to less than 0.2 under carbon-limiting conditions, but the bacteria were able to step up the EC to greater than 0.8 upon exposure to nutrient sugars. Similarly, nongrowing E. coli 25922, whose EC had been artificially lowered to less than 0.1 by the addition of the protonophore carbonyl cyanide m-chlorophenylhydrazone (CCCP), was able to immediately step up the EC to 0.8 to 0.9 upon the addition of glucose but was unable to respond to respiratory substrates.

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“…Neverthe less, the generation of hypochloric acid during PMN stimulation and its release into the medium can play a significant role in the phage inactivation. Since this acid affects the nucleophilic compounds [31,32], it is conceivable that this highly reactive metabolite dam ages both the proteins and the DNA of phages. This possibility seems to be corroborated by the fact that phage activity is preserved in the presence of taurine which acts as halide scavenger through the formation of N-chloramine derivatives [ 15].…”

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confidence: 99%

Polymorphonuclear Leukocyte Stimulation Measured by Phage Inactivation

Ferrini

Mileo

Nista³

et al. 1989

Int Arch Allergy Immunol

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A quantitative assay for determining the polymorphonuclear neutrophil (PMN) stimulation is described. The method is based on the inactivation of lambda vector phages that occurs after a brief exposure to stimulated PMNs. The determination of the number of residual plaque-forming units on the appropriate bacterial host allows a reproducible and sensitive quantitative assay for measuring the stimulation level of the PMN. In comparison with other methods that employ bacteria or eukaryotic cells, this assay provides several advantages and can be used for investigating the biochemical and physiological processes responsible for PMN stimulation.

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Oxidative inactivation of Escherichia coli by hypochlorous acid

Cited by 94 publications

References 20 publications

Hypochlorous acid stress in Escherichia coli: resistance, DNA damage, and comparison with hydrogen peroxide stress

Hypochlorous acid stress in Escherichia coli: resistance, DNA damage, and comparison with hydrogen peroxide stress

Viability and metabolic capability are maintained by Escherichia coli, Pseudomonas aeruginosa, and Streptococcus lactis at very low adenylate energy charge

Polymorphonuclear Leukocyte Stimulation Measured by Phage Inactivation

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