<i>IN SITU</i> HYDROGEN PEROXIDE PRODUCTION MAY ACCOUNT FOR A PORTION OF NUV (300–400 nm) INACTIVATION OF STATIONARY PHASE <i>Escherichia coli</i>

Hartman, Paul A.

doi:10.1111/j.1751-1097.1986.tb05595.x

Cited by 17 publications

(14 citation statements)

References 16 publications

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“…Although significant H 2 O 2 levels have never been measured in micro-organisms exposed to UVA (Hartman, 1986;Kramer & Ames, 1987), our data employing ROS scavengers and reporter strains support the hypothesis that H 2 O 2 is a major product of exposure to lethal UVA doses (Tyrrell, 1985;Hartman, 1986;Kramer & Ames, 1987;Khaengraeng & Reed, 2005). In addition, it is demonstrated that induction of katA and katB depends, at least in part, on the H 2 O 2 levels generated by UVA exposure, suggesting an OxyR-mediated response.…”

Section: Discussionsupporting

confidence: 67%

Exposure to low UVA doses increases KatA and KatB catalase activities, and confers cross-protection against subsequent oxidative injuries in Pseudomonas aeruginosa

et al. 2016

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Solar UVA radiation is one of the main environmental stress factors for Pseudomonas aeruginosa. Exposure to high UVA doses produces lethal effects by the action of the reactive oxygen species (ROS) it generates. P. aeruginosa has several enzymes, including KatA and KatB catalases, which provide detoxification of ROS. We have previously demonstrated that KatA is essential in defending P. aeruginosa against high UVA doses. In order to analyse the mechanisms involved in the adaptation of this micro-organism to UVA, we investigated the effect of exposure to low UVA doses on KatA and KatB activities, and the physiological consequences. Exposure to UVA induced total catalase activity; assays with non-denaturing polyacrylamide gels showed that both KatA and KatB activities were increased by radiation. This regulation occurred at the transcriptional level and depended, at least partly, on the increase in H 2 O 2 levels. We demonstrated that exposure to low UVA produced a protective effect against subsequent lethal doses of UVA, sodium hypochlorite and H 2 O 2 . Protection against lethal UVA depends on katA, whilst protection against sodium hypochlorite depends on katB, demonstrating that different mechanisms are involved in the defence against these oxidative agents, although both genes can be involved in the global cellular response. Conversely, protection against lethal doses of H 2 O 2 could depend on induction of both genes and/or (an)other defensive factor(s). A better understanding of the adaptive response of P. aeruginosa to UVA is relevant from an ecological standpoint and for improving disinfection strategies that employ UVA or solar irradiation.

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Section: Discussionsupporting

confidence: 67%

Exposure to low UVA doses increases KatA and KatB catalase activities, and confers cross-protection against subsequent oxidative injuries in Pseudomonas aeruginosa

et al. 2016

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“…Recently, Leowen and his colleagues have described mutants which are defective in catalase activity (21)(22)(23). In this paper, we present evidence that lesions in the katF gene, but not the katE or katG gene, result in sensitivity to broad-spectrum NUV as well as to 14 SAMMARTANO ET AL. Cells were grown at 37°C with shaking in sidearm flasks (Belco) containing 50 ml of LB broth to stationary phase as described previously (37,38).…”

mentioning

confidence: 94%

Control of sensitivity to inactivation by H2O2 and broad-spectrum near-UV radiation by the Escherichia coli katF locus

Sammartano¹,

Tuveson²,

Davenport³

1986

J Bacteriol

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Mutations in the Escherichia coli katF gene (hydroperoxidase II) result in sensitivity to inactivation by H202 and broad-spectrum near-UV (NUV; 300 to 400 nm) radiation. Another mutation, nur, originally described as conferring sensitivity to inactivation by broad-spectrum and monochromatic NUV, also confers sensitivity to inactivation by H202. Genetic analysis via transduction suggests that the nur mutation is a mutant allele of the katF locus. As previously reported for broad-spectrum and monochromatic NUV wavelengths, the sensitivity of a particular strain to H202 inactivation is also independent of the recA and uvrA alleles. Extracts of nur and katF strains lack catalase (hydroperoxidase II) as revealed by polyacrylamide gels stained for such activity, which is consistent with the genetic results.The mutagenic and inactivating effects of both monochromatic and broad-spectrum near-UV (NUV) wavelengths (300 to 400 nm) have been the subject of numerous investigations, which have been extensively reviewed (10,13,17,18,40).A mutation in an Escherichia coli gene (nur) has been described which sensitizes cells to inactivation by NUV without affecting sensitivity to far-UV (FUV) inactivation (35-37). Specifically, it was shown that the recA13, recAl, and uvrA6 mutations did not affect the sensitivity of stationary-phase cells to NUV inactivation. However, the polAl mutation did influence the sensitivity of E. coli cells to inactivation by NUV in an nur+ genetic background (36). The fact that the polAl mutation sensitizes E. coli to NUV inactivation and that E. coli xthA mutants (exonuclease III deficient) are sensitive to inactivation by H202 (8) and NUV (31) might mean that repair of or protection against NUVand H202-induced damage is based on a complex oxidative defense system (4).Further evidence that H202 is involved in NUV inactivation comes from the observation that incorporation of bovine catalase into the plating medium or the irradiated cell suspension protects E. coli cells from both inactivation and mutagenesis by broad-spectrum NUV (32). Hartman (14) has also presented evidence that H202 is involved with NUV inactivating events in stationary-phase E. coli cells.Pretreatment of E. coli or Salmonella typhimurium cells with a sublethal concentration of H202 results in protection against inactivation by a lethal concentration of H202 (4, 7) as well as by broad-spectrum NUV (33, 39). Tyrrell (39) has shown that pretreatment of growing E. coli cells with low fluences of NUV protects against inactivation by H202. If H202 were one product of NUV irradiation in cells, it would be expected that cells lacking catalase should be sensitive to inactivation by NUV. Recently, Leowen and his colleagues have described mutants which are defective in catalase activity (21)(22)(23). In this paper, we present evidence that lesions in the katF gene, but not the katE or katG gene, result in sensitivity to broad-spectrum NUV as well as to * Corresponding author.

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“…Peak et al (1987) have shown that a significant amount of DNA damage due to near-UV occurs by single-stand breaks. Near-UV radiation is also known to produce reactive oxygen species such as superoxide anion, singlet oxygen and hydrogen peroxide in bacteria (Webb, 1977;Hartman, 1986) and mammalian cells (Danpure and Tyrrell, 1976). However, the role of these photoproducts in UV carcinogenesis is unknown.…”

Section: Correlation Of Dna Photoproducts To Cell Lethality Mutationmentioning

confidence: 99%

Molecular Mechanisms of Ultraviolet Radiation Carcinogenesis

Ananthaswamy

Pierceall

1990

Photochem & Photobiology

357

198

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IN SITU HYDROGEN PEROXIDE PRODUCTION MAY ACCOUNT FOR A PORTION OF NUV (300–400 nm) INACTIVATION OF STATIONARY PHASE Escherichia coli

Cited by 17 publications

References 16 publications

Exposure to low UVA doses increases KatA and KatB catalase activities, and confers cross-protection against subsequent oxidative injuries in Pseudomonas aeruginosa

Exposure to low UVA doses increases KatA and KatB catalase activities, and confers cross-protection against subsequent oxidative injuries in Pseudomonas aeruginosa

Control of sensitivity to inactivation by H2O2 and broad-spectrum near-UV radiation by the Escherichia coli katF locus

Molecular Mechanisms of Ultraviolet Radiation Carcinogenesis

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