Lethal and Mutagenic Effects of Near-Ultraviolet Radiation

Webb, Robert B.

doi:10.1007/978-1-4684-2577-2_4

Cited by 191 publications

(91 citation statements)

References 229 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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

View full text Add to dashboard Cite

Section: Correlation Of Dna Photoproducts To Cell Lethality Mutationmentioning

confidence: 99%

Molecular Mechanisms of Ultraviolet Radiation Carcinogenesis

Ananthaswamy

Pierceall

1990

Photochem & Photobiology

357

198

View full text Add to dashboard Cite

“…The accumulation of DNA photoproducts can be lethal through the blockage of DNA replication and transcription. UVA can cause photodamage to a variety of molecules as well as physiological processes directly or indirectly by inducing the production of reactive oxygen species (5,6,17,53). Distinct differences between far-UV (UVC) and near-UV (UVB and UVA) damage have been observed in both bacteria and bacteriophages (6).…”

mentioning

confidence: 99%

Survival of Shewanella oneidensis MR-1 after UV Radiation Exposure

Qiu

Sundin

Chai

et al. 2004

Appl Environ Microbiol

View full text Add to dashboard Cite

؊2 , respectively. Photoreactivation conferred an increased survival rate to MR-1 of as much as 177-to 365-fold, 11-to 23-fold, and 3-to 10-fold following UVC, UVB, and solar light irradiation, respectively. A significant UV mutability to rifampin resistance was detected in both UVC-and UVB-treated samples, with the mutation frequency in the range of 10 ؊5 to 10 ؊6 . Unlike in E. coli, the expression levels of the nucleotide excision repair (NER) component genes uvrA, uvrB, and uvrD were not damage inducible in MR-1. Complementation of Pseudomonas aeruginosa UA11079 (uvrA deficient) with uvrA of MR-1 increased the UVC survival of this strain by more than 3 orders of magnitude. Loss of damage inducibility of the NER system appears to contribute to the high sensitivity of this bacterium to UVR as well as to other DNA-damaging agents.

show abstract

“…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.…”

mentioning

confidence: 99%

“…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).…”

mentioning

confidence: 99%

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

View full text Add to dashboard Cite

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.

show abstract

Lethal and Mutagenic Effects of Near-Ultraviolet Radiation

Cited by 191 publications

References 229 publications

Molecular Mechanisms of Ultraviolet Radiation Carcinogenesis

Molecular Mechanisms of Ultraviolet Radiation Carcinogenesis

Survival of Shewanella oneidensis MR-1 after UV Radiation Exposure

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

Contact Info

Product

Resources

About