Lethal effects of pyrimidine dimers induced at 365 nm in strains of E. coli differing in repair capability

Webb, Robert B.; Brown, Mickey S.; Tyrrell, Rex M.

doi:10.1016/0027-5107(76)90029-4

Cited by 30 publications

(7 citation statements)

References 17 publications

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“…Figure 2 shows that, indeed, this is the case. Moreover, the photoreactivable sector of 0.7 calculated by the method described by Webb et al (5) is nearly comparable with that obtained after 254 nm irradiation. When the cells were illuminated with flashes in dishes covered with common glass, no lethality was detected, but the very same glass did not interfere with the photoreactivation of 254 nm UV-irradiated cells.…”

Section: Photoreactivation Of Flash-light-induced Lesionssupporting

confidence: 83%

Damage to UV‐Sensitive Cells by Short UV in Photographic Flashes

Menezes

Monteiro

1996

Photochem & Photobiology

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Light emitted by electronic photographic flash units is shown to damage bacteria and human skin fibroblasts deficient in repair systems, with survival curves very similar to those produced by 254 nm short UV. The lesions induced by these flashes are as photorepairable by the photolyase enzyme as those induced by 254 nm UV and result in equivalent survival rates. Biological dosimetry performed with microorganisms highly sensitive to UV (Escherichia coli K12 AB2480, deficient in excision and recombinational-dependent repair systems and Bacillus subtilis UVSSP spores, deficient in excision and in a specific spore repair process) revealed that each 1 ms flash of light from the photographic unit used in this work contained the equivalent of 0.25 J m-2 of 254 nm UV, when measured at a distance of 7.0 cm. This dose of UV was found to be lethal to both repair-deficient E. coli bacteria and repair-deficient human skin fibroblasts obtained from xeroderma pigmentosum donors, as well as mutagenic in B/r wild-type and HCR-mutant bacteria.

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Section: Photoreactivation Of Flash-light-induced Lesionssupporting

confidence: 83%

Damage to UV‐Sensitive Cells by Short UV in Photographic Flashes

Menezes

Monteiro

1996

Photochem & Photobiology

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“…In contrast, whereas the number of dimers induced at 365 nm at 00C for a survival value of 0.37 under aerobic conditions was almost as great (66 dimers) as at 254 nm (75 dimers), no PR for lethality after 365-nm inactivation was detectable ( Fig. 3 and 4) (29).…”

Section: -mentioning

confidence: 87%

“…The procedures followed for photoreactivation (PR) were the same as those described previously (6,29). The primary source of PR radiation was a projector with a 500-W quartz iodine lamp operated at 135 V. The beam was filtered by a 1-cm-light path liquid filter, containing 5% copper sulfate and 15% cobalt sulfate, and an Optics Technology LP400 absorption filter that transmitted wavelengths of approximately 370 to 440 nm (9).…”

Section: Irradiation Procedures Stationary-phase Cellsmentioning

confidence: 99%

Near-UV mutagenesis: photoreactivation of 365-nm-induced mutational lesions in Escherichia coli WP2s

Webb¹

1978

J Bacteriol

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Reversion to tryptophan independence induced by 365-nm and 254-nm radiation was studied in Escherichia coli WP2s (B/r trp uvrA). Under aerobic conditions, the mutant frequency responses was of the fluence-square or "two-hit" type at both 365 and 254 nm when revertants were assayed on minimal agar supplemented with 2% nutrient broth (SEM plates). In contrast, when mutants were assayed on minimal agar supplemented with tryptophan only, the revertant yield was reduced to very low values at 365 nm, whereas values substantially greater than with SEM plates were obtained at 254 nm. Premutational lesions induced by both 365-nm and 254-nm radiation were photoreactivated more than 10-fold when assayed on SEM plates, implicating pyrimidine dimers as premutational lesions at both wavelengths. The strong photoreactivation of 365-nm-induced mutagenesis contrasted strikingly with the complete absence of photoreactivation of 365-nm-induced lethality in this strain.

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“…7B). The dose-response rates for UV-320 photobleaching were nonlinear and showed the typical shapes of processes in which a certain carrying capacity for protection exists in the cells, such as those of some UV-A survival curves (24,25). This indicates that the photobleaching of chl a was caused by different mechanisms under UV-365 and UV-320.…”

Section: Maximummentioning

confidence: 99%

Evidence Regarding the UV Sunscreen Role of a Mycosporine-Like Compound in the Cyanobacterium Gloeocapsa sp

García-Pichel

Wingard

Castenholz

1993

Appl Environ Microbiol

290

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The UV sunscreen role commonly ascribed to mycosporine-like amino acids (MAAs) was investigated with an isolate of the terrestrial cyanobacterium Gloeocapsa sp. strain C-90-Cal-G.(2), which accumulates intracellularly an MAA with absorbance maximum at 326 nm but produces no extracellular sunscreen compound (i.e., scytonemin). The intracellular concentrations of MAA achieved were directly related to the

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Lethal effects of pyrimidine dimers induced at 365 nm in strains of E. coli differing in repair capability

Cited by 30 publications

References 17 publications

Damage to UV‐Sensitive Cells by Short UV in Photographic Flashes

Damage to UV‐Sensitive Cells by Short UV in Photographic Flashes

Near-UV mutagenesis: photoreactivation of 365-nm-induced mutational lesions in Escherichia coli WP2s

Evidence Regarding the UV Sunscreen Role of a Mycosporine-Like Compound in the Cyanobacterium Gloeocapsa sp

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