“Sunlight”‐induced Mammalian Cell Killing: A Comparative Study of Ultraviolet and Near‐ultraviolet Inactivation

Elkind, M. M.; Han, A.; Chang-Liu, Chin Mei

doi:10.1111/j.1751-1097.1978.tb07668.x

Cited by 64 publications

(12 citation statements)

References 30 publications

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“…The results presented in Figure 1 indicate that 2-aminofluorene is also activated to a mutagen by light. The activation of 2-aminofluorene using a sun lamp, which emits wavelengths of light primarily below 350 nm [23], confirms the observations of DeFlora [5]. The activation seen using the black, blue, and coolwhite lamps indicates that lamps emitting wavelengths of light longer than those produced by the sun lamp are also effective in the mutagenic activation of this compound.…”

Section: Discussionsupporting

confidence: 83%

Mutagenic activation of 2‐aminofluorene by fluorescent light

White

Heflich

1985

Teratog Carcinog Mutagen

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To determine the effect of artificially produced light on the direct mutagenicity of 2-aminofluorene, that arylamine was irradiated with either sun, cool-white, black, blue, or yellow fluorescent light or held in the dark prior to assaying for mutagenicity using Salmonella typhimurium strain TA98. The effectiveness of these exposures in potentiating the mutagenicity of 2-aminofluorene was sun greater than black greater than cool-white greater than blue greater than yellow approximately equal to dark. By varying the radiant flux densities produced by the lamps and using optical filters, wavelengths of light up to approximately 450 nm were found to be effective in the mutagenic potentiation. Studies using radical scavengers and oxygen modifiers indicated that the light-induced mutagenicity was dependent on oxygen and that singlet oxygen may be an effective activator of 2-aminofluorene. The mutagenicity of fluorene was not increased by exposure to light, while only sunlight potentiated the mutagenicity of 2-acetylaminofluorene. This result suggested the importance of the primary amine in the mutagenic activation of 2-aminofluorene by light. Light-activated 2-aminofluorene was less mutagenic in strains TA98NR and TA98/1,8-DNP6 than in TA98. This observation, combined with the dependence of the photoactivation on oxygen and amino-substitution, indicated that the light-enhanced mutagenicity was at least partially due to N-oxidized photoproducts. These studies indicate that the effect of light on environmental contaminants must be considered in assessing their genotoxic potential.

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Section: Discussionsupporting

confidence: 83%

Mutagenic activation of 2‐aminofluorene by fluorescent light

White

Heflich

1985

Teratog Carcinog Mutagen

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“…Cyclobutane pyrimidine dimers were one of the main lesions produced after 254 nm UV [Setlow, 19681, and individuals afflicted with the disease xeroderma pigmentosum were sensitive to killing and mutation by UV [Maher and McCormick, 10761, and were defective in their ability to excise dimers [Cleaver, 1975;Setlow et al, 19691 and (6-4) photoproducts [Mitchell and Narin, 19891. Although lesions other than pyrimidine dimers (e.g., ( 6 4 ) photoproducts, thymine glycol, thymine-thymine adducts and their dehydration products, single strand breaks, alkali-labile bonds, DNA-DNA and DNA-protein cross links) were thought also to be responsible for the biological effects of SL in mammalian cells [Cleaver et al, 1988;Elkind et al, 1978;Hariharan and Cerutti, 1977;Smith and Paterson, 1981;Zelle et al, 19801, other work on human [Kantor and Setlow, 19821, frog [Rosenstein and Kantor, 198 I], Chinese hamster V-79 [Rothman and Setlow, 19791, and fish cells [Shima et al, 1981;Shima and Setlow, 19841 have shown that the mechanism of cell killing, at wavelength < 3 15 nm. is mainly the formation of pyrimidine dimers, as was observed for 254 nm.…”

Section: Discussionmentioning

confidence: 99%

DNA damage, photorepair, and survival in fish and human cells exposed to UV radiation

Ahmed

Setlow

Grist

et al. 1993

Environ and Mol Mutagen

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The effect of various wavelengths of UVB radiation on the induction of cyclobutane pyrimidine dimers in fish cells and human fibroblasts and the repair of these lesions were studied using an UV-endonuclease to measure dimers (endonuclease sensitive sites) by sedimentation of radioactive DNA, by gel electrophoresis of unlabeled DNA, and by cell survival. The data show that fish cells have an efficient photoreactivation system at wavelength > 304 nm that reverses cytotoxicity and dimer formation after exposure to filtered sunlamp irradiation of a shorter wavelength (lambda > 290 nm). Shorter wavelengths in UVB (> 304 nm) are more effective in photoreversal than longer ones (> 320 nm). As a consequence, 50-85% of dimers induced by these wavelengths in fish are photoreactivated while they are being formed. A major cytotoxicological lesion is the cyclobutane pyrimidine dimers. Cultured human fibroblasts do not possess such a repair system. These results indicate that sunlamp irradiation has wavelengths that both damage and repair DNA.

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“…has been studied extensively. Reports on the cytotoxic (Elkind et al, 1978), mutagenic (Hsie e f al., 1977), and oncogenic (Blum, 1959) effects of U V have been widely reported (Setlow, 1978). Many earlier studies employed "germicidal" lamps as the source of U V (eg, Cleaver, 1968).…”

Section: Introductionmentioning

confidence: 99%

A COMPARISON OF MAMMALIAN CELL SENSITIVITY TO EITHER 254 nm OR ARTIFICIAL “SOLAR” SIMULATED RADIATION

Gill

Coohill

1987

Photochem & Photobiology

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The sensitivity of six mammalian cell strains to either germicidal (254 nm) or artificial “solar” simulated radiation was tested. The solar simulator used had an output similar, in some respects, to natural sunlight. Cellular capacity for Herpes simplex virus production was used as the assay procedure. The tested cells were a strain of African green monkey kidney cells and five human skin fibroblast cell strains. The latter included a “normal” cell strain, and four photosensitive cell strains; three of which were strains of xeroderma pigmentosum cells, and one strain of Bloom's syndrome cells. When comparing the D10 values, the different cell strains varied by a factor of six in response to germicidal radiation, but only by a factor of two to artificial “solar” simulated radiation. The relative sensitivity of the cells to either type of radiation also varied from 1.7 to 10.9. Large variations in response occurred even among the xeroderma pigmentosum cell strains. These responses suggest that mammalian cell sensitivity to 254 nm radiation may not be a true indicator of a cell's responses to natural sunlight.

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“Sunlight”‐induced Mammalian Cell Killing: A Comparative Study of Ultraviolet and Near‐ultraviolet Inactivation

Cited by 64 publications

References 30 publications

Mutagenic activation of 2‐aminofluorene by fluorescent light

Mutagenic activation of 2‐aminofluorene by fluorescent light

DNA damage, photorepair, and survival in fish and human cells exposed to UV radiation

A COMPARISON OF MAMMALIAN CELL SENSITIVITY TO EITHER 254 nm OR ARTIFICIAL “SOLAR” SIMULATED RADIATION

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