[en] A mouse lymphoma cell assay system was used to determine relative mutagenicity and lethality of the radiation emitted by sunlight and several commonly encountered fluorescent-type artificial light sources. Comparison of the times required to either double the spontaneous mutation frequency or decrease cell survival by 50 percent showed that for 4 lamps, fluorescent radiation was 0.5 to 5 percent as mutagenic, and sunlamp radiation was 8 times as mutagenic, as sunlight. The fluorescent lamps ranged from less than 1 percent to more than 3 percent as lethal as sunlight while the sunlamp was more than 4 times more lethal than sunlight

[en] Exposure of L5178Y-S (but not L5178Y-R) cells to uv-fluences below 4 J/m² causes enhancement of both cell growth rate and cloning efficiency. No measurable increase in production of 6-thioguanine resistant mutants was observed when cells were stimulated by exposure to 0.5 J/m², however, a significant increase in mutation frequency accompanied growth stimulation caused by 2.5 J/m²

[en] Abstract only

[en] The wavelength dependence of ultraviolet radiation-induced cell killing and mutagenicity in L5178Y mouse lymphoma cells has been determined from 235 nm to 313 nm. Cells were irradiated in phosphate buffered saline at 20⁰C. The amount of cell killing was determined by cloning in soft agar medium immediately after irradiation. Mutation frequency was determined, after a 3-day expression time, by cloning in soft agar medium in the presence and the absence of 5-bromo-2' deoxyuridine (BrdUrd). The endpoint used to quantitate lethal effects was the exposure necessary to reduce the surviving fraction to 10%, while the endpoint for mutagenesis was the exposure necessary to increase the frequency of BrdUrd-resistant colonies ten-fold over the background level. Data were corrected for quantum energy and the action spectra for cell killing and mutagenesis were plotted as relative biological effectiveness per quantum vs wavelength, relative to the effect at 265.2 nm. Both action spectra show broad maxima at 270 nm, and are very similar to the action spectra determined by Rothman and Setlow (1979) for pyrimidine dimer formation and cell killing in V-79 cells. (author)

[en] Application is described of thymidine kinase (TK) and hypoxanthine-guanine phosphoribosyl transferase (HGPRT) mutation assay systems and sister chromatid exchange (SCE) in studies of light radiation effects on mammalian cells. Using the TK mutation assay system, we show that unfiltered radiation from a variety of broad spectrum fluorescent lamps and a sunlamp is both toxic and mutagenic to L5178Y TK+/- mouse lymphoma cells in culture. We present preliminary findings of our studies using Indian muntjac (Muntiacus muntjak) cells to determine the relationship between ultraviolet light-induced mutations at the HGPRT locus and ultraviolet light-induced SCE's

[en] Unfiltered broad spectrum radiation emitted by black light, cool white, and black light fluorescent lamps and a sunlamp, is both toxic and mutagenic to L5178Y mouse lymphoma cells when the cells are irradiated in phosphate-buffered saline. The increase in mutant frequency seen after exposure of the cells is linear throughout the range of exposures tested. The linear increase in mutagenesis is observed even at exposure levels which do not cause significant toxicity. To facilitate comparison of the differing rates of mutagenesis derived from exposure-response curves obtained for each light source, we have defined a parameter, joule-equivalent (jem), equal to mutants per 10⁵ survivors per joule per square meter. Jem values are calculated using the integrated irradiance of each lamp. Based on jem values, the relative mutagenicity of the various lamps tested (compared with a germicidal ultraviolet lamp) is 3x10^-3 for the sunlamp, 1x10^-4 for the black light and cool white lamps, and 3x10^-5 for the black light blue lamp. The toxic and mutagenic effects of the lamps are in reasonable agreement with their relative spectral output from 290 to 330 nm. (Auth.)

[en] Reports of the genetic effects of infrared radiation are summarized. A model is described for the action of far-red light on chromosomes in animal cells through disruption of hydrogen bonding in the double stranded DNA, in the complex structure of DNA, histones, and enzymes, or all. This is based upon earlier findings and physical, chemical and quantum mechanical considerations. Some predictions based upon the model are described along with experiments to test these predictions. Some of the studies presently being carried out in our laboratory are discussed

[en] The effect of ultraviolet (uv) radiation (235 to 313 nm) on cell killing and induction of mutants in L5178Y mouse lymphoma cells was compared to the effect of uv radiation (240 to 313 nm) on induction of pyrimidine dimers in Syrian hamster embryo cells. A very strong similarity among the three action spectra was found, suggesting that uv-induced pyrimidine dimer formation is a step common to both cell killing and mutagenesis in mammalian cells

[en] It was obtained by investigating the mutagenesis of UV-irradiated herpes simplex virus after the irradiated virus was grown in human cells that possess normal repair capacity (normal) or lack excision repair (XPA) or post-replication repair (XP var). Evidence is presented which indicate that XPA cells express no host cell reactivation, while XP var cells express the normal level. Viral mutagenesis was measured as the fraction of the progeny of the surviving virus capable of plaque formation in the presence of iododeoxycytidine. The UV exposure needed to yield a given mutagenesis level for virus grown in XPA cells was much lower than that for virus grown in normal cells. However, when the mutation frequencies were compared at similar virus survival levels, the data from virus grown in normal cells and in XPA cells were indistinguishable. Mutagenesis in XP var cells increased as dose squared and was similar in magnitude to that in normal cells. In human cells excision repair has been clearly demonstrated to be important in host cell reactivation of UV-irradiated viruses. (orig./AJ)

[en] Two strains of L5178Y mouse lymphoma cells, L5178Y-R (LY-R) and L5178Y-S (LY-S), differ markedly in their sensitivity to 254 nm UV radiation. In this study, the frequency of hypoxanthine-guanine-phosphoribosyl-transferase-deficient mutants was determined, using 6-thioguanine (TG) as a selective agent, in populations of LY-R and LY-S cells exposed to various fluences of UV radiation. The spontaneous mutation frequency for LY-R cells was (3.7+-0.6) X 10^-5 TGr mutants per viable cell, and the UV induction rate was (2.2+-0.8) X 10^-4 TGr mutants per viable cell per J/m². Both spontaneous and induced mutation frequencies were much lower for LY-S cells. Mutation induction rate was (4.2+-2.2) X 10^-7 TGr mutants per viable cell, per J/m². These differences in mutability do not appear to be due to gene duplication in LY-S cells, or to selective growth disadvantage of LY-S-derived TG-resistant mutants. Possible mechanisms underlying the differences in mutability of LY-R and LY-S cells are considered. (Auth.)