[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] 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] 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] 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] The authors report the results of experiments, using L5178Y mouse lymphoma cells, that implicate the ultraviolet-near ultraviolet region of the spectrum emitted by broad spectrum light sources (i.e. wavelengths shorter than 400 nm) as being responsible for the toxic and mutagenic effects of radiation from these sources. Cells were exposed to radiation from Cool White fluorecent lamps which was filtered either through Pyrex glass or through a sheet of clear plastic diffuser material. The results indicated that removal of wavelenghs below 388 nm effectively eliminates the toxic and mutagenic effects of radiation from Cool White fluorescent lamps, while removal of wavelengths below 270 nm only partially reduces these effects. (Auth.)

[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] 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.)

[en] The development of an information base of light-induced bioeffects data to support regulatory activities is a continuing process. Though standards covering the three spectral regions of light, ultraviolet (UV), visible, and infrared (IR), currently exist, attempts must regularly be made to assess the adequacy of these standards with respect to currently available biological information. In order to establish a starting point for these reassessments, the biological effects of light considered in establishing the standards must first be determined. Using this information, the strengths and weaknesses of each standard can be evaluated, and particularly important areas of future research can be determined. This document analyzes current standards covering non-coherent light with respect to the biological effects considered in their adoption. The current standards covering non-coherent light are based on few biological endpoints. The ACGIH standard for ultraviolet considers only skin erythema and eye keratitis; the visible light standard considers only retinal damage; and the infrared standard considers only lens cataracts. Clearly, other biological effects need to be considered. But any standard represents a state-of-the-art estimate of maximum allowable exposure levels, and while there is considerable qualitative information on many additional biological effects of light, there is little quantitative information. Without this information it is difficult either to incorporate these effects into the regulatory process or to determine if the current standards are adequate to cover them