| While mid-ultraviolet, near-ultraviolet and visible light are ubiquitous factors in our environment, relatively little information concerning the molecular or cellular effects of these radiations on human cells is available. Therefore, I measured DNA lesion induction and repair in DNA repair proficient and deficient cells after exposures to far-UV, mid-UV, near-UV and visible light and attempted to relate these molecular phenomena to the biological endpoint of cell lethality.;Pyrimidine dimers were detected using a dimer specific endonuclease that nicks DNA adjacent to dimers, while strand breaks were measured using an alkaline unwinding assay. The induction efficiencies of both lesions declined with increasing wavelength; however, the decrease in strand break induction was not as rapid as that of dimer induction. The ratio of strand breaks to dimers following cell exposure to 254 or 369 nm radiation was, respectively, 1.8 x 10('-4) or 0.19.;The kinetics of dimer repair (dimers remaining following irradiation and repair incubation were measured), as well as the size of repair synthesized patches (measured using BrdUrd photolysis techniques), remained constant with increasing wavelength, indicating a similar repair mechanism for dimers induced by all wavelengths tested. However, consistent with the detected decline in dimer induction with increasing wavelength the proportion of dimer repair to total DNA repair decreased with increasing wavelength.;The efficiency of cell killing, determined using clonagenic survival assays, dropped rapidly, but not as rapidly as that of dimer induction, with increasing wavelength. In addition, dimer repair deficient xeroderma pigmentosum cells became less lethally hypersensitive with increasing wavelength. These data suggest a decline in dimer induced cell lethality and the existence of non-dimer lethal lesions at longer wavelengths.;Pyrimidine dimer and strand break induction, DNA repair and cell killing were measured after cell exposure to polychromatic but narrow bandwidth light sources with peak emissions at 254, 305, 353, 369 and 445 nm.;Overall, this study presents molecular and cellular evidence that at longer wavelengths, the biological importance of pyrimidine dimers declines while the role of non-dimer, lethal injury increases. Patterns of non-dimer, lethal injury and DNA strand break induction are similar, suggesting that strand breaks contribute to such non-dimer injury. |
