Exposure to UVA light causes damage to cellular components such as DNA and membrane lipids. We showed previously that UVA irradiation can induce mutations in Drosophila larvae and that the major lesions responsible for mutations were not thymidine dimers when wavelengths tested became longer. The use of a longer wavelength with UVA laser apparatus (364 nm) has made it possible to test the effects of this powerful light in biological organisms. In the present study, we irradiated third instar larvae of the urate-null Drosophila mutant strain y v ma-l, which is sensitive to oxidative stress, and compared the effects of 364 nm light irradiation with the effects of X-rays. To assay viability, some of the larvae were kept at 25 degrees C until they eclosed in order to obtain a measure of viability. The remaining larvae were used to measure the amount of 8-hydroxydeoxyguanosine (8-OHdG), an indicator of oxidative DNA damage. The amount of 8-OHdG increased and viability decreased in response to increased UV dose in both the y v ma-l and wild-type strains. With irradiation of 600 kJ m(-2), 8-OHdG/10(6)dG was 7.2 +/- 3.2 and 6.2 +/- 2.0 in y v ma-l and wild-type strains, respectively, whereas the respective levels were 2.2 +/- 0.6 and 2.3 +/- 0.8 without irradiation. Our results indicated that irradiation with a 364-nm laser light caused significant oxidative damage in Drosophila larval DNA; however, induction of the damage was not prohibited by urate. To the best of our knowledge, this is the first report of a study in whole animals that shows increased levels of 8-OHdG in response to 364-nm UVA. X-ray ionizing radiation is also thought to generate reactive oxygen species in irradiated cells. We found that the amount of 8-OHdG in DNA following X-ray radiation remained unchanged in both strains, though survival rates were affected. X-ray-generated oxidative damage in Drosophila cells was followed by cell death but not DNA base oxidation, and the damage was suppressed by urate. The overall results suggest significant differences in the major in vivo oxidative damage caused by 364-nm light and X-rays.

The sunlight that reaches the surface of the earth is composed of polychromatic light with wavelengths ranging from 290 nm to 2500 nm. Ultraviolet (UV) light is a component of sunlight that is harmful to organisms. Although it is known that sunlight induces photoproducts and harmful eŠects such as major DNA damage caused by UV light in the tissues of many species including human skin, it is not clear whether sunlight induces oxidative damage in organisms. In this study, we investigated whether sunlight causes oxidative damage in exposed organisms using Drosophila. Third instar larvae were exposed to sunlight for an evaluation of viability and 8-hydroxydeoxyguanosine (8-OHdG) content. Urate-null Drosophila mutant larvae (ry 506 ), which are sensitive to active oxygen-producing agents, were more sensitive to sunlight lethality than the wild-type strain under limited conditions. This sunlight-induced toxicity in ry 506 larvae was partially prevented by pretreatment of larvae with 400 mM uric acid. The level of 8-OHdG in DNA showed no signiˆcant increase in both strains. In contrast, sunlight was signiˆcantly mutagenic for all seasons as reported previously. These results suggest that sunlight is partly responsible for oxidative damage in Drosophila and that 8-OHdG-formation plays little or no role in sunlight-induced mutation and toxicity.