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紫外线A(UVA)照射对黑腹果蝇的遗传毒性以及8-甲氧基补骨脂素与UVA的协同作用。

The genotoxicity of UVA irradiation in Drosophila melanogaster and the synergistic action of 8-methoxypsoralen and UVA.

作者信息

Negishi T, Tanabe F, Hayatsu H

机构信息

Faculty of Pharmaceutical Sciences, Okayama University, Japan.

出版信息

Carcinogenesis. 1992 Aug;13(8):1433-6. doi: 10.1093/carcin/13.8.1433.

DOI:10.1093/carcin/13.8.1433
PMID:1499094
Abstract

To study the genotoxicity of near-ultraviolet light (UVA) on a whole body, Drosophila melanogaster larvae were irradiated with UVA and the emerging flies were examined for the mutant wing spot formation. The genotoxicity of UVA was also assayed with the in vivo DNA-repair test using males with repair-deficiency at the mei-9 and mei-41 locus and the matching repair-proficient females. Third-instar larvae were placed in a plastic Petri dish, which was covered with soft glass, and irradiated with black light at 4-5 W/m2. This irradiation resulted in an increase in mutant wing-hair spots. After a 15 h irradiation (approximately 240 kJ/m2), the mutant clone frequencies found in the adult flies (spots/wing) were: 1.68 for the small single spots, 0.38 for the large single spots and 0.11 for the twin spots, while at zero time they were 0.68, 0.06 and 0.02 respectively. On the other hand, the UVA irradiation was negative in the in vivo DNA-repair test, indicating that the UVA-induced DNA lesion may not be subject to repair by the mei-9 and mei-41 functions. The presence of 8-methoxypsoralen (8-MOP) during the irradiation remarkably enhanced somatic mutations, and showed a strong DNA-damaging effect in the repair test. For example, a 15 h UVA irradiation with 26.7 microM 8-MOP resulted in a 14-fold increase in the number of twin spots per wing as compared with the frequency obtained on treatment with UVA alone. Treatment of the larvae with 8-MOP alone gave no mutant clones or DNA damage. A high frequency in twin spot formation was also observed in this UVA + 8-MOP treatment, indicating that extensive chromosomal recombinations took place in the somatic cells.

摘要

为研究近紫外光(UVA)对全身的遗传毒性,用UVA照射黑腹果蝇幼虫,然后检查羽化出的果蝇的突变翅斑形成情况。还使用在mei - 9和mei - 41位点具有修复缺陷的雄性果蝇和匹配的修复功能正常的雌性果蝇,通过体内DNA修复试验来测定UVA的遗传毒性。将三龄幼虫置于覆盖有软玻璃的塑料培养皿中,以4 - 5 W/m²的黑光进行照射。这种照射导致突变翅毛斑数量增加。照射15小时(约240 kJ/m²)后,在成年果蝇中发现的突变克隆频率(斑点/翅膀)为:小单斑为1.68,大单斑为0.38,双斑为0.11,而在照射起始时分别为0.68、0.06和0.02。另一方面,UVA照射在体内DNA修复试验中呈阴性,表明UVA诱导的DNA损伤可能无法通过mei - 9和mei - 41功能进行修复。照射期间8 - 甲氧基补骨脂素(8 - MOP)的存在显著增强了体细胞突变,并在修复试验中显示出强烈的DNA损伤效应。例如,与仅用UVA处理获得的频率相比,用26.7 microM 8 - MOP进行15小时的UVA照射导致每只翅膀双斑数量增加了14倍。单独用8 - MOP处理幼虫未产生突变克隆或DNA损伤。在这种UVA + 8 - MOP处理中也观察到双斑形成的高频现象,表明体细胞中发生了广泛的染色体重组。

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