Ikebuchi M, Osmak M, Han A, Hill C K
University of Southern California School of Medicine, Department of Experimental Radiotherapy, Albert Soiland Cancer Research Laboratory, Los Angeles 90015.
Radiat Res. 1988 May;114(2):248-67.
Chinese hamster V79 cells (subline MI2G) were exposed repeatedly to fractionated doses of germicidal 254 nm light (far-uv) at 6 J.m-2/fraction/day or sunlight-simulating 290-330 nm (mid-uv) at 150 J.m-2/fraction/day and sensitivities to cell killing action and mutation of far-uv and mid-uv were examined. As the number of exposure fractions increased, the cell cultures became resistant to cell killing induced by both far-uv and mid-uv. Increases in both Do and Dq were observed. Treatment with exposures of 6 J.m-2 far-uv is more efficient in yielding cell cultures that are resistant than exposures of 150 J.m-2 mid-uv. In contrast to the cells exposed to repeated far-uv, the cells exposed to repeated mid-uv were relatively more resistant to cell killing effects of mid-uv than far-uv, suggesting a possible role of photolesions other than pyrimidine dimers. When mutants resistant to 6-thioguanine were assayed during repeated exposure to far- or mid-uv light, the yield was initially linear with accumulating dose. At high total accumulated doses, the frequency decreased gradually (6 J.m-2 mid-uv) or reached a plateau (150 J.m-2 mid-uv). The sensitivity of N80 cells (exposed to 80 fractions of mid-uv) to mutation induction by uv light is higher than that of the original MI2G cells, whereas U81 cells (exposed to 81 fractions of far-uv) have a sensitivity similar to that of the original cells. Although an initial decrease in resistance to cell killing was observed, resistant cells retained their characteristics after 100 days in culture without further exposure. Cross-resistance to X rays was not shown. The data in this paper suggest that the capacity for repair of photolesions in DNA by repair processes was enhanced in cell cultures by repeated exposure to far-uv or mid-uv and that this altered the cells' ability to cope with lethal and mutagenic lesions. It remains to be seen if these changes in cell sensitivity were brought about by selective or inductive processes or a combination of both.
将中国仓鼠V79细胞(亚系MI2G)反复暴露于分次剂量的杀菌性254纳米光(远紫外线),剂量为6焦耳·平方米/分次/天,或模拟阳光的290 - 330纳米光(中紫外线),剂量为150焦耳·平方米/分次/天,并检测其对远紫外线和中紫外线细胞杀伤作用及突变的敏感性。随着照射分次数量的增加,细胞培养物对远紫外线和中紫外线诱导的细胞杀伤产生抗性。观察到Do和Dq均增加。6焦耳·平方米的远紫外线照射比150焦耳·平方米的中紫外线照射在产生抗性细胞培养物方面更有效。与反复暴露于远紫外线的细胞相比,反复暴露于中紫外线的细胞对中紫外线的细胞杀伤作用相对比对远紫外线更具抗性,这表明除嘧啶二聚体外的光损伤可能起作用。当在反复暴露于远紫外线或中紫外线期间检测对6 - 硫鸟嘌呤抗性的突变体时,产量最初与累积剂量呈线性关系。在高总累积剂量时,频率逐渐降低(6焦耳·平方米的中紫外线)或达到平稳状态(150焦耳·平方米的中紫外线)。N80细胞(暴露于80次中紫外线分次)对紫外线诱导突变的敏感性高于原始MI2G细胞,而U81细胞(暴露于81次远紫外线分次)的敏感性与原始细胞相似。尽管观察到对细胞杀伤的抗性最初有所下降,但抗性细胞在无进一步照射的情况下培养100天后仍保留其特性。未显示对X射线的交叉抗性。本文数据表明,通过反复暴露于远紫外线或中紫外线,细胞培养物中DNA光损伤的修复能力通过修复过程得到增强,这改变了细胞应对致死性和诱变性损伤的能力。这些细胞敏感性的变化是由选择性过程、诱导性过程还是两者结合引起的,还有待观察。