Pero R W, Bryngelsson T, Högstedt B, Akesson B
Carcinogenesis. 1982;3(6):681-5. doi: 10.1093/carcin/3.6.681.
Lymphocytes from 38 individuals occupationally exposed to styrene concentrations in workroom air of 1 p.p.m. t0 40 p.p.m. were examined for any genotoxic effects using unscheduled DNA synthesis (UDS) as the indicator of DNA damage. The mean level of N-acetoxy-2-acetylaminofluorene (NA-AAF) induced UDS was significantly increases (p less than 0.001) for the styrene exposed group when compared to the mean level for the unexposed controls. There was no significant effect on u.v.-induced UDS from the in vivo styrene exposure. Lymphocyte cultures exposed in in vitro to styrene concentrations up to 100 micro M have confirmed the UDS data collected on individuals occupationally exposed to styrene. In addition, the in vitro study has also shown that the increased NA-AAF induced UDS resulting from styrene exposure was paralleled by a similar increase in NA-AAF binding to DNA. Taken together these results indicate that styrene exposure does not inhibit DNA repair synthesis, but rather it predisposes lymphocytes to an increased risk for DNA damage induction from subsequent genotoxic exposures.
对38名职业接触工作场所空气中苯乙烯浓度为百万分之一至百万分之四十的个体的淋巴细胞,以程序外DNA合成(UDS)作为DNA损伤指标,检测其是否存在遗传毒性效应。与未接触对照组的平均水平相比,苯乙烯接触组中N - 乙酰氧基 - 2 - 乙酰氨基芴(NA - AAF)诱导的UDS平均水平显著升高(p小于0.001)。体内苯乙烯暴露对紫外线诱导的UDS没有显著影响。体外暴露于高达100微摩尔苯乙烯浓度的淋巴细胞培养证实了在职业接触苯乙烯个体中收集到的UDS数据。此外,体外研究还表明,苯乙烯暴露导致的NA - AAF诱导的UDS增加与NA - AAF与DNA结合的类似增加平行。综合这些结果表明,苯乙烯暴露并不抑制DNA修复合成,而是使淋巴细胞更容易受到后续遗传毒性暴露诱导DNA损伤的风险增加。