对 styrene 和 styrene-7,8-oxide 基因毒性文献的批判性审查:一个更新
Lynn H Pottenger1, Marcy Banton2, Wade T Barranco3
1LHP Tox Consult, LLC, Midland, MI, USA.
概括
styrene 和 styrene 氧化物在体外表现出突变性潜力. 然而,最近的研究证实,烯不是动物体内的突变原体,也不是人类细胞遗传损伤的原因.
科学领域:
- 毒理学 毒理学 毒理学
- 遗传学 是一个遗传学.
- 职业健康 职业健康 职业健康
背景情况:
- 最近对 styrene 和 styrene 氧化物 (SO) 致变性/细胞遗传效应的评估从2019年开始进行了更新.
- 首次包括关于 styrene/SO 基因毒性的转录学研究.
- 考虑了初级DNA损伤终点数据.
研究的目的:
- 批判性地评估最近关于 styrene 和 SO 的突变性和细胞遗传效应的数据.
- 为了解决烯体内突变性研究中的数据缺口.
- 更新关于烯在实验动物和人类中的基因毒性证据权重.
主要方法:
- 关于烯和SO的突变/细胞遗传作用的最近研究的综述.
- 包括与基因毒性相关的转录组学研究.
- 考虑主要的DNA损伤终点.
- 对动物体内致变性和基因毒性研究的分析符合经合组织指导方针.
- 审查最近关于工作场所烯暴露的流行病学研究.
主要成果:
- 最近对小鼠和老鼠进行的符合经合组织指导方针的研究表明,在多种组织或骨髓中没有突变性.
- 最近的重复剂量动物研究对DNA损伤和微核产生了负面结果.
- 流行病学研究没有提供额外的证据表明烯暴露会导致细胞遗传损伤增加.
- 在某些条件下,烯和SO在体外表现出致变体或细胞遗传作用.
结论:
- 没有令人信服的证据表明,烯在实验动物中是一种体内变异原体或克拉斯托根/新原体.
- 目前的证据不支持工作场所的施烯暴露导致人类细胞遗传损伤的频率增加.
- 虽然 styrene 和 SO 可以在体外诱导效应,但在动物和人类体内数据没有显示出令人信服的基因毒性证据.
关键词:
在DNA中,添加物是DNA的添加物.造成的DNA损伤是DNA损伤.致变性 致变性 致变性可持续发展目标12:负责任的消费和生产可持续发展目标8:体面的工作和经济增长这就是克拉斯托基性 (clastogenicity).翻译学 翻译学 翻译学 翻译学更多相关视频
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