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N-OH-MOCA(4-氨基-4'-羟基氨基-双-3,3'-二氯二苯甲烷)和PBQ(2-苯基-1,4-苯醌)对人淋巴母细胞的致突变性。

Mutagenicity of N-OH-MOCA (4-amino-4'-hydroxylamino-bis-3,3'-dichlorodiphenylmethane) and PBQ (2-phenyl-1,4-benzoquinone) in human lymphoblastoid cells.

作者信息

Reid T M, DeBord D G, Cheever K L, Savage R E

机构信息

Division of Biomedical and Behavioral Sciences, National Institute for Occupational Safety and Health, Cincinnati, OH 45226, USA.

出版信息

Toxicol Lett. 1998 May;95(3):205-10. doi: 10.1016/s0378-4274(98)00039-3.

Abstract

The genotoxic potential of two occupationally significant chemicals, 4,4'-methylene-bis-2-chloroaniline (MOCA) and 2-phenyl-1,4-benzoquinone (PBQ), was explored by monitoring the induction of mutations at the HPRT locus of AHH-1 human lymphoblastoid cells. Exposure of AHH-1 cells to the putative carcinogenic metabolite of MOCA, N-OH-MOCA, induced a 6-fold increase in mutant frequency and resulted in base pair substitutions primarily at A:T base pairs. In contrast, exposure to PBQ did not result in an increased mutant frequency although this compound was significantly more cytotoxic than N-OH-MOCA at equimolar doses. The induction of mutations at A:T sites by N-OH-MOCA is consistent with the type of DNA damage known to be produced by MOCA and provides a specific marker of genotoxic damage for exposed populations.

摘要

通过监测AHH-1人淋巴母细胞系HPRT位点的突变诱导情况,探究了两种具有职业重要性的化学物质,4,4'-亚甲基双-2-氯苯胺(MOCA)和2-苯基-1,4-苯醌(PBQ)的遗传毒性潜力。将AHH-1细胞暴露于MOCA的假定致癌代谢物N-OH-MOCA中,可使突变频率增加6倍,并主要导致A:T碱基对处的碱基对替换。相比之下,暴露于PBQ并未导致突变频率增加,尽管在等摩尔剂量下该化合物的细胞毒性明显高于N-OH-MOCA。N-OH-MOCA在A:T位点诱导突变与已知由MOCA产生的DNA损伤类型一致,并为暴露人群提供了遗传毒性损伤的特定标志物。

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