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生物活化,变异性,DNA损伤和由3,4-二甲基氨林诱导的氧化应激

Mariam R Habil¹, Raúl A Salazar-González¹, Mark A Doll¹

¹Department of Pharmacology & Toxicology, University of Louisville School of Medicine, Louisville, KY 40202, USA.

|January 8, 2025

概括

3,4-二甲基氨 (3,4-DMA) 暴露会导致DNA损伤和突变. 常见的NAT1*14B变异显示出比NAT1*4参考等位基因更高的HPRT突变,表明了基因毒性.

科学领域:

毒理学毒理学毒理学
遗传学是一个遗传学.
生物化学生物化学

背景情况:

3,4-Dimethylaniline (3,4-DMA) 是一种在香烟烟雾中发现的化学物质,用于工业应用.
在N-乙转移酶1 (NAT1) 的遗传变异可以影响化学代谢和毒性.

研究的目的:

为了研究3,4-DMA在表达不同NAT1等位基因的中国仓鼠卵巢 (CHO) 细胞中的基因毒性.
评估NAT1遗传变异在3,4-DMA诱导的DNA损伤,氧化应激和突变中的作用.

主要方法:

使用的核酸切除修复缺陷的CHO细胞稳定地感染了人类CYP1A2和NAT1*4 (参考) 或NAT1*14B (变异) 等位基因.
评估了3,4-DMA N-乙化速率,反应性氧物种 (ROS) 生产,双链DNA断裂和素基转移酶 (HPRT) 突变.

主要成果:

具有NAT1*4的CHO细胞显示3,4-DMA N-乙化显著高于具有NAT1*14B.B的细胞.
在表达CYP1A2和NAT1.1.的细胞中,3,4-DMA诱导的ROS,DNA损伤和HPRT突变的度依赖性增加.
虽然NAT1*4和NAT1*14B细胞之间的ROS和DNA损伤水平相似,但NAT1*14B细胞表现出明显更高的HPRT突变.

结论:

3,4-DMA表现出基因毒性,与潜在的致癌性一致.
虽然NAT1*14B变异具有较低的N-乙化,但与增加的HPRT突变有关,这表明它在3,4-DMA诱导的基因毒性中发挥了作用.

关键词:

3,4-二甲基亚氨基氨酸的3,4-二甲基亚氨基氨酸.在NAT1中使用NAT1.双链断裂是双链断裂的原因之一.遗传毒性遗传毒性遗传毒性遗传毒性突变是发生在突变中的突变.

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