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诱导体细胞中牙科树脂单体的 DNA 损伤。

Induced DNA damage by dental resin monomers in somatic cells.

机构信息

Post-graduation Program in Genetics and Applied Toxicology (PPGGTA), Lutheran University of Brazil (ULBRA), Genetic Toxicity Laboratory (TOXIGEN), Canoas, RS, Brazil.

出版信息

Basic Clin Pharmacol Toxicol. 2010 Feb;106(2):124-9. doi: 10.1111/j.1742-7843.2009.00479.x. Epub 2009 Nov 11.

Abstract

The present in vivo study investigated the genotoxicity of four dental resin monomers: triethyleneglycoldimethacrylate (TEGDMA), hydroxyethylmethacrylate (HEMA), urethanedimethacrylate (UDMA) and bisphenol A-glycidylmethacrylate (BisGMA). The Somatic Mutation and Recombination Test (SMART) in Drosophila melanogaster was applied to analyse their genotoxicity expressed as homologous mitotic recombination, point and chromosomal mutation. SMART detects the loss of heterozygosity of marker genes expressed phenotypically on the fly's wings. This fruit fly has an extensive genetic homology to mammalians, which makes it a suitable model organism for genotoxic investigations. The present findings provide evidence that the mechanistic basis underlying the genotoxicity of UDMA and TEGDMA is related to homologous recombination and gene/chromosomal mutation. A genotoxic pattern can correspondingly be discerned for both UDMA and TEGDMA: their genotoxicity is attributed respectively to 49% and 44% of mitotic recombination, as well as 51% and 56% of mutational events, including point and chromosomal alterations. The monomer UDMA is 1.6 times more active than TEGDMA to induce mutant clones per treatment unit. BisGMA and HEMA had no statistically significant effect on total spot frequencies - suggesting no genotoxic action in the SMART assay. The clinical significance of these observations has to be interpreted for data obtained in other bioassays.

摘要

本体内研究调查了四种牙科树脂单体的遗传毒性

三乙二醇二甲基丙烯酸酯(TEGDMA)、羟乙基甲基丙烯酸酯(HEMA)、尿烷二甲基丙烯酸酯(UDMA)和双酚 A 缩水甘油基甲基丙烯酸酯(BisGMA)。利用黑腹果蝇体细胞突变和重组测试(SMART)分析它们的遗传毒性,表现为同源有丝分裂重组、点突变和染色体突变。SMART 检测到标记基因的杂合性丢失,这些标记基因在果蝇的翅膀上表现出表型。这种果蝇与哺乳动物有广泛的遗传同源性,使其成为遗传毒性研究的合适模型生物。本研究结果提供了证据,证明 UDMA 和 TEGDMA 的遗传毒性的机制基础与同源重组和基因/染色体突变有关。可以相应地为 UDMA 和 TEGDMA 识别出遗传毒性模式:它们的遗传毒性分别归因于 49%和 44%的有丝分裂重组,以及 51%和 56%的突变事件,包括点突变和染色体改变。单体 UDMA 比 TEGDMA 每处理单位诱导突变克隆的活性高 1.6 倍。BisGMA 和 HEMA 对总斑点频率没有统计学上的显著影响——这表明在 SMART 试验中没有遗传毒性作用。必须根据其他生物测定中获得的数据来解释这些观察结果的临床意义。

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