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TEM study of chronic alcoholism effects on early carcinogenesis by probing the nanoscale structural alterations of cell nuclei
Physical Biology ( IF 2 ) Pub Date : 2021-01-12 , DOI: 10.1088/1478-3975/abcbdd
Prakash Adhikari 1, 2 , Pradeep K Shukla 2, 3 , Hemendra M Ghimire 2, 4 , Mehedi Hasan 1 , Peeyush Sahay 1 , Huda Almabadi 4, 5 , Vibha Tripathi 4 , Omar Skalli 6 , Radhakrishna Rao 3 , Prabhakar Pradhan 1
Affiliation  

Nanoscale structural alteration in the nuclei of cells with the progression of carcinogenesis is due to the rearrangements of the basic building blocks in the cell such as DNA, RNA, lipids, etc. Although epigenetic modifications underlie the development of cancer, exposure to carcinogenic chemicals such as alcohol also enhances the development of cancer. We report the effects of chronic alcoholism on early-carcinogenesis based on changes in the degree of nanoscale structural alterations (L d) in nuclei. For this, transmission electron microscopy (TEM) imaging of the nuclei of colonic cells is performed for the following four mouse models: control mice; chronic alcoholic mice treated with ethanol (i.e., EtOH mice); mice treated with colonic carcinogen azoxymethane (AOM) and dextran sulfate sodium (DSS) that induced colitis (i.e., AOM + DSS mice); and chronic alcoholic or EtOH treated mice, together with AOM and DSS treatment (i.e., AOM + DSS + EtOH mice). The disordered optical lattices are constructed from their respective TEM images of thin colonic cell nuclei and the L d values are calculated using the inverse participation ratio (IPR) technique from the spatially localized eigenfunctions of these lattices. Results show no significant difference in the average L d value of the colon cell nuclei of alcohol treated mice relative to its control [i.e., L d(C) ∼ L d(EtOH)]; however, an increase in the L d value of alcohol treated precancerous cells [i.e., L d(AOM + DSS + EtOH) > L d(AOM + DSS)], indicating that alcohol accelerates the early carcinogenic process.



中文翻译:

通过探测细胞核的纳米级结构改变,慢性酒精中毒对早期致癌作用的 TEM 研究

随着致癌作用的进展,细胞核中的纳米级结构改变是由于细胞中基本构建块(如 DNA、RNA、脂质等)的重排。虽然表观遗传修饰是癌症发展的基础,但暴露于致癌化学物质如因为酒精也会促进癌症的发展。我们根据纳米级结构改变程度的变化报告了慢性酒精中毒对早期致癌作用的影响(L d) 在原子核中。为此,对以下四种小鼠模型进行了结肠细胞核的透射电子显微镜 (TEM) 成像:对照小鼠;用乙醇治疗的慢性酒精性小鼠(即 EtOH 小鼠);用引起结肠炎的结肠致癌物氧化偶氮甲烷 (AOM) 和葡聚糖硫酸钠 (DSS) 治疗的小鼠(即 AOM + DSS 小鼠);和慢性酒精或 EtOH 治疗的小鼠,以及 AOM 和 DSS 治疗(即 AOM + DSS + EtOH 小鼠)。无序光学晶格是根据它们各自的薄结肠细胞核的 TEM 图像构建的,L d值是使用反参与比 (IPR) 技术根据这些晶格的空间局部特征函数计算的。结果显示平均L无显着差异 酒精处理小鼠的结肠细胞核与其对照相比的d值 [即,L d (C) ∼ L d (EtOH)];然而,酒精处理的癌前细胞的L d值增加[即,L d (AOM + DSS + EtOH) > L d (AOM + DSS)],表明酒精加速了早期致癌过程。

更新日期:2021-01-12
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