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0.5 至 30 eV 电子诱导的聚集 DNA 损伤。

Clustered DNA Damages induced by 0.5 to 30 eV Electrons.

机构信息

State Key Laboratory of Photocatalysis on Energy and Environment, Fuzhou University, Fuzhou 350116, China.

Département de Médecine Nucléaire et Radiobiologie et Centre de Recherche Clinique, Faculté de Médecine, Université de Sherbrooke, Sherbrooke, QC J1H 5N4, Canada.

出版信息

Int J Mol Sci. 2019 Jul 31;20(15):3749. doi: 10.3390/ijms20153749.

DOI:10.3390/ijms20153749
PMID:31370253
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6695612/
Abstract

Low-energy electrons (LEEs) of energies ≤30 eV are generated in large quantities by ionizing radiation. These electrons can damage DNA; particularly, they can induce the more detrimental clustered lesions in cells. This type of lesions, which are responsible for a large portion of the genotoxic stress generated by ionizing radiation, is described in the Introduction. The reactions initiated by the collisions of 0.5-30 eV electrons with oligonucleotides, duplex DNA, and DNA bound to chemotherapeutic platinum drugs are explained and reviewed in the subsequent sections. The experimental methods of LEE irradiation and DNA damage analysis are described with an emphasis on the detection of cluster lesions, which are considerably enhanced in DNA-Pt-drug complexes. Based on the energy dependence of damage yields and cross-sections, a mechanism responsible for the clustered lesions can be attributed to the capture of a single electron by the electron affinity of an excited state of a base, leading to the formation of transient anions at 6 and 10 eV. The initial capture is followed by electronic excitation of the base and dissociative attachment-at other DNA sites-of the electron reemitted from the temporary base anion. The mechanism is expected to be universal in the cellular environment and plays an important role in the formation of clustered lesions.

摘要

低能电子(LEEs)的能量≤30eV 是由电离辐射大量产生的。这些电子可以破坏 DNA;特别是,它们可以在细胞中诱导更具危害性的簇状损伤。这种类型的损伤是由电离辐射产生的大部分遗传毒性应激的原因,在引言中进行了描述。随后的部分解释和回顾了 0.5-30eV 电子与寡核苷酸、双链 DNA 和与化疗铂药物结合的 DNA 碰撞引发的反应。用 LEE 辐照和 DNA 损伤分析的实验方法进行了描述,重点是检测簇状损伤,这些损伤在 DNA-Pt-药物复合物中大大增强。基于损伤产率和截面的能量依赖性,可以将导致簇状损伤的机制归因于单个电子被碱基的激发态的电子亲和力捕获,从而在 6 和 10eV 处形成瞬态阴离子。初始捕获后,碱基发生电子激发,从临时碱基阴离子中重新发射的电子在其他 DNA 位点上发生离解附着。该机制预计在细胞环境中是普遍存在的,并在簇状损伤的形成中起着重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3bd1/6695612/35851d667a58/ijms-20-03749-sch001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3bd1/6695612/070757b296c3/ijms-20-03749-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3bd1/6695612/67dff93aec19/ijms-20-03749-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3bd1/6695612/35851d667a58/ijms-20-03749-sch001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3bd1/6695612/070757b296c3/ijms-20-03749-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3bd1/6695612/67dff93aec19/ijms-20-03749-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3bd1/6695612/35851d667a58/ijms-20-03749-sch001.jpg

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