【摘要】：在輻射生物效應(yīng)的研究中,探索DNA損傷與效應(yīng)之間的關(guān)聯(lián)性是一個(gè)重要的研究課題。DNA損傷與效應(yīng)之間的關(guān)聯(lián),將輻射生物效應(yīng)的機(jī)理指向了原初的DNA損傷信息,而探索本源的損傷機(jī)理,在DNA分子水平上建立細(xì)致的損傷信息與輻射終點(diǎn)效應(yīng)的關(guān)聯(lián),將具有根本的索源意義。早期基于靶理論提出的L-Q模型建立了一個(gè)初略的輻射所致DNA雙鏈斷裂數(shù)與細(xì)胞存活的關(guān)聯(lián),該模型本質(zhì)上反映的是劑量和效應(yīng)的關(guān)聯(lián)。細(xì)胞響應(yīng)閾值模型建立了靶元中能量沉積與輻射終點(diǎn)效應(yīng)的關(guān)聯(lián),該模型仍是反映劑量和效應(yīng)的關(guān)聯(lián)。顯然,以上兩類關(guān)聯(lián)模型沒有將損傷的機(jī)理指向原初的DNA損傷譜,不能揭示基本的DNA損傷信息與終點(diǎn)效應(yīng)的關(guān)聯(lián)性。因此,研究DNA損傷譜與靶元能量沉積的關(guān)聯(lián)性,是搭建輻射生物效應(yīng)和原初損傷關(guān)聯(lián)的重要環(huán)節(jié),是理論上解釋輻射生物效應(yīng)機(jī)理的關(guān)鍵,因而具有重要的科學(xué)意義。實(shí)驗(yàn)和理論研究已表明,幾乎所有類型的電離輻射都會(huì)產(chǎn)生大量的低能電子(能量低于幾keV),也稱"δ射線",它們會(huì)進(jìn)一步與生物分子相互作用,使之激發(fā)或電離。而DNA分子作為遺傳信息的攜帶者,是最重要的生物靶分子,DNA損傷,可能會(huì)導(dǎo)致基因突變、細(xì)胞死亡以及其他嚴(yán)重的生物學(xué)后果。因此,低能電子誘導(dǎo)的DNA損傷一直是輻射生物學(xué)研究的一個(gè)重要課題。獲得DNA損傷譜是對(duì)輻射生物效應(yīng)機(jī)理解釋并預(yù)測(cè)生物效應(yīng)的第一步。低能電子輻照DNA時(shí),會(huì)產(chǎn)生大量不同類型的DNA損傷,包括單鏈斷裂(SSB)、雙鏈斷裂(DSB)、堿基損傷以及鏈斷裂與堿基損傷結(jié)合形成的簇?fù)p傷。DNA簇?fù)p傷是輻射所致細(xì)胞死亡和突變的關(guān)鍵損傷,被認(rèn)為是難以修復(fù)且對(duì)細(xì)胞是致命的。因此,DNA簇?fù)p傷譜分布的研究具有更重要的生物學(xué)意義。然而,由于實(shí)驗(yàn)條件和理論計(jì)算的局限性,目前有關(guān)的研究基本上是針對(duì)高能粒子所誘導(dǎo)的簡(jiǎn)單DNA簇?fù)p傷,未能給出各種不同復(fù)雜類型DNA簇?fù)p傷的定量分析。本文應(yīng)用Monte Carlo徑跡結(jié)構(gòu)模擬法,對(duì)包括亞電離電子作用的低能電子誘導(dǎo)的DNA簇?fù)p傷及其與DNA靶元和核小體靶元能量沉積的關(guān)聯(lián)性作系統(tǒng)深入的研究。建立了一個(gè)更為嚴(yán)格的低能電子在液態(tài)水中的徑跡結(jié)構(gòu)模擬方法,計(jì)算了低能電子誘導(dǎo)的DNA直接損傷譜,定量分析了不同初始能量下,亞電離電子對(duì)于DNA單鏈斷裂、雙鏈斷裂以及堿基損傷產(chǎn)額的貢獻(xiàn),研究不同類型DNA簇?fù)p傷以及核小體DNA損傷與靶元能量沉積的關(guān)聯(lián)性。本文的研究工作,主要包含以下方面的內(nèi)容和結(jié)果:1、論文的第一章,簡(jiǎn)要介紹了低能電子誘導(dǎo)DNA損傷與能量沉積關(guān)聯(lián)性研究的背景及意義,綜述了國(guó)內(nèi)外在該領(lǐng)域的研究現(xiàn)狀和研究方法。2、論文的第二章,描述了低能電子與液態(tài)水相互作用的兩個(gè)彈性散射的模型,即Tan模型和Champion模型。前者主要應(yīng)用基于解相對(duì)論性Dirac方程的Mott模型的平均散射截面方法,后者使用解非相對(duì)論性Schrodinger方程的分波法,并考慮了液態(tài)水的凝聚態(tài)相效應(yīng)。應(yīng)用Emfietzoglou等發(fā)展的基于介電響應(yīng)理論的光學(xué)數(shù)據(jù)模型計(jì)算低能電子在液態(tài)水中的非彈性散射,比較研究了基于兩個(gè)彈性散射模型的低能電子在液態(tài)水中徑跡結(jié)構(gòu)的模擬,計(jì)算分析了液態(tài)水凝聚態(tài)相效應(yīng)對(duì)表征徑跡結(jié)構(gòu)的能量沉積和非彈性散射事件空間分布的影響。結(jié)果表明,液態(tài)水凝聚態(tài)相效應(yīng)的影響主要發(fā)生在較低的電子能量�；诖�,并由于電子能量較高時(shí)Mott模型考慮了電子的相對(duì)論效應(yīng),提出并建立了一個(gè)更為嚴(yán)格的低能電子在液態(tài)水中徑跡結(jié)構(gòu)模擬方法。本章建立的模型可為輻射誘導(dǎo)DNA損傷的研究提供更為可靠的電子徑跡結(jié)構(gòu)。3、論文的第三章,建立了一個(gè)計(jì)及亞電離電子作用的低能電子誘導(dǎo)DNA直接損傷譜的模擬方法。尤其,這一方法中對(duì)低能電子與DNA各組分(四個(gè)堿基:腺嘌呤-Adenine(A)、胸腺嘧啶-Thymine(T)、鳥嘌呤-Guanine(G)、胞嘧啶-Cytosine(C),糖環(huán)-sugar moiety和磷酸基團(tuán)-phosphate group)之間的彈性相互作用,使用了最新的理論計(jì)算截面�；诮⒌哪M方法,系統(tǒng)地模擬研究了計(jì)及亞電離電子作用的低能電子誘導(dǎo)DNA堿基損傷、DNA鏈斷裂及相應(yīng)的簇?fù)p傷,定量分析了亞電離電子對(duì)不同復(fù)雜類型DNA鏈斷裂和堿基損傷產(chǎn)額的貢獻(xiàn)。結(jié)果表明:亞電離電子對(duì)DNA鏈斷裂產(chǎn)額的貢獻(xiàn)約為40-70%,且SSB為最主要的鏈斷裂類型,隨著初始能量的增高,SSB的相對(duì)產(chǎn)額逐漸增大;雙鏈斷裂類型的鏈斷裂所占比重較小,并隨著初始能量的升高而減小;亞電離電子誘導(dǎo)的DSB產(chǎn)額比相應(yīng)的SSB產(chǎn)額要小約230-290%;亞電離電子對(duì)DNA堿基損傷產(chǎn)額的貢獻(xiàn)約為20-40%,且A-T堿基對(duì)的損傷產(chǎn)額要比G-C堿基對(duì)的明顯的高;由亞電離電子誘導(dǎo)的SSB和A-T堿基對(duì)損傷之間具有較強(qiáng)的關(guān)聯(lián)性。本章的結(jié)果,尤其是亞電離電子的貢獻(xiàn),為輻射生物效應(yīng)的研究提供了原初的損傷信息,是研究低能電子誘導(dǎo)的各類DNA簇?fù)p傷與能量沉積關(guān)聯(lián)性研究的基礎(chǔ)。4、論文的第四章,提出并建立確定六種類型的DNA簇?fù)p傷靶單元的方法,將DNA簇?fù)p傷分為簡(jiǎn)單簇?fù)p傷和復(fù)雜簇?fù)p傷兩類,前者由每種類型的單鏈斷裂與鄰近堿基損傷結(jié)合構(gòu)成,后者包括每種類型的雙鏈斷裂與鄰近堿基損傷的結(jié)合。應(yīng)用Monte Carlo徑跡結(jié)構(gòu)模擬法,系統(tǒng)地模擬不同初始能量下低能電子誘導(dǎo)的DNA簇?fù)p傷譜,定量研究簡(jiǎn)單簇?fù)p傷和復(fù)雜簇?fù)p傷關(guān)聯(lián)的能量沉積分布特征,定量研究能量沉積與DNA簇?fù)p傷的關(guān)聯(lián)規(guī)律。本章的研究獲得了如下的結(jié)果:(1)不同初始能量下,總的簇?fù)p傷相對(duì)產(chǎn)額隨能量沉積的變化規(guī)律一致,約90%簇?fù)p傷的能量沉積分布在約低于150 eV的范圍,簡(jiǎn)單簇?fù)p傷為最主要的簇?fù)p傷,約占全部簇?fù)p傷的90%;(2)不同初始能量下,簡(jiǎn)單簇?fù)p傷的能量沉積分布規(guī)律相似,能量沉積主要分布在約低于150 eV的范圍,峰值出現(xiàn)在約50 eV處;(3)在考慮的電子初始能量范圍內(nèi)(≤4.5keV),SSB+BD(單鏈斷裂與鄰近的堿基損傷結(jié)合)簇?fù)p傷譜由1個(gè)單鏈斷裂分別結(jié)合1到5個(gè)堿基損傷構(gòu)成,SSB+BD類型的簇?fù)p傷約占簡(jiǎn)單簇?fù)p傷的75-90%。隨著堿基損傷數(shù)目的增加,SSB+BD簇?fù)p傷靶元內(nèi)的平均能量沉積逐漸增大。堿基損傷數(shù)一定,不同初始能量下的SSB+BD簇?fù)p傷靶元內(nèi)的平均能量沉積變化不大,即靶元內(nèi)的能量沉積主要取決于DNA損傷的復(fù)雜性,對(duì)初始能量的依賴很小,這是DNA靶元能量沉積與DNA簇?fù)p傷關(guān)聯(lián)的一個(gè)重要特征。此外,1個(gè)單鏈斷裂結(jié)合1個(gè)堿基損傷是最主要的SSB+BD簇?fù)p傷,約占SSB+BD簇?fù)p傷總產(chǎn)額的80%,SSB+BD簇?fù)p傷復(fù)雜性越高,能量沉積越大。(4)在復(fù)雜簇?fù)p傷中,DSB+BD(雙鏈斷裂與鄰近的堿基損傷結(jié)合)簇?fù)p傷占主導(dǎo)地位。在考慮的電子初始能量范圍,DSB+BD損傷譜由1個(gè)雙鏈斷裂分別結(jié)合1到5個(gè)堿基損傷構(gòu)成。其中,1個(gè)雙鏈鏈斷裂結(jié)合1個(gè)堿基損傷構(gòu)成的DSB+BD是最主要的復(fù)雜簇?fù)p傷,約占全部DSB+BD簇?fù)p傷的83%,其平均能量沉積約為106 eV。隨著復(fù)雜性增加,能量沉積逐漸增大,平均能量沉積亦明顯的大,但很難形成。然而,盡管復(fù)雜簇?fù)p傷的產(chǎn)額很小,但它們的生物效應(yīng)不可忽略。本章的工作定量地研究了不同復(fù)雜性DNA簇?fù)p傷與DNA靶元能量沉積的關(guān)聯(lián)性,揭示了相應(yīng)的關(guān)聯(lián)特征,為輻射生物效應(yīng)和原初損傷的關(guān)聯(lián)搭建起關(guān)鍵的環(huán)節(jié),從而使輻射生物效應(yīng)機(jī)理的研究能夠指向原初的損傷譜。5、論文的第五章,建立了核小體的體積模型以及模擬核小體DNA損傷譜的Monte Carlo方法,并提出DNA鏈斷裂關(guān)聯(lián)損傷的概念。應(yīng)用建立的Monte Carlo方法,模擬獲得了核小體靶元中的DNA鏈斷裂關(guān)聯(lián)損傷和DNA簇?fù)p傷譜,定量研究了核小體靶元能量沉積與其上的DNA損傷的關(guān)聯(lián)規(guī)律,獲得了如下的結(jié)果:(1)不同初始能量下,核小體靶元DNA鏈斷裂關(guān)聯(lián)損傷的相對(duì)產(chǎn)額隨靶元能量沉積的變化規(guī)律一致,具有DNA鏈斷裂關(guān)聯(lián)損傷的核小體靶元中90%的能量沉積分布在約低于180 eV的范圍。(2)簡(jiǎn)單的單鏈斷裂SSB,是核小體DNA中最主要的鏈斷裂類型,約占全部鏈斷裂產(chǎn)額的80-90%。不同初始能量下,SSB關(guān)聯(lián)損傷的能量沉積分布規(guī)律相似,主要分布在約低于180eV的范圍,且SSB關(guān)聯(lián)損傷的譜分布峰值出現(xiàn)在約30 eV處。SSB關(guān)聯(lián)損傷中,堿基損傷數(shù)為0和1的SSB關(guān)聯(lián)損傷是核小體DNA的SSB關(guān)聯(lián)損傷最主要的損傷類型,約分別占全部核小體DNA的SSB關(guān)聯(lián)損傷的70-90%和10-20%。(3)DSB是核小體DNA最主要的雙鏈斷裂類型,約占全部雙鏈斷裂產(chǎn)額的85-95%。在所考慮的初始能量范圍(≤3keV),核小體DNA發(fā)生DSB關(guān)聯(lián)損傷時(shí),結(jié)合的堿基損傷數(shù)從0到3,所對(duì)應(yīng)的核小體靶元內(nèi)的平均能量沉積分別為101.86 eV、122.79 eV、159.80 eV和229.28 eV。這表明了結(jié)合的堿基損傷數(shù)越多,損傷復(fù)雜性越高,能量沉積越大。其中,堿基損傷數(shù)為0的核小體DSB關(guān)聯(lián)損傷是最主要的DSB關(guān)聯(lián)損傷類型,約占全部核小體DSB鏈斷裂關(guān)聯(lián)損傷的 70-80%。(4)簇?fù)p傷是復(fù)雜性較高的鏈斷裂關(guān)聯(lián)損傷,其產(chǎn)額很小,占核小體DNA鏈斷裂關(guān)聯(lián)損傷的12.48%。不同初始能量下,SSB+BD簇?fù)p傷是最主要的DNA簇?fù)p傷。在核小體靶元中,當(dāng)DNA分別發(fā)生簡(jiǎn)單簇?fù)p傷和復(fù)雜簇?fù)p傷時(shí),核小體靶元的平均能量沉積約分別為112.68 eV和170.88 eV,明顯高于相應(yīng)的鏈斷裂關(guān)聯(lián)損傷的平均能量沉積。本章對(duì)于核小體DNA損傷譜與相應(yīng)靶元能量沉積的關(guān)聯(lián)性研究,為輻射生物效應(yīng)機(jī)理研究提供了相應(yīng)的理論參考。
[Abstract]:In the study of biological effects of radiation, it is an important research topic to explore the relationship between DNA damage and effect. The relationship between DNA damage and effect points the mechanism of biological effects of radiation to the original DNA damage information, and explores the original damage mechanism, and establishes detailed damage information and radiation end point at the DNA molecular level. The early L-Q model based on target theory established a preliminary association between the number of DNA double strand breaks induced by radiation and cell survival, which essentially reflects the correlation between dose and effect. It is obvious that the two models do not point the damage mechanism to the original DNA damage spectrum and can not reveal the correlation between the basic DNA damage information and the end effect. Experimental and theoretical studies have shown that almost all types of ionizing radiation produce large quantities of low-energy electrons (energies less than a few keV), also known as "delta-rays", which further interact with biological molecules to make them interact. DNA molecule, as the carrier of genetic information, is the most important biological target molecule. DNA damage may lead to gene mutation, cell death and other serious biological consequences. Therefore, DNA damage induced by low-energy electrons has always been an important subject in radiation biology. The first step in explaining and predicting biological effects is to irradiate DNA with low-energy electrons, resulting in a large number of different types of DNA damage, including single-strand breaks (SSB), double-strand breaks (DSB), base damage, and cluster damage resulting from the combination of strand breaks and base damage. However, due to the limitations of experimental conditions and theoretical calculations, the current studies are basically aimed at the simple DNA cluster damage induced by high-energy particles, and fail to provide a variety of complex types of DNA cluster damage. Quantitative analysis. A more rigorous method for simulating the track structure of low-energy electrons in liquid water has been developed by using Monte Carlo method to study the damage of DNA clusters induced by low-energy electrons including subionized electrons and their correlation with the energy deposition of DNA and nucleosome targets. The direct DNA damage spectra induced by low energy electrons were calculated. The contribution of subionized electrons to the yield of DNA single-strand breakage, double-strand breakage and base damage at different initial energies was quantitatively analyzed. The relationship between different types of DNA cluster damage and DNA damage in nucleosomes and target energy deposition was studied. The contents and results are as follows: 1. In the first chapter, the background and significance of the study on the correlation between low-energy electron-induced DNA damage and energy deposition are briefly introduced. The research status and methods in this field at home and abroad are reviewed. 2. In the second chapter, two elastic scattering models of the interaction between low-energy electrons and liquid water, namely T, are described. The former is mainly based on the average scattering cross section method of the Mott model for solving the relativistic Dirac equation, while the latter is based on the wave-splitting method for solving the non-relativistic Schrodinger equation, taking into account the condensed phase effect of liquid water. The inelastic scattering of low-energy electrons in liquid water is calculated. The simulation of the track structure of low-energy electrons in liquid water based on two elastic scattering models is compared. The effect of condensed phase effect of liquid water on the spatial distribution of energy deposition and inelastic scattering events is calculated and analyzed. Based on this, and considering the relativistic effect of electrons in the Mott model when the electron energy is high, a more rigorous simulation method for the trajectory structure of low energy electrons in liquid water is proposed and established. The model established in this chapter can provide more information for the study of radiation-induced DNA damage. In order to obtain a reliable electron track structure, the third chapter of this paper establishes a simulation method for the direct DNA damage spectra induced by low-energy electrons, taking into account the effect of subionized electrons. In particular, this method is applied to the low-energy electrons and DNA components (four bases: adenine-Adenine (A), thymine-Thymine (T), guanine (G), cytosine-Cytosine (G). (C), the elastic interaction between the glycocycle-sugar moiety and the phosphate group, using the latest theoretical calculation cross section. Based on the established simulation method, the low-energy electron-induced DNA base damage, DNA strand breakage and the corresponding cluster damage were systematically simulated and analyzed quantitatively. The results show that the contribution of sub-ionized electrons to the yield of DNA strand breakage is about 40-70%, and SSB is the most important type of strand breakage. Subionization electron-induced DSB yields were about 230-290% less than the corresponding SSB yields; the contribution of subionization electron to DNA base damage yields was about 20-40%, and the damage yields of A-T base pairs were significantly higher than those of G-C base pairs; there was a strong correlation between SSB and A-T base pairs induced by subionization electron and DNA damage. The results of this chapter, especially the contribution of subionized electrons, provide the original damage information for the study of biological effects of radiation, and are the basis for the study of the correlation between various DNA cluster damage induced by low-energy electrons and energy deposition. 4. Chapter 4 of this paper proposes and establishes a method for identifying six types of DNA cluster damage target units, namely, DN. Cluster A damage can be divided into two types: simple cluster damage and complex cluster damage. The former consists of each type of single-strand breakage combined with adjacent base damage, and the latter includes each type of double-strand breakage combined with adjacent base damage. Damage spectra are used to quantitatively study the distribution of energy deposition associated with simple and complex cluster damage, and to quantitatively study the correlation between energy deposition and DNA cluster damage. Deposition is distributed in the range of about 150 eV, and simple cluster damage is the main cluster damage, accounting for about 90% of the total cluster damage; (2) The distribution of energy deposition of simple cluster damage is similar under different initial energies, the energy deposition mainly distributes in the range of about 150 eV, and the peak value appears at about 50 eV; (3) The initial electron energy norm is considered. In the periphery (< 4.5 keV), the damage spectra of SSB+BD clusters consist of one single strand break combined with one or five base damage respectively. The damage of SSB+BD clusters accounts for 75-90% of the damage of simple clusters. With the increase of the number of base damage, the average energy deposition in the damage targets of SSB+BD clusters increases gradually. The average energy deposition in SSB+BD cluster damage target cells at different initial energies does not change much, that is, the energy deposition in the target cells mainly depends on the complexity of DNA damage and has little dependence on the initial energy. This is an important feature of the association between DNA target energy deposition and DNA cluster damage. Injury is the main damage of SSB+BD cluster, accounting for about 80% of the total damage yield of SSB+BD cluster. The higher the damage complexity of SSB+BD cluster, the greater the energy deposition. Among them, DSB+BD composed of one double-strand break and one base break is the most important complex cluster damage, accounting for about 83% of all DSB+BD cluster damage, and its average energy deposition is about 106 eV. Although the yield of complex cluster damage is very small, its biological effects should not be neglected. In this chapter, we quantitatively studied the correlation between DNA cluster damage and DNA target energy deposition, and revealed the corresponding correlation characteristics, which is the key link for the correlation between radiation biological effects and primary damage, thus making the radiation biological effects possible. In chapter 5, the volume model of nucleosome and Monte Carlo method to simulate the DNA damage spectrum of nucleosome are established, and the concept of DNA strand breakage associated damage is proposed. The results are as follows: (1) At different initial energies, the relative yield of DNA strand breakage associated damage of nucleosome target element is consistent with the variation of energy deposition of target element, and 90% of the energy of nucleosome target element with DNA strand breakage associated damage is obtained. (2) Simple SSB is the most important type of strand breakage in nucleosome DNA, accounting for 80-90% of the total strand breakage yield. Under different initial energies, the energy deposition pattern of SSB associated damage is similar, mainly distributed in the range of less than 180 eV, and the peak value of spectrum distribution of SSB associated damage. SSB-related damage is the most important type of SSB-related damage in nucleosome DNA, accounting for 70-90% and 10-20% of SSB-related damage in nucleosome DNA, respectively. (3) DSB is the most important type of double-strand breakage in nucleosome DNA, accounting for 85-95% of the total double-strand breakage yield. In the initial energy range considered (< 3 keV), the number of binding base damage ranged from 0 to 3, and the average energy deposition in the corresponding nucleosome target cells were 101.86 eV, 122.79 eV, 159.80 eV and 229.28 eV, respectively. Among them, nucleosome DSB-related damage with zero base damage is the most important type of DSB-related damage, accounting for 70-80% of all nucleosome DSB-related damage. (4) Cluster damage is a more complex chain breakage-related damage, and its yield is very small, accounting for 12.48% of nucleosome DNA-chain breakage-related damage at different initial energies. The average energy deposition of nucleosome target cells is about 112.68 eV and 170.88 eV respectively, which is significantly higher than that of the corresponding chain breakage associated damage. The study of product correlation provides a theoretical reference for studying the mechanism of biological effects of radiation.
【學(xué)位授予單位】：山東大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2017
【分類號(hào)】：Q691

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