紫外辐射诱导植物叶片DNA损伤敏感性差异

单细胞凝胶电泳(彗星检测, comet assay)技术已广泛应用于动物细胞DNA损伤检测, 但在植物细胞DNA损伤检测中的应用尚不多见。本研究通过对动物细胞彗星检测方法的改进, 利用植物细胞原生质体作为材料, 研究了不同发育期九里香(Murraya panicuata)叶片对UV-B诱导的DNA损伤的敏感性差异。彗星检测结果表明, 九里香叶片DNA的损伤程度与UV-B辐射的剂量呈正相关; 在相同UV-B辐射剂量下, 九里香幼嫩叶片比成熟叶片的DNA损伤量大, 表明其幼嫩叶片对UV-B辐射的敏感性比成熟叶片高。     

紫外辐射诱导植物叶片DNA损伤敏感性差异

单细胞凝胶电泳（彗星检测,cometassay）技术已广泛应用于动物细胞DNA损伤检测,但在植物细胞DNA损伤检测中的应用尚不多见。本研究通过对动物细胞彗星检测方法的改进,利用植物细胞原生质体作为材料,研究了不同发育期九里香（Murraya panicuata）叶片对UV-B诱导的DNA损伤的敏感性差异。彗星检测结果表明,九里香叶片DNA的损伤程度与UV-B辐射的剂量呈正相关：在相同UV—B辐射剂量下,九里香幼嫩叶片比成熟叶片的DNA损伤量大,表明其幼嫩叶片对UV-B辐射的敏感性比成熟叶片高。     

DNA损伤修复基本方式的研究进展

DNA损伤修复基因可修复由不同原因导致的DNA损伤．从而保护遗传信息的完整性。DNA损伤修复有3种基本形式,即碱基切除修复、核苷酸切除修复和错配修复。本文综述了DNA损伤修复3种基本形式的研究进展情况并讨论了DNA链断裂重组和重接合修复及DNA聚合酶绕道修复DNA损伤。     

天然产物产生菌自抗性中DNA损伤修复的研究进展

临床上使用的抗生素大多是由微生物次级代谢产生的天然产物及其衍生物,这类化合物可以抑制微生物的生长,具有显著的细胞毒性.产生菌在合成这些抗生素的同时,也需要通过多种自抗性机制来应对其对自身的毒害作用.本文总结了近年来DNA损伤修复途径参与的天然产物产生菌自抗性机制的研究进展,重点介绍了 DNA损伤类抗生素产生菌中的碱基切...     

从DNA修复机理看细胞癌变的发生机制

DNA损伤是引起基因突变,导致细胞恶性转化的重要原因．DNA损伤的修复过程非常复杂,是与细胞周期调节、DNA复制和DNA转录等生命活动紧密相连的．首先DNA修复需要细胞周期停滞,避免DNA损伤进入子代细胞．其次,参与DNA转录的某些基因产物参与DNA损伤的识别,有利于转录链的优先修复．最后,DNA修复系统NER、MMR参与损伤修复．上述DNA修复过程任何环节的异常,都将造成DNA修复功能减弱,导致某些功能基因突变,从而导致细胞的恶性转化．     

紫外辐射诱导烟草原生质体中DNA损伤的彗星电泳检测

以烟草原生质体为材料,采用彗星电泳检测用0.5W·m^-2紫外线以不同时间（0、5、10、30、60和120s）诱导的烟草原生质体中DNA的损伤。结果表明,在0～10s的时间内代表DNA损伤程度的尾矩、Olive尾矩等参数与紫外线照射时间具有良好的时间依赖关系。本文建立的烟草原生质体体系采用彗星电泳技术,可以快速而灵敏地检测紫外线对植物细胞的损伤程度。     

DNA损伤修复机制——解读2015年诺贝尔化学奖

Tomas Lindahl, Paul Modrich和Aziz Sancar三位科学家因发现“DNA损伤修复机制”获得了2015年诺贝尔化学奖．Lindahl首次发现Escherichia Coli中参与碱基切除修复的第一个蛋白质--尿嘧啶 DNA糖基化酶（UNG）; Modrich重建了错配修复的体外系统,从大肠杆菌到哺乳动物深入探究了错配修复的机制; Sancar利用纯化的UvrA、UvrB、UvrC重建了核苷酸切除修复的关键步骤,阐述了核苷酸切除修复的分子机制．DNA损伤是由生物所处体外环境和体内因素共同导致的,面对不同种类的损伤,机体启动多种不同的修复机制修复损伤,保护基因组稳定性．这些修复机制包括：光修复(light repairing);核苷酸切除修复（nucleotide excision repair, NER）;碱基切除修复（base excision repair, BER）;错配修复（mismatch repair, MMR）;以及DNA双链断裂修复（DNA double strand breaks repair, DSBR）．其中DNA双链断裂修复又分同源重组（homologous recombination, HR）和非同源末端连接（non homologous end joining, NHEJ）两种方式．本文将对上述几种修复的机制进行总结与讨论．     

DNA修复的分子机制

ＤＮＡ是遗传信息的载体,需要有极高的保真度,这不仅有赖于完善的复制体系,而且还需要有能纠正已存在的错误的修复系统。对于不同的ＤＮＡ损伤,生物体内存在许多不同的修复系统。本文介绍三种主要修复系统即核苷酸切割修复,错配修复及转录偶联修复的分子机制,深入研究ＤＮＡ修复作用对了解某些癌症成因及细胞衰老等过程有重要意义。     

RNA聚合酶监视的DNA修复机制

生物体在正常生命过程中面临内/外因来源的DNA损伤,DNA损伤不仅影响基因正确复制,也阻碍其正常转录.为避免DNA损伤带来的灾难性后果,生物体进化出一整套修复机制,以保证复制和转录的正确性、基因组的完整性和遗传的稳定性.本文重点综述了RNA聚合酶监视(RNA polymerase-surveilled,RNAP-S)的DNA修复机制.首先从RNA聚合酶(RNA polymerase,RNAP)的结构出发介绍了RNAP对DNA损伤的感知机制;其次讨论了滞留RNAP的回溯、与其模板DNA的解离以及后续修复机制的启动,真核细胞科凯恩综合征B蛋白(Cockayne syndrome protein B,CSB)及其泛素化和8-氧代鸟嘌呤DNA糖基化酶1 (8-oxoguanine DNA glycosylase1,OGG1)介导的RNAP-S修复;最后探讨了RNAP-S损伤修复的生物学意义并展望其前景.     

哺乳动物卵母细胞的DNA损伤与修复研究进展

DNA损伤是影响配子发生和胚胎发育的关键因素之一。卵母细胞容易被各种内外源因素(如活性氧、辐射、化疗药物等)诱发DNA损伤。目前研究发现,对于各类DNA损伤,各发育阶段的卵母细胞能够做出相应的DNA损伤反应,通过复杂的机制对DNA进行修复或者启动细胞凋亡。相比于进入生长阶段的卵母细胞,原始卵泡卵母细胞更容易被DNA损伤诱导凋亡。DNA损伤不易诱导卵母细胞减数分裂成熟进程停滞,然而携带DNA损伤的卵母细胞的发育能力明显下降。在临床上,衰老、放疗和化疗是导致女性卵母细胞DNA损伤、卵巢储备降低和不孕的常见原因。为此,人们尝试了能够减轻卵母细胞DNA损伤和增强DNA修复能力的多种方法,试图保护卵母细胞。本文对哺乳动物的各发育阶段卵母细胞的DNA损伤与修复的相关研究进行了梳理和总结,并讨论了其潜在的临床价值,以期为生育力保护提供新的策略。     

Repair of DNA Damage Induced by Solar UV

Solar UV radiation induces significant levels of DNA damage in living things. This damage, if left unrepaired, is lethal in humans. Recent work has demonstrated that plants possess several repair pathways for UV-induced DNA damage, including pathways for the photoreactivation of both 6-4 products and cyclobutane pyrimidine dimers (CPDs), the two lesions most frequently induced by UV. Plants also possess the more general nucleotide excision repair (NER) pathway as well as bypass polymerases that enable the plant to replicate its DNA in the absence of DNA repair.This revised version was published online in October 2005 with corrections to the Cover Date.     

Molecular Mechanisms of DNA Damage and Repair: Progress in Plants

Dedicated to Prof. Jan H. J. Hoeijmakers.

Referee: Dr. Nawin C. Mishra, Professor of Genetics, University of South Carolina, Department of Biological Sciences, Columbia, SC 29208

Despite stable genomes of all living organisms, they are subject to damage by chemical and physical agents in the environment (e.g., UV and ionizing radiations, chemical mutagens, fungal and bacterial toxins, etc.) and by free radicals or alkylating agents endogenously generated in metabolism. DNA is also damaged because of errors during its replication. The DNA lesions produced by these damaging agents could be altered base, missing base, mismatch base, deletion or insertion, linked pyrimidines, strand breaks, intra- and inter-strand cross-links.     

亚硒酸钠诱发的晶状体上皮细胞DNA损伤及修复

观察了亚硒酸钠（Ｎａ２ＳｅＯ３）在体外作用于大鼠晶状体上皮细胞（ＲＬＥｃｅｌｌｓ）而造成的ＤＮＡ单链断裂（ｓｉｎｇｌｅｓｔｒａｎｄｂｒｅａｋｓ,ＳＳＢ）,并对其ＤＮＡ损伤、修复动力学做了初步研究．发现ＳＳＢ严重程度与亚硒酸钠的浓度呈线性相关,其ＳＳＢ重接修复约在３０～６０ｍｉｎ内完成．还作了有关非程序ＤＮＡ合成（ＵＤＳ）的检测,发现与ＳＳＢ相比,ＵＤＳ发生迟且持续时间更长,提示Ｎａ２ＳｅＯ３可能在体外对大鼠晶状体上皮细胞除造成ＳＳＢ以外,还可能造成其它种类的ＤＮＡ损伤．     

The Role of Melanocytes in the Repair of UV Related DNA Damage in Keratinocytes

Epidermal pigmentation and UV exposure are related to the incidence of skin tumors. There is a higher incidence of UV related skin tumors in populations with low pigment and in vitiligo patients, resulting from DNA damage. Normally DNA repair processes set in with the expression of PCNA in the keratinocyte. The present study was conducted on the marginal zone skin in vitiligo. Whole skin organ cultures irradiated with increasing doses of UV in the 280–400 nm range show that in the depigmented area there is no expression of PCNA by the keratinocytes. In comparison, the marginal zone keratinocytes show a dose related positivity in the presence of UV responsive melanocytes. These photoresponsive melanocytes show dendricity and cytoplasmic PCNA positivity. The melanocytes interact with keratinocytes by active melanosome transfer. From this study it is suggested that this involves transfer of PCNA as well. The present study indicates the differentiating keratinocytes in skin do not express PCNA but appear to be dependent on active UV responding melanocytes for DNA repair. This factor could play an important role in the occurrence of UV-related skin tumors.     

脂质过氧化引起的DNA损伤研究进展

脂质过氧化可以引起各种碱基损伤、DNA链断裂和各种荧光产物生成,并对DNA分子鸟嘌呤碱基具有选择性损伤.过渡金属离子可以明显加深脂质过氧化对DNA的损伤程度.多种抗氧化剂、活性氧自由基清除剂对脂质过氧化引起的DNA损伤有一定程度的保护作用.具有致突、致癌作用的8－羟基鸟嘌呤已经观察到．脂质过氧化的致突变、致癌变作用机制引起了人们的极大兴趣．     

5-氮胞苷对贵州小型猪淋巴细胞DNA损伤及修复的影响

目的　研究贵州小型猪淋巴细胞对化学物或药物引起的DNA损伤及修复影响的反应。方法　用单细胞凝胶电泳技术检测比较 5 氮胞苷对PHA刺激和未刺激淋巴细胞的DNA损伤及其修复过程。结果　 5 氮胞苷引起未刺激淋巴细胞明显的DNA泳动 (彗星尾 ) ,经修复孵育 2h后 ,DNA泳动与孵育前比较无显著差异 ,而 5 氮胞苷引起的刺激细胞DNA泳动经 2h修复孵育后与孵育前比较显著减少。结论　 5 氮胞苷引起贵州小型猪未刺激淋巴细胞DNA损伤经 2h孵育未能修复 ,而刺激细胞的DNA损伤明显修复。     

Induced Repair of Genetic Damage in Neurospora

Repair of genetic damage in Neurospora has been studied using a procedure in which one strain is exposed to a potentially lethal dose of UV before being joined in a heterokaryon with an undamaged strain. We have monitored the ability of the second strain to rescue the first. The extent of rescue is greatly enhanced when the rescuing strain has itself received a small, nonlethal dose of UV, thus demonstrating an inducible repair system.--The experiment was modified by substituting X rays or nitrous acid for UV as either the damaging agent or the inducing agent. In every combination, induced rescue was observed.--Three repair-deficient mutants (uvs-2, uvs-3 and uvs-6) were substituted for wild type (uvs+) as the rescuing component to find out whether any of them lacked the inducible repair system. Both uvs-2 and uvs-6 demonstrated inducible repair; uvs-3 showed none, but gave a high level of repair without induction, suggesting that it is a regulation (derepressed) mutant of an inducible repair system.