共查询到18条相似文献,搜索用时 78 毫秒
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金霉素链霉菌噬菌体的分布DistributionofbacteriophagesofStreptoinycesaureofaciens张菊英ZhangJuying(福州抗生素总厂,福州350002)(FuzhouAntibioticGeneralFa... 相似文献
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本文研究了柞蚕核多角体病毒的分离、纯化、纯化后的病毒DNA经限制性内切酶Pat Ⅰ、Hind Ⅲ、BamH Ⅰ、XhoⅠ、SalⅠ、EcoRⅠ及EcoRⅠ+BamHⅠ等酶解后电泳分别形成31、26、6、15、24、5及7条区带。据内切酶图谱测算柞蚕核多角体病毒的分子量为75.16±2.3×10~6道尔顿。并比较了柞蚕、蓖麻蚕及家蚕等核多角体病毒的亲缘关系。 相似文献
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红霉素链霉菌抗噬菌体菌株的选育 总被引:1,自引:0,他引:1
目的筛选红霉素链霉菌抗噬菌体菌株。方法以红霉素链霉菌B-27#为出发菌株,采用经过紫外诱变过的孢子悬浮液与噬菌体接触的方法进行处理。结果筛选到一株抗噬菌体高产菌株。通过噬菌体的侵染试验和摇瓶发酵生产能力验证,其抗噬菌体能力十分稳定,红霉素发酵摇瓶效价比对照有所提高。该菌株经纯化后投入生产,有效地控制和预防了噬菌体的污染。结论采用经过紫外诱变过的孢子悬浮液与噬菌体接触的方法进行处理,可以有效的获得抗噬菌体菌株。在试验中我们还发现,在紫外灯(253.7 nm、15 W、30 cm)下照射120 s,菌株出现抗噬菌体突变的几率最高。 相似文献
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目的筛选红霉素链霉菌抗噬菌体菌株.方法以红霉素链霉菌B-27#为出发菌株,采用经过紫外诱变过的孢子悬浮液与噬菌体接触的方法进行处理.结果筛选到一株抗噬菌体高产菌株.通过噬菌体的侵染试验和摇瓶发酵生产能力验证,其抗噬菌体能力十分稳定,红霉素发酵摇瓶效价比对照有所提高.该菌株经纯化后投入生产,有效地控制和预防了噬菌体的污染.结论采用经过紫外诱变过的孢子悬浮液与噬菌体接触的方法进行处理,可以有效的获得抗噬菌体菌株.在试验中我们还发现,在紫外灯(253.7 nm、15 W、30 cm)下照射120 s,菌株出现抗噬菌体突变的几率最高. 相似文献
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螺旋霉素链霉菌噬菌体的分离和鉴定 总被引:1,自引:0,他引:1
从螺旋霉素的异常发酵液及土壤样品中分离到19株螺旋霉素链霉素噬菌体,对每一噬菌体进行了纯化,根据血清中和反应,这些噬菌体可分为4种血清型(P_(11)型、1010型、1012型及4031型)。P_(11)型和1012型噬斑小而清晰,4031型和1010型大而不清晰。观察了4种血清型的代表性噬菌体形态和它们的DNA的限制性内切酶酶切片断长度,多态性。 相似文献
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金霉素链霉菌污染噬菌体后的菌丝形态特征ThemorphologicalcharateristicsofmyceliaofStreptomycesaureofaciensaftersufferingbacteriophagecontamination张... 相似文献
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在抗肿瘤抗生素(C-1027)产生菌球孢链霉菌(Streptomyces globisporus)中发现一新的质粒pSGL1,其分子量为7.40Kb。 采用Katz等的方法分离提取了质粒pSGL1,pSGL1经单酶切实验证明:PvuⅡ,PstⅠ、XbaⅠ、XhoⅠ和KpnⅠ为单切点;SmnaⅠ为双切点;SalⅠ和BamHⅠ为四切点;而EcoRⅠ、HindⅢ、BgⅢ和PvuⅠ则没有切点,经一系列双酶切实验,构建了质粒pSGLⅠ的限制性内切酶图谱。 相似文献
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发展链霉菌宿主载体系统有可能进行抗生素耐药性,抗生素生物合成和各种酶基因的克隆。由于这类微生物染色体DNA的G+C含量很高,引起了人们对被克隆基因转录调节区的极大兴趣。为了克隆含有启动子的DNA片断,所以组建了许多启动子探针载体。详细分析几种启动子,表明它们在—10区域存在着共同的碱基顺序。 相似文献
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结核分支杆菌稳定L型染色体DNA的限制性酶切分析 总被引:2,自引:0,他引:2
目的 探讨结核分支杆菌稳定L型变异的分子机制。方法 对结核分支杆菌稳定L型纯培养物的染色体DNA的特异性PCR扩增片段进行HaeⅢ限制性内切酶分析。结果 结核分支杆菌稳定L型的染色体DNA具有与其亲代细菌型一致的主要酶切片段,但也显示出不同于其亲代细菌型DNA的酶切片段。结论 结核分支杆菌稳定L型可保留与其亲代细菌型一致的特异性染色体基因,但也发生了染色体基因的改变。 相似文献
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Peter Møller Ditte Marie Jensen Regitze Sølling Wils Maria Helena Guerra Andersen Pernille Høgh Danielsen Martin Roursgaard 《Nanotoxicology》2017,11(9-10):1237-1256
Nanosized titanium dioxide (TiO2) has been investigated in numerous studies on genotoxicity, including comet assay endpoints and oxidatively damaged DNA in cell cultures and animal models. The results have been surprisingly mixed, which might be attributed to physico-chemical differences of the tested TiO2. In the present review, we assess the role of certain methodological issues and publication bias. The analysis shows that studies on DNA strand breaks without proper assay controls or very low intra-group variation tend to show statistically significant effects. Levels of oxidatively damaged DNA, measured by the enzyme-modified comet assay, tend to show no effect in studies that have not included proper assay controls or they have uncertainty about the measurement. In addition, there are indications of publication and reporting bias. Nevertheless, the analysis shows that Aeroxide P25 generates DNA strand breaks in a concentration-dependent manner, which is not dependent on the duration of exposure. The standard comet assay seems to be able to discriminate between the genotoxicity of different types of TiO2, where anatase TiO2 seems to be the form with strongest genotoxic potential. Cell culture studies also demonstrate increased levels of oxidatively damaged DNA after exposure to TiO2. There are relatively few studies on animal models where DNA strand breaks and oxidatively damaged DNA have been tested with reliable methods. Collectively, this review shows that exposure to nanosized TiO2 is associated with genotoxicity in cells, whereas there are still too few reliable studies to assess the genotoxic potential in animal models. 相似文献
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用黄曲霉毒素B1(AFB1)、苯并(a)芘(BaP)和2-乙基氨基芴(2-AAF)作为致癌物代表,研究限量饮食(Dietaryrestriction,DR)对雄性F344大鼠和B6C3F1小鼠代谢活化致癌物的影响。以几种致癌物主要的DNA加合物作为代谢活化的生物指标。结果显示:限量饮食降低大鼠和小鼠的体重,降低AFB1-DNA加合物(ADA)的生成,增加AFB1-谷胱甘肽结合物(AFB1-SG)的生成,增加BaP-DNA加合物(Bp-N2-dG)的生成,但对2-AAF-DNA加合物(AF-C8-dG)的作用有双重性,染毒后24,48小时AF-C8-dG在两组动物肝中无差别,而72小时后则明显降低AF-C8-dG的生成。结果说明:对于不同的致癌物,DR有选择性改变代谢酶活性的作用,这种作用可以改变致癌物的活化进而影响致癌过程的起始阶段 相似文献
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Structure‐based virtual screening toward the discovery of novel inhibitors of the DNA repair activity of the human apurinic/apyrimidinic endonuclease 1
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Patrícia S. Guerreiro Sílvia G. Estácio Fernando Antunes Ana S. Fernandes Pedro F. Pinheiro João G. Costa Matilde Castro Joana P. Miranda Rita C. Guedes Nuno G. Oliveira 《Chemical biology & drug design》2016,88(6):915-925
The DNA repair activity of human apurinic/apyrimidinic endonuclease 1 (APE1) has been recognized as a promising target for the development of small‐molecule inhibitors to be used in combination with anticancer agents. In an attempt to identify novel inhibitors of APE1, we present a structure‐based virtual screening (SBVS) study based on molecular docking analysis of the compounds of NCI database using the GOLD 5.1.0 (Genetic Optimization for Ligand Docking) suite of programs. Compounds selected in this screening were tested with a fluorescence‐based APE1 endonuclease activity assay. Two compounds ( 37 and 41 ) were able to inhibit the multifunctional enzyme APE1 in the micromolar range, while compound 22 showed inhibitory effects at nanomolar concentrations. These results were confirmed by a plasmid DNA nicking assay. In addition, the potential APE1 inhibitors did not affect the cell viability of non‐tumor MCF10A cells. Overall, compounds 22 , 37, and 41 appear to be important scaffolds for the design of novel APE1 inhibitors and this study highlights the relevance of in silico‐based approaches as valuable tools in drug discovery. 相似文献
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The effect of aphidicolin on DNA synthesis in herpes simplex virus type 1 (HSV-1) infected and uninfected Vero cells was determined by isodensity banding of [32P]-labelled DNA. A 50% inhibition of HSV-1 DNA synthesis was observed at 0.07 μM aphidicolin while 2.1 and 1.3 μM were required to inhibit the cellular DNA synthesis to 50% in infected and uninfected Vero cells, respectively. When the viral DNA synthesis was totally inhibited by 10 μM aphidicolin, the cellular DNA synthesis was inhibited to about 90% in both infected and uninfected cells. Aphidicolin inhibited the cellular DNA synthesis in HSV-1 infected and uninfected Vero cells remaining in the presence of 250 μM foscarnet to the same extent as the DNA synthesis in the absence of foscarnet. 相似文献
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Modulation of DNA polymerase beta-dependent base excision repair in cultured human cells after low dose exposure to arsenite 总被引:1,自引:0,他引:1
Base excision repair (BER) is crucial for development and for the repair of endogenous DNA damage. However, unlike nucleotide excision repair, the regulation of BER is not well understood. Arsenic, a well-established human carcinogen, is known to produce oxidative DNA damage, which is repaired primarily by BER, whilst high doses of arsenic can also inhibit DNA repair. However, the mechanism of repair inhibition by arsenic and the steps inhibited are not well defined. To address this question we have investigated the regulation of DNA polymerase beta (Pol beta) and AP endonuclease (APE1), in response to low, physiologically relevant doses of arsenic. GM847 lung fibroblasts and HaCaT keratinocytes were exposed to sodium arsenite, As(III), and mRNA, protein levels and BER activity were assessed. Both Pol beta and APE1 mRNA exhibited significant dose-dependant down regulation at doses of As(III) above 1 microM. However, at lower doses Pol beta mRNA and protein levels, and consequently, BER activity were significantly increased. In contrast, APE1 protein levels were only marginally increased by low doses of As(III) and there was no correlation between APE1 and overall BER activity. Enzyme supplementation of nuclear extracts confirmed that Pol beta was rate limiting. These changes in BER correlated with overall protection against sunlight UV-induced toxicity at low doses of As(III) and produced synergistic toxicity at high doses. The results provide evidence that changes in BER due to low doses of arsenic could contribute to a non-linear, threshold dose response for arsenic carcinogenesis. 相似文献
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Periodontitis is a common chronic inflammatory condition that results in increased levels of inflammatory cytokines and inflammatory mediators. In addition to oral disease and tooth loss, it also causes low-grade systemic inflammation that contributes to development of systemic conditions including cardiovascular disease, pre-term birth, diabetes and cancer. Chronic inflammation is associated with epigenetic change, and it has been suggested that such changes can alter cell phenotypes in ways that contribute to both ongoing inflammation and development of associated pathologies. Here we show that exposure of human gingival fibroblasts to IL-1β increases expression of maintenance methyltransferase DNMT1 but decreases expression of de novo methyltransferase DNMT3a and the demethylating enzyme TET1, while exposure to PGE2 decreases expression of all three enzymes. IL-1β and PGE2 both affect global levels of DNA methylation and hydroxymethylation, as well as methylation of some specific CpG in inflammation-associated genes. The effects of IL-1β are independent of its ability to induce production of PGE2, and the effects of PGE2 on DNMT3a expression are mediated by the EP4 receptor. The finding that exposure of fibroblasts to IL-1β and PGE2 can result in altered expression of DNA methylating/demethylating enzymes and in changing patterns of DNA methylation suggests a mechanism through which inflammatory mediators might contribute to the increased risk of carcinogenesis associated with inflammation. 相似文献