简介:IntroductionIn1963,MoorA.M.[1]firstlyreportedthephosphateefect,i.e.,intheUVirradiation(253.7nm)ofaqueoussolutionsof4-amino-2-...
简介:cytosine的tautomers和相关含水的tautomers上的AbinitioMP2和DFT研究被执行了。cytosine和相关转变状态的四tautomers的地面状态结构充分被优化。震动的频率分析在所有优化结构上被执行。详细内在的反应坐标(IRC)计算被执行保证被连接到相关tautomers的优化转变状态结构。我们为cytosine的tautomers和相关含水的tautomers获得了相对稳定性顺序。在里面孤立并且含水的条件,C(2)O(7)的契约类型和C(4)N(8)极大地影响cytosinetautomers的稳定性。而且,我们在在keto和cytosinetautomers的enol形式之间的intramolecular质子转移上探索了水分子的影响。第一个水分子显然减少为monohydratedcytosinetautomers的异构化激活精力。第二和第三个水分子什么时候在反应环被增加,被显示出异构化精力障碍仅仅有点变化。溶剂效果在孤立的cytosine的质子转移障碍上有明显的影响。然而,溶剂效果似乎为monohydrated,dihydrated和trihydratedcytosine的异构化精力障碍不足道。在这些建筑群的水分子能被看作明确的水。因此,明确的水模型可能是更可信的探索intramolecular质子转移,与是含蓄的水模型的PCM比较。
简介:Objective:Toexploretheeffectsofdexamethasone(DXM)andvincristine(VCR)oncytosinearabinoside(Ara-C)inducedapoptosisandactivationofnuclearfactor-κ-genebinding(NF-κB)inleukemiccelllineHL60-n.Methods:ApoptosisofHL60-ncellswasanalysedbyTdT-mediatedX-dUTPnickandendlabeling(TUNEL)andDNAelectrophoresis.NF-κBactivityofHL60-ncellswasdetectedbyelectrophoreticmobilityshiftassay(EMSA).Results:TherewasslightactivationofNF-κBinHL60-ncellswithoutdruginduction.Ara-Cat1μmol/LsignificantlyenhancedtheactivationofNF-κBinHL60-ncells.ThelevelofNF-κBactivationinducedbyDXMat1μmol/LorVCRat0.1μmol/Lhadnosignificantdifferencecomparedwiththatofthecontrolgroup.However,inHL60-ncellspre-treatedwith1μmol/LofDXMor0.1μmol/LofVCR,theactivationofNF-κBinducedby1μmol/LofAra-Cwassignificantlysuppressedwithinhibitionratesof31.0%and47.0%,respectively.TheapoptosisratesofHL60-ncellsinducedby1.0μmol/L,10μmol/Land100μmot/LAra-Cwere45.00±3.16%,61.88±3.40%and77.62±4.75%,respectively.TheapoptoticratesofHL60-ncellsinducedbyDXMat1μmol/LorVCRat0.1μmol/Lweresimilartothatofthecontrolgroup.However,eitherDXMat1μmol/LorVCRat0.lμmol/LcouldenhancetheapoptosisofHL60-ncellsinducedbyAra-Cat1μmol/Lwithratesof39.1%and59.2%,respectively.Conclusion:Ara-CcaninduceapoptosisandactivationofNF-κBinHL60-ncells.ThemechanismofincreasedapoptosisofHL60-ncellsbyDXMorVCRmayberelatedtosuppressionofNF-κBactivation.