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SSCP检测内毒素致mtDNA基因突变及阳离子A的保护作用

detection of endotoxin-induced mtDNA gene mutation and protection effect of CA
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摘要 将60只健康试验大鼠随机分为3组:正常对照组(A组)、ET处理组(B组)、CA+ET处理组(C组),运用PCR-SSCP技术对肝脏mtDNA tRNACys-Tyr、COI基因片段一等基因进行了分析,同时运用分光光度计法对血清丙二醛的含量进行测定,观察ET致mtDNA的突变效应以及CA对该效应的保护作用。,结果发现,B组mtDNA tRNACys-Tyr基因片段在第5238与5242碱基处发生了插入1个碱基T的插入突变,COI一基因片段发生T5322G和T5331G处置换点突变,其他各组无基因突变发生。B组血清MDA含量均明显高于其他二组(P<0.05)、C组明显低于B组但高于A组(P<0.05)。结果表明,ET可导致mtDNA基因发生突变,而CA对ET致基因突变具有保护效应。 To investigate the mutational effect of endotoxin (ET)-induced mtDNA and the protec- tive effect of cation A (CA),sixty experimental rats were divided randomly into 3 groups:normal control group (group A),ET treated group (group B),and CA+ET treated group (group C). The liver mtDNA was extracted for detecting the mutations of tRNAcys-Tyr ,COI fragment one gene by polymerase chain reaction-single stranded conformation polymorphism (PCR-SSCP) tech- nique. The results revealed that a mutation was tRNAcys-Tyr of group B,which was inserted T be- tween 5238 and 5242 region,another mutation happened in T5322G and T5331G of the mtDNA COI one gene, no mutations of this gene was detected in group A and C. Serum MDA contents of group B were significantly higher than those of group A and C (P〈0.05) ,those of group C were significantly lower than those of group B and higher than group A (P〈0.05). It can be concluded that ET could cause the mutation of mtDNA gene,and CA has antagonistic and protective effect on the mutation of mtDNA gene caused by ET.
出处 《中国兽医学报》 CAS CSCD 北大核心 2013年第11期1707-1711,共5页 Chinese Journal of Veterinary Science
基金 国家自然科学基金资助项目(30560113) 云南省高端科技人才引进计划项目(2009CI125) 云南省现代农业生猪产业技术体系建设专项基金 云南省高校科技创新团队支持计划资助(云教科[2011]14号)
关键词 内毒素 聚合酶链式反应单股构象多态性分析 mtDNA基因突变 阳离子A 保护效应 endotoxin polymerase chain reaction-single stranded conformation polymorphism cat-ion A protective effect
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  • 1郭萌,李冠民,黄清泉.细菌内毒素研究进展[J].中国实验动物学报,2009,17(5):397-400. 被引量:58
  • 2蒋旭宏,黄小民.内毒素性急性肝损伤实验动物模型的建立和检测指标[J].中国中医急症,2009,18(8):1309-1310. 被引量:7
  • 3祝晨,黄小民.细胞凋亡与内毒素性肝损伤[J].医学研究杂志,2009,38(2):101-103. 被引量:3
  • 4Suliman H B, Carraway M S, Piantadosi C A. Postli- popolysaccharide oxidative damage of mitochondrial DNA[J]. Am J Respir Crit Care Med, 2002,167 (4) :570-579.
  • 5Wang Z,Wang H Y,Feng H. A. Simple and Reproduci- ble Method for Directed Evolution.. Combination of Random Mutation with dITP and DNA Fragmentation with Endonuelease V[J]. Mol Biotechnol, 2013,53 ( 1 ) .. 49-54.
  • 6Orita M, Suzuki Y T, Sekiya T, et al. Rapid and sensi tive detection of point mutations and DNA polymor- phisms using the polymerase chain reaction [J]. Ge- nomics, 1989,5 ~ 874-879.
  • 7周海洋,时多,王学敏.核呼吸因子-1:细胞核调控线粒体功能的一种重要因子[J].生命的化学,2005,25(3):202-204. 被引量:8
  • 8Brown G G. , DesRosiers L J. Rat mitochondrial DNA polymorphisrn: sequence analysis of a hypervariable site for insertions/deletions {-J~. Nucl Acids Res, 1983, 11(19) =6699-6708.
  • 9Guan M X, Antonio J. The Deafness-Associated Mito- chondrial DNA Mutation at Position7445, Which Af- fects tRNASer(UCN) Precursor Processing, Has Long- Range Effects on NADH Dehydrogenase Subunit ND6 Gene Expression[J]. Mol Cell Biol, 1998, 18 (10) : 5868-5879.
  • 10闻剑飞,刘玉倩,王海涛,赵斌,袁克星.运动中线粒体活性氧产生机制的研究进展[J].河北师范大学学报(自然科学版),2009,33(2):271-275. 被引量:6

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