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  本文關鍵詞：陰道毛滴蟲鐵氧還蛋白基因的克隆與表達　出處：《四川大學》2005年碩士論文　論文類型：學位論文

  更多相關文章： 陰道毛滴蟲 鐵氧還蛋白 基因克隆 原核表達 真核表達質粒

【摘要】：研究背景及目的:陰道毛滴蟲(Trichomonas vaginalis)是寄生在人體泌尿生殖道的一種常見病原體,可引起陰道毛滴蟲病(Xrichomoniasis)。自1836年Donné首次描述該蟲的特點及所致疾病的癥狀以來,至今仍是威脅人類健康的主要的性傳播疾病之一。鐵氧還蛋白(Ferredoxin Fd)是自然界分布很廣的低分子量鐵硫蛋白,最常見的是[2Fe-2S]Fd,在陰道毛滴蟲中它是氫化酶體(Hydrogenosome)電子傳遞鏈的主要成分,它參與丙酮酸鹽:鐵氧還蛋白氧化還原酶(pyruvate:ferredoxin oxidoreductase PFOR)介導的丙酮酸鹽氧化脫羧形成乙酰輔酶A和ATP反應,是此過程中的電子供體,通過電子傳遞參與了—線抗滴蟲藥物甲硝唑(metronidazole)在體內的活化。盡管應用甲硝唑已經(jīng)數(shù)十年,其抗藥性的發(fā)展還是較緩慢。然而,近年來臨床上甲硝唑抗性株的發(fā)現(xiàn)和不斷增加,使得對甲硝唑在體內的作用機制和抗藥性的發(fā)展的研究就尤為重要。Quon和Johnson等發(fā)現(xiàn)滴蟲抗性株細胞中Fd明顯低于敏感株,Northern雜交分析,Fd的mRNA水平下降50-65%,基因轉錄下降40-65%,Land等通過實驗發(fā)現(xiàn)藥物高度抵抗的蟲株內Fd mRNA的水平下降90%,免疫印記顯示,在高度抵抗株內幾乎檢測不到PFOR和Fd,甲硝唑在抗藥株內活化減少。本課題對Fd基因及蛋白質的研究將有助于闡明陰道毛滴蟲抗藥株抗性機制。 本研究分兩個部分,第一部分:目的:Fd基因的克隆。方法:從我國四川地區(qū)臨床分離陰道毛滴蟲(陰道毛滴蟲四川分離株—1),應用螯合樹脂
[Abstract]:Background and objective: Trichomonas vaginalis is a common pathogen in human genitourinary tract. Trichomonas vaginalis can cause trichomonas vaginalis. Since 1836, Donn 茅 first described the characteristics and symptoms of the disease. Ferredoxin Fd is one of the major sexually transmitted diseases that threaten human health. Ferredoxin Fd is a widely distributed low molecular weight ferrithionein in nature, the most common of which are. [2Fe-2S] FD, which is the main component of the electron transport chain of Hydrogenosome in Trichomonas vaginalis. It participates in pyruvate: ferredoxin oxidoreductase redoxin pyruvate: ferredoxin, pyruvate: ferredoxin, pyruvate: ferredoxin). The oxidative decarboxylation of pyruvate into acetyl coenzyme A and ATP reaction was mediated. Metronidazole is the electron donor involved in the activation of metronidazole, a novel antitrichomonium drug, although metronidazole has been used for decades. The development of resistance to metronidazole is still slow. However, in recent years, metronidazole resistant strains have been found and increased. It is very important to study the mechanism of metronidazole in vivo and the development of drug resistance. Quon and Johnson showed that the FD of trichomonas resistant strain was significantly lower than that of susceptible strain. Northern blot analysis showed that the mRNA level of Fd decreased by 50-65%, and the transcription of Fd gene decreased by 40-65%. Land et al. found that the level of FD mRNA in the highly resistant strains decreased 90%. The immunological imprinting showed that PFOR and FD could hardly be detected in the highly resistant strains. Metronidazole activates less in resistant strains. The study of FD gene and protein will be helpful to elucidate the resistance mechanism of Trichomonas vaginalis resistance strain. This study is divided into two parts. Part one: to clone the gene of: Fd. Methods: to isolate Trichomonas vaginalis (Trichomonas vaginalis) (Trichomonas vaginalis strain-1) from the clinic in Sichuan, china, and apply chelating resin
【學位授予單位】：四川大學
【學位級別】：碩士
【學位授予年份】：2005
【分類號】：R383

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相關期刊論文 前2條

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本文編號：1399645