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本文引用的文献

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How Trypanosoma cruzi deals with oxidative stress: Antioxidant defence and DNA repair pathways.克氏锥虫如何应对氧化应激:抗氧化防御和 DNA 修复途径。
Mutat Res Rev Mutat Res. 2016 Jan-Mar;767:8-22. doi: 10.1016/j.mrrev.2015.12.003. Epub 2015 Dec 29.
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Interferences in the Optimization of the MTT Assay for Viability Estimation of Proteus mirabilis.奇异变形杆菌活力评估中MTT法优化的干扰因素。
Avicenna J Med Biotechnol. 2015 Oct-Dec;7(4):159-67.
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Dibenzylideneacetones Are Potent Trypanocidal Compounds That Affect the Trypanosoma cruzi Redox System.二苄叉丙酮是强效杀锥虫化合物,可影响克氏锥虫的氧化还原系统。
Antimicrob Agents Chemother. 2015 Nov 23;60(2):890-903. doi: 10.1128/AAC.01360-15. Print 2016 Feb.
4
Mitochondrial Dysfunction Induced by N-Butyl-1-(4-Dimethylamino)Phenyl-1,2,3,4-Tetrahydro-β-Carboline-3-Carboxamide Is Required for Cell Death of Trypanosoma cruzi.N-丁基-1-(4-二甲基氨基)苯基-1,2,3,4-四氢-β-咔啉-3-甲酰胺诱导的线粒体功能障碍是克氏锥虫细胞死亡所必需的。
PLoS One. 2015 Jun 18;10(6):e0130652. doi: 10.1371/journal.pone.0130652. eCollection 2015.
5
Proliferation and differentiation of Trypanosoma cruzi inside its vector have a new trigger: redox status.克氏锥虫在其传播媒介体内的增殖和分化有了一个新的触发因素:氧化还原状态。
PLoS One. 2015 Feb 11;10(2):e0116712. doi: 10.1371/journal.pone.0116712. eCollection 2015.
6
Trypanosoma cruzi cell death induced by the Morita-Baylis-Hillman adduct 3-Hydroxy-2-methylene-3-(4-nitrophenylpropanenitrile).由森田-贝利斯-希尔曼加合物3-羟基-2-亚甲基-3-(4-硝基苯基)丙腈诱导的克氏锥虫细胞死亡。
PLoS One. 2014 Apr 8;9(4):e93936. doi: 10.1371/journal.pone.0093936. eCollection 2014.
7
Further evidence of the trypanocidal action of eupomatenoid-5: confirmation of involvement of reactive oxygen species and mitochondria owing to a reduction in trypanothione reductase activity.进一步证实 eupomatenoid-5 的杀锥虫作用:由于还原型谷胱甘肽还原酶活性降低,确认活性氧物质和线粒体的参与。
Free Radic Biol Med. 2013 Jul;60:17-28. doi: 10.1016/j.freeradbiomed.2013.01.008. Epub 2013 Jan 31.
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Autophagy and skeletal muscles in sepsis.脓毒症中的自噬和骨骼肌。
PLoS One. 2012;7(10):e47265. doi: 10.1371/journal.pone.0047265. Epub 2012 Oct 9.
9
Severe heat shock induces nucleolar accumulation of mRNAs in Trypanosoma cruzi.严重热休克诱导克氏锥虫核仁中 mRNAs 的积累。
PLoS One. 2012;7(8):e43715. doi: 10.1371/journal.pone.0043715. Epub 2012 Aug 27.
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In vivo and in vitro Leishmania amazonensis infection induces autophagy in macrophages.在体和体外感染导致巨噬细胞自噬。
Tissue Cell. 2012 Dec;44(6):401-8. doi: 10.1016/j.tice.2012.08.003. Epub 2012 Aug 30.

不同应激条件对人体寄生虫克氏锥虫诱导的超微结构和生理变化。

Ultrastructural and physiological changes induced by different stress conditions on the human parasite Trypanosoma cruzi.

作者信息

Pérez-Morales Deyanira, Hernández Karla Daniela Rodríguez, Martínez Ignacio, Agredano-Moreno Lourdes Teresa, Jiménez-García Luis Felipe, Espinoza Bertha

机构信息

Laboratorio de Estudios sobre Tripanosomiasis. Departamento de Inmunología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, A.P. 70228, C.P. 04510, Ciudad de México, México.

Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de México, A.P. 70228, C.P. 04510, México, D.F., México.

出版信息

Cell Stress Chaperones. 2017 Jan;22(1):15-27. doi: 10.1007/s12192-016-0736-y. Epub 2016 Oct 6.

DOI:10.1007/s12192-016-0736-y
PMID:27714535
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5225055/
Abstract

Trypanosoma cruzi is the etiological agent of Chagas disease. The life cycle of this protozoan parasite is digenetic because it alternates its different developmental forms through two hosts, a vector insect and a vertebrate host. As a result, the parasites are exposed to sudden and drastic environmental changes causing cellular stress. The stress response to some types of stress has been studied in T. cruzi, mainly at the molecular level; however, data about ultrastructure and physiological state of the cells in stress conditions are scarce or null. In this work, we analyzed the morphological, ultrastructural, and physiological changes produced on T. cruzi epimastigotes when they were exposed to acid, nutritional, heat, and oxidative stress. Clear morphological changes were observed, but the physiological conditions varied depending on the type of stress. The maintenance of the physiological state was severely affected by heat shock, acidic, nutritional, and oxidative stress. According to the surprising observed growth recovery after damage by stress alterations, different adaptations from the parasite to these harsh conditions were suggested. Particular cellular death pathways are discussed.

摘要

克氏锥虫是恰加斯病的病原体。这种原生动物寄生虫的生命周期是双宿主型的,因为它通过两种宿主(一种媒介昆虫和一种脊椎动物宿主)交替其不同的发育形式。因此,寄生虫会暴露于导致细胞应激的突然而剧烈的环境变化中。对克氏锥虫对某些类型应激的反应进行了研究,主要是在分子水平上;然而,关于应激条件下细胞的超微结构和生理状态的数据很少或根本没有。在这项工作中,我们分析了克氏锥虫前鞭毛体在暴露于酸、营养、热和氧化应激时所产生的形态、超微结构和生理变化。观察到了明显的形态变化,但生理状况因应激类型而异。热休克、酸性、营养和氧化应激严重影响了生理状态的维持。根据应激改变造成损伤后令人惊讶的生长恢复情况,提出了寄生虫对这些恶劣条件的不同适应方式。文中还讨论了特定的细胞死亡途径。