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豚鼠气单胞菌改变实验感染的银鲶鱼的胞质和线粒体肌酸激酶活性:对肾脏生物能量学的损害。

Aeromonas caviae alters the cytosolic and mitochondrial creatine kinase activities in experimentally infected silver catfish: Impairment on renal bioenergetics.

作者信息

Baldissera Matheus D, Souza Carine F, Júnior Guerino B, Verdi Camila Marina, Moreira Karen L S, da Rocha Maria Izabel U M, da Veiga Marcelo L, Santos Roberto C V, Vizzotto Bruno S, Baldisserotto Bernardo

机构信息

Department of Microbiology and Parasitology, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.

Department of Physiology and Pharmacology, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.

出版信息

Microb Pathog. 2017 Sep;110:439-443. doi: 10.1016/j.micpath.2017.07.031. Epub 2017 Jul 19.

Abstract

Cytosolic and mitochondrial creatine kinases (CK), through the creatine kinase-phosphocreatine (CK/PCr) system, provide a temporal and spatial energy buffer to maintain cellular energy homeostasis. However, the effects of bacterial infections on the kidney remain poorly understood and are limited only to histopathological analyses. Thus, the aim of this study was to investigate the involvement of cytosolic and mitochondrial CK activities in renal energetic homeostasis in silver catfish experimentally infected with Aeromonas caviae. Cytosolic CK activity decreased in infected animals, while mitochondrial CK activity increased compared to uninfected animals. Moreover, the activity of the sodium-potassium pump (Na, K-ATPase) decreased in infected animals compared to uninfected animals. Based on this evidence, it can be concluded that the inhibition of cytosolic CK activity by A. caviae causes an impairment on renal energy homeostasis through the depletion of adenosine triphosphate (ATP) levels. This contributes to the inhibition of Na, K-ATPase activity, although the mitochondrial CK activity acted in an attempt to restore the cytosolic ATP levels through a feedback mechanism. In summary, A. caviae infection causes a severe energetic imbalance in infected silver catfish, which may contribute to disease pathogenesis.

摘要

胞质和线粒体肌酸激酶(CK)通过肌酸激酶-磷酸肌酸(CK/PCr)系统,提供一个时间和空间上的能量缓冲,以维持细胞能量稳态。然而,细菌感染对肾脏的影响仍知之甚少,且仅局限于组织病理学分析。因此,本研究的目的是调查在实验性感染豚鼠气单胞菌的胡子鲇中,胞质和线粒体CK活性在肾脏能量稳态中的作用。与未感染动物相比,感染动物的胞质CK活性降低,而线粒体CK活性增加。此外,与未感染动物相比,感染动物的钠钾泵(Na,K-ATPase)活性降低。基于这些证据,可以得出结论,豚鼠气单胞菌对胞质CK活性的抑制通过三磷酸腺苷(ATP)水平的消耗导致肾脏能量稳态受损。这导致了Na,K-ATPase活性的抑制,尽管线粒体CK活性试图通过反馈机制恢复胞质ATP水平。总之,豚鼠气单胞菌感染在感染的胡子鲇中引起严重的能量失衡,这可能有助于疾病的发病机制。

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