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黄嘌呤氧化酶活性与实验感染无乳链球菌的银鲑鱼氧化和炎症性肾损伤的关系:与活性氧和一氧化氮的相互作用。

Involvement of xanthine oxidase activity with oxidative and inflammatory renal damage in silver catfish experimentally infected with Streptococcus agalactiae: Interplay with reactive oxygen species and nitric oxide.

机构信息

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

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

出版信息

Microb Pathog. 2017 Oct;111:1-5. doi: 10.1016/j.micpath.2017.08.010. Epub 2017 Aug 10.

DOI:10.1016/j.micpath.2017.08.010
PMID:28804017
Abstract

Xanthine oxidase (XO) is a final enzyme of purine metabolism linked with initiation and progression of infectious diseases, since is considered an important source of reactive oxygen species (ROS) and nitric oxide (NO), developing a pro-oxidant and pro-inflammatory profile in some infectious diseases. Thus, the aim of this study was to evaluate the involvement of XO activity in the renal oxidative and inflammatory damage, as well as the interplay with ROS and metabolites of nitric oxide (NOx) levels in silver catfish experimentally infected with Streptococcus agalactiae. Xanthine oxidase activity, and uric acid, ROS and NOx levels increased in renal tissue of infected animals compared to uninfected animals. Moreover, the histopathological analyses revealed the presence of necrosis, generalized edema and nuclear degeneration of renal tubules. Based on these evidences, the upregulation on renal XO activity exerts a pro-oxidant and pro-inflammatory profile in kidney of fish infected with S. agalactiae. The excessive uric acid levels induced the release of oxidative and inflammatory mediators, such as ROS and NOx, that directly contribute to renal oxidative and inflammatory damage. In summary, the upregulation on XO activity may be considered a pathway involved in the renal injury during S. agalactiae infection.

摘要

黄嘌呤氧化酶(XO)是嘌呤代谢的最后一种酶,与传染病的发生和进展有关,因为它被认为是活性氧(ROS)和一氧化氮(NO)的重要来源,在一些传染病中产生促氧化剂和促炎作用。因此,本研究旨在评估 XO 活性在银鲈肾脏氧化和炎症损伤中的作用,以及与活性氧(ROS)和一氧化氮(NO)代谢物水平的相互作用。与未感染动物相比,感染链球菌的银鲈肾脏组织中的黄嘌呤氧化酶活性、尿酸、ROS 和 NOx 水平增加。此外,组织病理学分析显示出肾小管坏死、弥漫性水肿和核变性。基于这些证据,肾脏 XO 活性的上调在感染 S.agalactiae 的鱼的肾脏中表现出促氧化剂和促炎作用。尿酸水平升高会导致氧化和炎症介质(如 ROS 和 NOx)的释放,这些介质直接导致肾脏氧化和炎症损伤。总之,XO 活性的上调可能被认为是链球菌感染引起肾脏损伤的一种途径。

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