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Superoxide radical formation in diverse organs of rats with experimentally induced obstructive jaundice.
Redox Report ( IF 3.8 ) Pub Date : 2008-07-24 , DOI: 10.1179/135100008x308902
Stelios F Assimakopoulos 1 , Adamantios G Mavrakis , Konstantinos Grintzalis , Ioannis Papapostolou , George Zervoudakis , Dimitris Konstantinou , Elisabeth Chroni , Constantine E Vagianos , Christos Georgiou
Affiliation  

Oxidative stress seems to be a cardinal feature of cholestasis, implicated in the pathophysiology of organ injury not only in the liver, but also in several extrahepatic tissues. The present study was designed to assess directly oxidative stress in vital organs of experimentally jaundiced rats by measuring the key oxidative stress marker superoxide radical (O2(*-)). Twelve male Wistar rats underwent laparotomy and were divided into two groups - group I (n = 6) sham operated, and group II (n = 6) bile-duct ligated. Ten days later, the O2(*-) formation rate was quantified in liver, intestine, kidney and heart of all animals. These measurements were done by application of a new ultrasensitive fluorescent assay for the in vivo quantification of O2(*-), which is based on the 1:1 molar stoichiometric reaction of O2(*-) with dihydroethidine (DHE, an O2(*-) trap) that results in the formation of the specific product 2-OH-ethidium. 2-OH-Ethidium was measured by fluorescence in rats' organs and its formation rate was converted to O2(*-) production rate. As compared to sham-operated rats, in jaundiced rats there was a significant increase of O2(*-) in the intestine (136%, P < 0.01), liver (104%, P < 0.01), and kidney (95%, P < 0.01), whereas there was no significant difference in heart O2(*-) levels. Superoxide radical may play an important role in the pathophysiology of cholestatic liver injury, intestinal barrier failure and renal failure, associated with postoperative morbidity and mortality in obstructive jaundice. On the contrary, O2(*-) and oxidative stress are possibly not implicated in the pathophysiology of hepatic cardiomyopathy.

中文翻译:

实验性梗阻性黄疸大鼠不同器官中超氧化物自由基的形成。

氧化应激似乎是胆汁淤积的主要特征,不仅与肝脏有关,而且与肝外一些组织的器官损伤有关。本研究旨在通过测量关键的氧化应激标记物超氧化物自由基(O2(*-))来直接评估实验性黄疸大鼠重要器官的氧化应激。将十二只雄性Wistar大鼠进行剖腹手术,分为两组:I组(n = 6)进行假手术,II组(n = 6)结扎胆管。十天后,对所有动物的肝,肠,肾和心脏中的O2(*-)形成率进行了定量。这些测量是通过应用新的超灵敏荧光测定法对O2(*-)进行体内定量而完成的,该方法基于O2(*-)与二氢乙啶(DHE,O2(*-)捕集阱),导致形成特定的产物2-OH-乙啶。通过荧光在大鼠器官中测量2-OH-乙啶,并将其形成速率转换为O2(*-)产生速率。与假手术大鼠相比,在黄疸大鼠中,肠道(136%,P <0.01),肝脏(104%,P <0.01)和肾脏(95%, P <0.01),而心脏O2(*-)水平没有显着差异。超氧化物自由基可能在胆汁淤积性肝损伤,肠屏障功能障碍和肾功能衰竭的病理生理中起重要作用,与梗阻性黄疸的术后发病率和死亡率有关。相反,O2(*-)和氧化应激可能与肝性心肌病的病理生理无关。
更新日期:2019-11-01
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