Differential regulation of tissue thiol-disulfide redox status in a murine model of peritonitis

• Type of Material: Article
• Authors: Shana M. Benton, Emory University; Zhe Liang, Emory University; Li Hao, Emory University; Youngliang Liang, Emory University; Gautam Hebbar, Emory University; Dean P Jones, Emory University; Craig Coopersmith, Emory University; Thomas R Ziegler, Emory University
• Language: English
• Date: 2012-10-04
• Publisher: BioMed Central
• Publication Version: Final Published Version
• Copyright Statement: © 2012 Benton et al.; licensee BioMed Central Ltd.
• License: Creative Commons Attribution 2.0 Generic
• Final Published Version (URL): http://www.journal-inflammation.com/content/9/1/36
• Title of Journal or Parent Work: Journal of Inflammation
• ISSN: 1476-9255
• Volume: 9
• Issue: 36
• Start Page: 1
• End Page: 6
• Grant/Funding Information: This work was supported by National Institutes of Health grant K24 RR023356 (TRZ), T32 DK 007734 (SMB), ES009047 (DPJ), ES011195 (DPJ) and R01 GM072808 (CMC).
• Research Categories: Health Sciences, Medicine and Surgery

Abstract

Background Glutathione (GSH)/glutathione disulfide (GSSG) and cysteine (Cys)/cystine (CySS) are major redox pools with important roles in cytoprotection. We determined the impact of septic peritonitis on thiol-disulfide redox status in mice. Methods FVB/N mice (6–12 week old; 8/group) underwent laparotomy with cecal ligation and puncture (CLP) or laparotomy alone (control). Sections of ileum, colon, lung and liver were obtained and GSH, GSSG, Cys and CySS concentrations determined by HPLC 24 h after laparotomy. Redox potential [Eh in millivolts (mV)] of the GSH/GSSG and Cys/CySS pools was calculated using the Nernst equation. Data were analyzed by ANOVA (mean ± SE). Results GSH/GSSG Eh in ileum, colon, and liver was significantly oxidized in septic mice versus control mice (ileum: septic −202±4 versus control −228±2 mV; colon: -195±8 versus −214±1 mV; and liver: -194±3 vs. -210±1 mV, all P<0.01). Lung GSH/GSSG redox was similar in each group (−191±3 versus −190±2 mV). In contrast, ileal and colonic Cys/CySS Eh was unchanged with CLP, while liver and lung Cys/CySS Eh became significantly more reducing (liver: septic = −103±3 versus control −90±2 mV; lung: -101±5 versus −81±1 mV, each P<0.05). Conclusions Septic peritonitis induced by CLP oxidizes ileal and colonic GSH/GSSG redox but Cys/CySS Eh remains unchanged in these intestinal tissues. In liver, CLP oxidizes the GSH/GSSG redox pool and CyS/CySS Eh becomes more reducing; in lung, CLP does not alter GSH/GSSG Eh, and Cys/CySS Eh is less oxidized. CLP-induced infection/inflammation differentially regulates major thiol-disulfide redox pools in this murine model.