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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 [E h  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 E h  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 E h  was unchanged with CLP, while liver and lung Cys/CySS E h  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 E h  remains unchanged in these intestinal tissues. In liver, CLP oxidizes the GSH/GSSG redox pool and CyS/CySS E h  becomes more reducing; in lung, CLP does not alter GSH/GSSG E h , and Cys/CySS E h  is less oxidized. CLP-induced infection/inflammation differentially regulates major thiol-disulfide redox pools in this murine model.

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