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

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 e h becomes more reducing; in lung,clp does not alter gsh/gssg e h,and cys/cyss eh is less oxidized. clp-induced infection/inflammation differentially regulates major thiol-disulfide redox pools in this murine model. © 2012 benton et al.; licensee biomed central ltd.