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01.12.2012 | Research | Ausgabe 1/2012 Open Access

Journal of Inflammation 1/2012

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

Zeitschrift:
Journal of Inflammation > Ausgabe 1/2012
Autoren:
Shana M Benton, Zhe Liang, Li Hao, Youngliang Liang, Gautam Hebbar, Dean P Jones, Craig M Coopersmith, Thomas R Ziegler
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1476-9255-9-36) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

TRZ and CMC conceived the study, SMB, ZL, and LH collected the samples; ZL performed the CLP surgeries and maintained the mice; DPJ and YL performed redox analysis; SMB and DPJ analyzed the data; SMB and TRZ authored the manuscript; SMB, GH, TRZ, DPJ, and CMC prepared the manuscript. All authors read and approved the final manuscript.

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.
Zusatzmaterial
Authors’ original file for figure 1
12950_2012_250_MOESM1_ESM.tiff
Authors’ original file for figure 2
12950_2012_250_MOESM2_ESM.tiff
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