HPB Surg. 2011;2011:789323. doi: 10.1155/2011/789323. Epub 2011 Sep 18.

Disturbances in the glutathione/ophthalmate redox buffer system in the woodchuck model of hepatitis virus-induced hepatocellular carcinoma.

HPB surgery : a world journal of hepatic, pancreatic and biliary surgery

Rafael Andres Ibarra, R Abbas, R S Kombu, Guo-Fang Zhang, G Jacobs, Z Lee, H Brunengraber, J R Sanabria

PMID: 21941408 PMCID: PMC3175733 DOI: 10.1155/2011/789323

Abstract

Purpose. The incidence of liver tumors is rising in USA. The purpose of this study was to evaluate liver oxido-reductive status in the presence of chronic liver disease and hepatocellular carcinoma (HCC). Methods. Glutathione species and ophthalmate (OA) concentrations were measured by LC-MS in processed plasma and red blood cells (RBC) from infected Woodchuck with hepatitis virus (WHV). Blood samples were obtained from: (i) infected animals with tumors (WHV+/HCC+), (ii) infected animals without tumors (WHV+/HCC-) and (iii) healthy animals (WHC-/HCC-). Results. The concentration of reduced glutathione (GSH) and the ratio GSH/GSG were lower in plasma from WHV+/HCC+ animals when compared to WHV+/HCC- and WHV-/HCC- (P < 0.01). In contrast, the concentration of oxidized glutathione (GSSG) was found to be higher in plasma from WHV+/HCC+ animals when compared to WHV+/HCC- and WHV-/HCC- (P < 0.01). The Glutathione species and its ratio from the RBC compartment were similar among all groups. OA concentration in both plasma and RBC was significantly higher from WHV+/HCC+ when compared to WHV+/HCC- and WHV-/HCC- (P < 0.01). Conclusions. Disturbances of the glutathione redox buffer system and higher concentrations of OA were found in the WCV+/HCC+ animal model. The role of these compounds as biomarkers of early tumor development in patients with end stage liver disease remains to be determined.

References

1. Ann Surg Oncol. 2004 Feb;11(2):130-8 - PubMed
2. FEBS Lett. 1994 Mar 14;341(1):59-64 - PubMed
3. Cell Biochem Funct. 2004 Nov-Dec;22(6):343-52 - PubMed
4. J Biol Chem. 1994 Aug 5;269(31):19731-7 - PubMed
5. Mol Imaging Biol. 2011 Feb;13(1):140-51 - PubMed
6. Int J Cancer. 2001 Jan 1;91(1):55-9 - PubMed
7. Int J Cancer. 2002 Mar 1;98(1):84-91 - PubMed
8. HPB Surg. 2011;2011:709052 - PubMed
9. Proc Natl Acad Sci U S A. 1978 Sep;75(9):4533-7 - PubMed
10. Free Radic Biol Med. 2003 Jan 1;34(1):1-10 - PubMed
11. J Biol Chem. 2001 Jul 27;276(30):27846-54 - PubMed
12. Free Radic Biol Med. 1999 Feb;26(3-4):410-8 - PubMed
13. Gastroenterology. 2004 Nov;127(5 Suppl 1):S27-34 - PubMed
14. J Hepatol. 2002 Jul;37(1):56-62 - PubMed
15. Clin Biochem. 2007 Oct;40(15):1157-62 - PubMed
16. J Gastroenterol Hepatol. 2009 Apr;24(4):605-17 - PubMed
17. Q J Nucl Med Mol Imaging. 2009 Apr;53(2):144-56 - PubMed
18. J Biol Chem. 2006 Jun 16;281(24):16768-76 - PubMed
19. Am J Physiol Endocrinol Metab. 2009 Jul;297(1):E260-9 - PubMed
20. Cancer Detect Prev. 1989;14(2):227-9 - PubMed
21. Clin Exp Metastasis. 1999;17(7):567-74 - PubMed
22. Biochem Biophys Res Commun. 1980 Sep 30;96(2):848-53 - PubMed
23. Prostaglandins Leukot Essent Fatty Acids. 2009 Nov-Dec;81(5-6):391-9 - PubMed
24. Cancer Epidemiol Biomarkers Prev. 2004 Oct;13(10):1651-9 - PubMed
25. Hepatol Res. 2007 Sep;37 Suppl 2:S152-65 - PubMed
26. Cell Death Differ. 2009 Oct;16(10):1303-14 - PubMed
27. J Nucl Med. 2011 Jan;52(1):98-106 - PubMed
28. J Biol Chem. 1998 Jul 24;273(30):18898-905 - PubMed
29. Crit Rev Clin Lab Sci. 2006;43(2):143-81 - PubMed
30. Hepatology. 2011 Mar;53(3):1020-2 - PubMed
31. FASEB J. 1996 May;10(7):709-20 - PubMed
32. World J Gastroenterol. 2010 Jan 28;16(4):418-24 - PubMed
33. Hepatology. 2005 Nov;42(5):1208-36 - PubMed

Publication Types

• Journal Article

Grant support

• R01 ES013925/ES/NIEHS NIH HHS/United States
• R33 DK070291/DK/NIDDK NIH HHS/United States
• T32 DK007319/DK/NIDDK NIH HHS/United States