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dc.contributor.authorRahman, S.H.*
dc.contributor.authorSrinivasan, Asha R.*
dc.contributor.authorNicolaou, Anna*
dc.date.accessioned2010-12-16T16:29:16Z
dc.date.available2010-12-16T16:29:16Z
dc.date.issued2009
dc.identifier.citationRahman, S. H., Srinivasan, A. R. and Nicolaou, A. (2009). Transsulfuration Pathway Defects and Increased Glutathione Degradation in Severe Acute Pancreatitis. Digestive Diseases and Sciences, Vol. 54, No. 3, pp. 675-682.en
dc.identifier.urihttp://hdl.handle.net/10454/4588
dc.descriptionnoen
dc.description.abstractGlutathione depletion is a consistent feature of the progression of mild to severe acute pancreatitis. In this study, we examined the temporal relationship between cysteine, homocysteine, and cysteinyl-glycine levels; total reduced erythrocyte glutathione; gamma-glutamyl transpeptidase activity; and disease severity. Initially, cysteine concentration was low, at levels similar to those of healthy controls. However, glutathione was reduced whilst cysteinyl glycine and gamma-glutamyl transpeptidase activity were increased in both mild and severe attacks. As the disease progressed, glutathione and cysteinyl glycine were further increased in mild attacks and cysteine levels correlated with homocysteine (r = 0.8, P < 0.001) and gamma-glutamyl transpeptidase activity (r = 0.75, P < 0.001). The progress of severe attacks was associated with glutathione depletion, reduced gamma-glutamyl transpeptidase activity, and increased cysteinyl glycine that correlated with glutathione depletion (r = 0.99, P = 0.01). These results show that glutathione depletion associated with severe acute pancreatitis occurs despite an adequate cysteine supply and could be attributed to heightened oxidative stress coupled to impaired downstream biosynthesis.en
dc.language.isoenen
dc.subjectSulfur amino acidsen
dc.subjectOxidative stressen
dc.subjectGamma glutamyl transpeptidaseen
dc.subjectAcute pancreatitisen
dc.subjectGlutathione depletionen
dc.subjectHomocysteineen
dc.subjectCysteineen
dc.titleTranssulfuration Pathway Defects and Increased Glutathione Degradation in Severe Acute Pancreatitis.en
dc.status.refereedyesen
dc.typeArticleen
dc.identifier.doihttps://doi.org/10.1007/s10620-008-0382-z


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