View : 18 Download: 0

Irreversible inactivation of glutathione peroxidase 1 and reversible inactivation of peroxiredoxin ii by H2O2 in red blood cells

Title
Irreversible inactivation of glutathione peroxidase 1 and reversible inactivation of peroxiredoxin ii by H2O2 in red blood cells
Authors
Cho C.-S.Lee S.Lee G.T.Woo H.A.Choi E.-J.Rhee S.G.
Ewha Authors
이서구우현애
SCOPUS Author ID
이서구scopusscopus; 우현애scopus
Issue Date
2010
Journal Title
Antioxidants and Redox Signaling
ISSN
1523-0864JCR Link
Citation
vol. 12, no. 11, pp. 1235 - 1246
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Catalase, glutathione peroxidase1 (GPx1), and peroxiredoxin (Prx) II are the principal enzymes responsible for peroxide elimination in RBC. We have now evaluated the relative roles of these enzymes by studying inactivation of GPx1 and Prx II in human RBCs. Mass spectrometry revealed that treatment of GPx1 with H2O2 converts the selenocysteine residue at its active site to dehydroalanine (DHA). We developed a blot method for detection of DHA-containing proteins, with which we observed that the amount of DHA-containing GPx1 increases with increasing RBC density, which is correlated with increasing RBC age. Given that the conversion of selenocysteine to DHA is irreversible, the content of DHA-GPx1 in each RBC likely reflects total oxidative stress experienced by the cell during its lifetime. Prx II is inactivated by occasional hyperoxidation of its catalytic cysteine to cysteine sulfinic acid during catalysis. We believe that the activity of sulfiredoxin in RBCs is sufficient to counteract the hyperoxidation of Prx II that occurs in the presence of the basal level of H2O2 flux resulting from hemoglobin autoxidation. If the H2O2 flux is increased above the basal level, however, the sulfinic Prx II begins to accumulate. In the presence of an increased H2O2 flux, inhibition of catalase accelerated the accumulation of sulfinic Prx II, indicative of the protective role of catalase. Antioxid. Redox Signal. 12, 1235-1246. © 2010 Mary Ann Liebert, Inc.
DOI
10.1089/ars.2009.2701
Appears in Collections:
일반대학원 > 생명·약학부 > Journal papers
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE