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Roles of reactive oxygen species, NF-κB, and peroxiredoxins in glycochenodeoxycholic acid-induced rat hepatocytes death
- Roles of reactive oxygen species, NF-κB, and peroxiredoxins in glycochenodeoxycholic acid-induced rat hepatocytes death
- Chu S.H.; Lee-Kang J.; Lee K.-H.; Lee K.
- Ewha Authors
- 이지희; 이경은
- SCOPUS Author ID
- 이지희; 이경은
- Issue Date
- Journal Title
- vol. 69, no. 1, pp. 12 - 19
- SCI; SCIE; SCOPUS
- The aim of this study was to determine the roles of reactive oxygen species (ROS), NF-κB and antioxidants in glycochenodeoxycholic acid (GCDC, 0-400 μmol/l, 0.5-3 h)-induced hepatocytes death. The differential uptake of ethidium bromide and acridine orange revealed that apoptotic death occurred dose-dependently in GCDC-treated hepatocytes whereas necrotic death was prominent especially at higher GCDC concentrations (≥200 μmol/l). ROS generation measured fluorometrically either by a confocal laser microscope or by a microplate fluorescence reader was increased dose-dependently. The dose-dependent NF-κB activation with the significant IκB-α decrease preceded both hepatocyte cell death and the alteration of antioxidant enzymes. The Cu/Zn-SOD level among several antioxidants, we checked, remained unchanged. In contrast, the catalase level and its enzymatic activity were markedly decreased only at 400 μmol/l. The Prx I and Prx II, newly defined antioxidant enzymes reducing H2O2 levels were decreased at the 200 and 400 μmol/l. These observations point to ROS generation in the GCDC-treated hepatocyte as the proximate event that triggers NF-κB activation, IκB-α proteolysis, Prx depletion, and finally cell death. And oxidative stress may be more related to necrotic cell death in GCDC-treated hepatocytes. Copyright © 2003 S. Karger AG, Basel.
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