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Mol. Cells 2006; 22(1): 21-29

Published online January 1, 1970

© The Korean Society for Molecular and Cellular Biology

Hydrogen Peroxide Induces Apoptosis of BJAB Cells Due to Formation of Hydroxyl Radicals Via Intracellular Iron-mediated Fenton Chemistry in Glucose Oxidase-mediated Oxidative Stress

Jeong-Chae Lee, Young-Ok Son, Ki-Choon Choi, Yong-Suk Jang

Abstract

The aim of this study was to determine if hydrogen peroxide (H2O2) generated by glucose oxidase (GO) induces apoptosis or necrosis of BJAB cells and which radical is the direct mediator of cell death. We found that GO produced H2O2 continuously in low concentrations, similar to in vivo conditions, and decreased proliferation and cell viability in a dose-dependent manner. The GO-mediated cytotoxicity resulted from apoptosis, and was confirmed by monitoring the cells after H33342/Annexin V/propidium iodide staining. Decreases of mitochondrial membrane potential and intracellular glutathione level were found to be critical events in the H2O2-mediated apoptosis. Additional experiments revealed that H2O2 exerted its apoptotic action through the formation of hydroxyl radicals via the Fenton rather than the Haber-Weiss reaction. Moreover, intracellular redox-active iron, but not copper, participated in the H2O2-mediated apoptosis.

Keywords Apoptosis; BJAB Cells; Glucose Oxidase; Hydroxyl Radicals; Metal Ions.

Article

Research Article

Mol. Cells 2006; 22(1): 21-29

Published online August 31, 2006

Copyright © The Korean Society for Molecular and Cellular Biology.

Hydrogen Peroxide Induces Apoptosis of BJAB Cells Due to Formation of Hydroxyl Radicals Via Intracellular Iron-mediated Fenton Chemistry in Glucose Oxidase-mediated Oxidative Stress

Jeong-Chae Lee, Young-Ok Son, Ki-Choon Choi, Yong-Suk Jang

Abstract

The aim of this study was to determine if hydrogen peroxide (H2O2) generated by glucose oxidase (GO) induces apoptosis or necrosis of BJAB cells and which radical is the direct mediator of cell death. We found that GO produced H2O2 continuously in low concentrations, similar to in vivo conditions, and decreased proliferation and cell viability in a dose-dependent manner. The GO-mediated cytotoxicity resulted from apoptosis, and was confirmed by monitoring the cells after H33342/Annexin V/propidium iodide staining. Decreases of mitochondrial membrane potential and intracellular glutathione level were found to be critical events in the H2O2-mediated apoptosis. Additional experiments revealed that H2O2 exerted its apoptotic action through the formation of hydroxyl radicals via the Fenton rather than the Haber-Weiss reaction. Moreover, intracellular redox-active iron, but not copper, participated in the H2O2-mediated apoptosis.

Keywords: Apoptosis, BJAB Cells, Glucose Oxidase, Hydroxyl Radicals, Metal Ions.

Mol. Cells
Jun 30, 2023 Vol.46 No.6, pp. 329~398
COVER PICTURE
The cellular proteostasis network is adaptively modulated upon cellular stress, thereby protecting cells from proteostasis collapse. Heat shock induces the translocation of misfolded proteins and the chaperone protein HSP70 into nucleolus, where nuclear protein quality control primarily occurs. Nuclear RNA export factor 1 (green), nucleolar protein fibrillarin (red), and nuclei (blue) were visualized in NIH3T3 cells under basal (left) and heat shock (right) conditions (Park et al., pp. 374-386).

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