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Centrosome amplification and multinuclear phenotypes are Induced by hydrogen peroxide
Sunyoung Chae1, Chawon Yun, Haeryun Um
1Department of Biochemistry and Molecular Biology, Chronic Inflammatory Disease Research Center, Ajou University School of Medicine, Suwon 442-749, Korea.
Experimental & Molecular Medicine
|November 3, 2005
Summary
Oxidative stress, induced by hydrogen peroxide (H2O2), causes cell cycle delays and multinucleated cell formation by promoting centrosome amplification. Antioxidants can reverse these effects, suggesting a link between oxidative stress and cellular dysfunction.
Area of Science:
- Cell Biology
- Molecular Biology
- Pathophysiology
Background:
- Multinucleated cells arise from mitosis defects and are observed in inflammation, senescence, and cancer.
- Oxidative stress is linked to various pathophysiological conditions.
Purpose of the Study:
- To investigate the effect of hydrogen peroxide (H2O2)-induced oxidative stress on cell cycle progression and multinucleated cell formation.
- To explore the role of signaling pathways and reactive oxygen species (ROS) in H2O2-induced cellular changes.
Main Methods:
- Chang liver cells were treated with H2O2.
- Cell cycle progression, centrosome amplification, spindle formation, and phospho-ERK levels were analyzed.
- The effects of MEK1/2 inhibitor (PD98059) and antioxidants (N-acetylcysteine, PDTC) were evaluated.
Main Results:
- H2O2 significantly delayed cell cycle progression in Chang liver cells.
- H2O2 induced centrosome hyperamplification (n≥3) and multipolar spindle formation, leading to increased multinucleated cells.
- Increased phospho-ERK levels were observed, but PD98059 did not prevent centrosome amplification.
- Both H2O2 and adriamycin increased intracellular ROS and multinucleated cells, effects suppressed by antioxidants.
Conclusions:
- Oxidative stress can trigger centrosome hyperamplification and multinucleated cell formation.
- These events may contribute to the progression of pathophysiological states.
- Antioxidant intervention may mitigate H2O2-induced cellular abnormalities.