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Nickel (II)-induced apoptosis and G2/M enrichment
1Department of Biochemistry, College of Medicine, Soonchunhyang University, Cheon-An, Korea.
Abstract:
Treatment with certain DNA-damaging agents induce a complex cellular response comprising pertubation of cell cycle progression and/or apoptosis on proliferating mammalian cells. Our studies were focused on the cellular effects of nickel (II) acetate, DNA-damaging agent, on Chinese hamster ovary (CHO) cells. Fragmented DNAs were examined by agarose gel electrophoresis and cell cycle was determined by DNA flow cytometry using propidium iodide fluorescence. Apparent DNA laddering was observed in cells treated with 240 microM nickel (II) and increased with a concentration-dependent manner. Treatment of nickel (II) acetate resulted in apoptosis which was accompanied by G2/M cell accumulation. Proportion of CHO cells in G2/M phase was also significantly increased in cells exposed to at least 480 microM nickel (II) from 57.7% of cells in the G0/G1 phase, 34.7% in the S phase, and 7.6% in the G2/M1 phase for 0 microM nickel (II), to 58.6%, 14.5%, and 26.9% for 640 microM nickel (II). These findings suggest that nickel (II) can modulate cellular response through some common effectors involving in both apoptotic and cell cycle regulatory pathways.
Insights
Nickel (II) acetate, a DNA-damaging agent, induces apoptosis and G2/M cell cycle arrest in Chinese hamster ovary cells. This study reveals nickel
Area of Science:
- Cellular and Molecular Biology
- Toxicology
- Genetics
Background:
- DNA-damaging agents trigger complex cellular responses, including apoptosis and cell cycle perturbation.
- Nickel (II) acetate is a known DNA-damaging agent with potential cellular effects.
Purpose of the Study:
- To investigate the cellular effects of nickel (II) acetate on Chinese hamster ovary (CHO) cells.
- To determine the impact of nickel (II) acetate on DNA fragmentation, apoptosis, and cell cycle progression.
Main Methods:
- Agarose gel electrophoresis to examine DNA fragmentation.
- DNA flow cytometry with propidium iodide staining to analyze cell cycle distribution.
Main Results:
- Nickel (II) acetate treatment induced DNA laddering in a concentration-dependent manner.
- Apoptosis was observed in nickel (II) acetate-treated cells, accompanied by G2/M cell cycle accumulation.
- Significant increase in G2/M phase cells occurred at nickel (II) concentrations of 480 microM and above.
Conclusions:
- Nickel (II) acetate induces apoptosis and G2/M cell cycle arrest in CHO cells.
- Nickel (II) appears to modulate cellular responses through common effectors in apoptotic and cell cycle pathways.