Nickel (II)-induced apoptosis and G2/M enrichment

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 μM 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 μM nickel (II) from 57.7% of cells in the G₀/G₁ phase, 34.7% in the S phase, and 7.6% in the G₂/M phase for 0 μM nickel (II), to 58.6%, 14.5%, and 26.9% for 640 μM nickel (II). These findings suggest that nickel (II) can modulate cellular response through some common effecters involving in both apoptotic and cell cycle regulatory pathways.