Nickel (II)-induced apoptosis and G2/M enrichment.
- Author:
Sang Han LEE
1
;
Do Kwon KIM
;
Young Rok SEO
;
Kee Min WOO
;
Chang Se KIM
;
Man Hee CHO
Author Information
1. Department of Biochemistry, College of Medicine, Soonchunhyang University, Cheon-An, Korea.
- Publication Type:Original Article
- Keywords:
DNA damage;
apoptosis;
cell cycle;
flow cytometry;
Sub-G1;
DNA ladder
- MeSH:
Animal;
Apoptosis/drug effects*;
CHO Cells/drug effects*;
CHO Cells/cytology;
Cell Cycle/drug effects*;
DNA Fragmentation/drug effects;
Flow Cytometry;
G2 Phase/drug effects;
Hamsters;
Mitosis/drug effects;
Nickel/pharmacology*
- From:Experimental & Molecular Medicine
1998;30(3):171-176
- CountryRepublic of Korea
- Language:English
-
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.
