Apoptosis, bcl2 expression, and cell cycle analyses in nickel(II)-treated normal rat kidney cells.
10.3346/jkms.2001.16.2.165
- Author:
Sang Han LEE
1
;
Joong Geun CHOI
;
Man Hee CHO
Author Information
1. Department of Biochemistry, College of Medicine, Soonchunhyang University, Cheonan, Korea. L1037624@sch.ac.kr
- Publication Type:Original Article
- Keywords:
Nickel(II);
Apoptosis;
Cell Cycle;
Bcl2
- MeSH:
Acetates/*toxicity;
Animal;
Apoptosis/*drug effects/physiology;
Cell Cycle/drug effects/physiology;
Cells, Cultured;
Gene Expression/drug effects;
Kidney/cytology;
Organometallic Compounds/*toxicity;
Protein p53/genetics;
Proto-Oncogene Proteins c-bcl-2/*genetics;
Rats
- From:Journal of Korean Medical Science
2001;16(2):165-168
- CountryRepublic of Korea
- Language:English
-
Abstract:
Nickel compounds are carcinogenic to human and are potent inducers of kidney and lung tumors in experimental animals. In this study, the effects of nickel(II) acetate on apoptosis, cell cycle and bcl2 expression in normal rat kidney (NRK- 52E) cells were investigated. Nickel(II) induced apoptosis in NRK-52E cells as demonstrated by DNA laddering. Apparent DNA laddering was observed in cells treated with 480 microM for 48 hr. In the flow cytometric analysis using propidium iodide fluorescence, an increase of cell proportion in G2/M phase was shown in cells exposed to at least 320 microM of nickel(II) acetate, from 7.7% for 0 microM of nickel(II) to 16.5% for 480 microM of nickel(II) acetate. Induction of apoptotic cell death by nickel(II) was accompanied by reduction of bcl2 protein expression, while the level of p53 protein was not changed. Taken together, our data indicate that nickel(II)-induced apoptosis in NRK-52E cells is accompanied by G2/M cell cycle arrest, regardless of p53 function, and that bcl2-mediated signaling pathway may be involved in positive regulation of nickel(II)-induced apoptotic cell death in NRK-52E cells.
