J Korean Med Sci.  2001 Apr;16(2):165-168. 10.3346/jkms.2001.16.2.165.

Apoptosis, bcl2 expression, and cell cycle analyses in nickel(II)-treated normal rat kidney cells

• Lee SH
• Choi JG
• Cho MH

• KMID: 648251
• DOI: http://doi.org/10.3346/jkms.2001.16.2.165

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.

Keyword

Nickel(II); Apoptosis; Cell Cycle; Bcl2

MeSH Terms

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