Carcinogenesis, Vol 19, 1203-1207, Copyright © 1998 by Oxford University Press
YH Shiao, SH Lee and KS Kasprzak
Nickel(II) compounds are known human and animal carcinogens. In this study,
the effects of nickel(II) acetate on cell cycle, apoptosis and p53
expression were investigated in order to unveil the elements of early
cellular responses to the metal. Chinese hamster ovary (CHO) cells were
grown for 72 h in Ham's F-12 medium containing 0, 40, 80, 160, 240, 320,
480 or 640 microM nickel(II) acetate. DNA fragmentation, representative of
apoptosis, was examined by agarose gel electrophoresis. The distribution of
cells among various phases of cell cycle was determined by DNA flow
cytometry. Expression of p53 protein was measured by the Western blotting
technique. DNA fragmentation was detectable in cells treated with > or =
160 microM nickel(II) and its intensity increased with increasing
nickel(II) concentration. The proportion of cells at S phase declined in a
nickel(II) concentration- dependent manner. The decline was accompanied by
an increase of cell proportion in G2/M phase and the increase became
statistically significant in cells exposed to at least 480 microM
nickel(II). Expression of p53 protein was not different from that in the
control among samples treated with < or = 480 microM nickel(II).
However, an extra fraction that migrated close to the p53 protein fraction
was detected in cells treated with 640 microM nickel(II). Our findings
suggest that nickel(II) modulates cellular response through effectors
involved in both G2/M arrest and apoptosis regulatory pathways. The
proportion of cells arrested at G2/M phase or undergoing apoptosis depends
directly on nickel(II) concentration. High concentration of nickel(II)
appears to up-regulate protein(s) other than the common form of p53
protein.
ARTICLES
Cell cycle arrest, apoptosis and p53 expression in nickel(II) acetate- treated Chinese hamster ovary cells
Laboratory of Comparative Carcinogenesis, NCI-FCRDC, NIH, Frederick, MD 21702, USA. shiao@ncifcrf.gov
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