Carcinogenesis, Vol 18, 1021-1026, Copyright © 1997 by Oxford University Press
H Dally and A Hartwig
Compounds of nickel(II) and cadmium(II) are carcinogenic to humans and to
experimental animals. One frequently discussed mechanism involved in tumor
formation is an increase in reactive oxygen species by both metals with the
subsequent generation of oxidative DNA damage. In the present study we used
human HeLa cells to investigate the potential of nickel(II) and cadmium(II)
to induce DNA lesions typical for oxygen free radicals in intact cells and
the effect on their repair. As indicators of oxidative DNA damage, we
determined the frequencies of DNA strand breaks and of lesions recognized
by the bacterial formamidopyrimidine-DNA glycosylase (Fpg protein),
including 7,8- dihydro-8-oxoguanine (8-hydroxyguanine), a pre-mutagenic DNA
base modification. Nickel(II) caused a slight increase in DNA strand breaks
at 250 microM and higher, while the frequency of Fpg-sensitive sites was
enhanced only at the cytotoxic concentration of 750 microM. The repair of
oxidative DNA lesions induced by visible light was reduced at 50 microM and
at 100 microM nickel(II) for Fpg-sensitive sites and DNA strand breaks,
respectively; the removal of both types of lesions was blocked nearly
completely at 250 microM nickel(II). In the case of cadmium(II), DNA strand
breaks occurred at 10 microM and no Fpg- sensitive sites were detected.
However, the repair of Fpg-sensitive DNA lesions induced by visible light
was reduced at 0.5 microM cadmium(II) and higher, while the closure of DNA
strand breaks was not affected. Since oxidative DNA damage is continuously
induced during aerobic metabolism, an impaired repair of these lesions
might well explain the carcinogenic action of nickel(II) and cadmium(II).
ARTICLES
Induction and repair inhibition of oxidative DNA damage by nickel(II) and cadmium(II) in mammalian cells
University of Bremen, Department of Biology and Chemistry, Germany.
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