Carcinogenesis, Vol 18, 271-277, Copyright © 1997 by Oxford University Press
KS Kasprzak, P Jaruga, TH Zastawny, SL North, CW Riggs, R Olinski and M Dizdaroglu
DNA base damage was assayed using gas chromatography/ mass spectrometry
with selected ion monitoring (GC/MS-SIM) in renal and hepatic chromatin of
male F344 rats up to 14 days after a single i.p. injection of 90 micromol
Ni(II) acetate/kg body wt. Ten different damaged bases were quantified. No
damage was found in either organ 12 h after Ni(II) treatment. The damage
became significant only from day 1, with magnitude and persistence
depending on the organ and base. In livers, levels of five DNA base
products were significantly elevated over those in control rats. They were:
8-oxoguanine (by 46% at day 1 postinjection);
2,6-diamino-4-hydroxy-5-formamidopyrimidine (by 107% at day 1);
5-(hydroxymethyl)uracil (by 94% at day 1); 5,6-dihydroxyuracil (by 128% at
day 1); and 5-hydroxyhydantoin (by 39% in terms of the overall adjusted
means for days 1-14 post-injection). The elevation was highest at day 1
post-injection followed by a decrease at later days, except for
5-hydroxyhydantoin. In kidneys, the levels of only three damaged bases,
8-oxoguanine, 5-hydroxyhydantoin and 5,6-dihydroxyuracil were increased
significantly (by 31, 73 and 60%, respectively) and one base, 8-oxoadenine,
was increased by 26%, just below significance, all in terms of overall
adjusted means for days 1-14 post-injection. Hence, unlike those in the
liver, the renal increases persisted for 14 days. The results reveal a
tissue specific response to Ni(II)-mediated oxidative DNA base damage with
apparently faster DNA repair in liver than in kidney, the main target of
Ni(II) carcinogenicity.
ARTICLES
Oxidative DNA base damage and its repair in kidneys and livers of nickel(II)-treated male F344 rats
Laboratory of Comparative Carcinogenesis, National Cancer Institute, FCRDC, Frederick, MD 21702, USA.
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