Carcinogenesis, Vol 19, 2081-2084, Copyright © 1998 by Oxford University Press
J Nair, A Gal, S Tamir, SR Tannenbaum, GN Wogan and H Bartsch
In order to investigate specific DNA damage caused by nitric oxide (NO)
induced lipid peroxidation, levels of promutagenic etheno adducts 1,N6-
ethenodeoxyadenosine (epsilondA) and 3,N4-ethenodeoxycytidine (epsilondC)
were measured in spleen DNA of SJL mice induced to produce high levels of
NO by injection of RcsX (pre-B-cell lymphoma) cells. epsilondA and
epsilondC levels were quantified by an ultrasensitive
immunoaffinity-32P-post-labeling method. Spleen DNA of control mice (n = 5)
had background levels of 9.2+/-5.4 epsilondA adducts per 10(9) dA and
13.1+/-5.7 epsilondC adducts per 10(9) dC. In RcsX cell-injected mice (n =
7), levels of these adducts were elevated approximately 6- fold, i.e.
53.9+/-39.4 epsilondA per 10(9) dA and 83.5+/-57.8 epsilondC per 10(9) dC
(P < 0.05). Mice injected with RcsX cells and also treated with
NG-methyl-L-arginine (NMA), an inhibitor of inducible nitric oxide synthase
(n = 6), had significantly reduced levels (P < 0.05) of both epsilondA
and epsilondC (13.5+/-5.7 epsilondA per 10(9) dA and 28.2+/- 15.7 epsilondC
per 10(9) dC). These findings constitute the first available evidence of
formation of etheno adducts associated with NO overproduction in vivo. The
adducts were presumably formed from lipid peroxidation products such as
trans-4-hydroxy-2-nonenal (HNE), generated via oxidation of lipids by
peroxynitrite. The results suggest that etheno-DNA adducts, among other
types of damage, may contribute to the etiology of cancers associated with
chronic infection/inflammation in which NO is overproduced.
ARTICLES
Etheno adducts in spleen DNA of SJL mice stimulated to overproduce nitric oxide
Division of Toxicology and Cancer Risk Factors, German Cancer Research Center, Heidelberg.
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