Carcinogenesis, Vol 19, 1275-1283, Copyright © 1998 by Oxford University Press
C Ji, CA Rouzer, LJ Marnett and JA Pietenpol
We have investigated the effect of the endogenous genotoxin malondialdehyde
(MDA) on cell cycle kinetics and the expression and biochemical activity of
several cell cycle regulatory proteins. MDA treatment of two human cell
lines (RKO and H1299) resulted in a 3- to 6- fold elevation in the levels
of the major detectable MDA-DNA adduct, M1G-dR. The increase in M1G-dR was
accompanied by irreversible cell cycle arrest, elevation in p53 and p21
protein levels, and inhibition of cyclin E- and cyclin B-associated kinase
activities. The decrease in cyclin E- and cyclin B-dependent kinase
activities was caused by increased p21 and decreased cdc2 levels,
respectively. Comparable levels of p21 induction were observed in RKO
(wild-type p53) and H1299 (p53-null) cells. Thus, MDA was able to engage
cell cycle checkpoint function in human cell lines when used at
concentrations that produce M1G-dR levels of the same magnitude found in
human tissues.
ARTICLES
Induction of cell cycle arrest by the endogenous product of lipid peroxidation, malondialdehyde
Department of Biochemistry, Vanderbilt Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
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