Carcinogenesis, Vol 19, 1389-1392, Copyright © 1998 by Oxford University Press
RM Whyatt, DA Bell, W Jedrychowski, RM Santella, SJ Garte, G Cosma, DK Manchester, TL Young, TB Cooper, R Ottman and FP Perera
This study investigated the relationship in human placenta between
polycyclic aromatic hydrocabon (PAH)-DNA adduct levels and two biomarkers
of cytochrome P4501A1 (CYP1A1): gene induction evidenced by CYP1A1 mRNA,
and a genetic polymorphism, the CYP1A1 MspI RFLP. CYP1A1 codes for an
inducible enzyme system that catalyzes the bioactivation of PAHs. Prior
research found a high correlation in human lung tissue between CYP1A1
activity and DNA damage from PAHs. The CYP1A1 Mspi RFLP has been linked in
some studies to risk of lung cancer. The relationships in human placenta
between DNA damage, CYP1A1 activity and genotype have not been well
characterized and may be relevant to risks from transplacental PAH
exposure. The study cohort consisted of 70 newborns from Krakow, Poland, a
city with elevated air pollution, and 90 newborns from nearby Limanowa, an
area with lower air pollution but greater indoor coal use. Contrary to
results seen previously in lung tissue, CYP1A1 mRNA was not significantly
correlated with PAH-DNA adduct levels in the placenta. Smoking
(self-reported maternal and infant plasma cotinine) was significantly
associated with CYP1A1 mRNA levels (P < 0.01), but not with PAH-DNA
adduct levels. Placental PAH- DNA adduct levels were significantly higher
in infants with the CYP1A1 MspI restriction site compared with infants
without the restriction site (P < 0.01), implicating a genetic factor in
inter-individual variation in DNA damage in human placenta. Further studies
are needed to determine the relevance of this finding to risk of
transplacental carcinogenesis.
ARTICLES
Polycyclic aromatic hydrocarbon-DNA adducts in human placenta and modulation by CYP1A1 induction and genotype
Columbia University School of Public Health, Division of Environmental Health Sciences, New York, NY 10032, USA.
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