CYP1A1 MESSENGER-RNA LEVELS IN PLACENTAL TISSUE AS A BIOMARKER OF ENVIRONMENTAL EXPOSURE

Citation
Rm. Whyatt et al., CYP1A1 MESSENGER-RNA LEVELS IN PLACENTAL TISSUE AS A BIOMARKER OF ENVIRONMENTAL EXPOSURE, Cancer epidemiology, biomarkers & prevention, 4(2), 1995, pp. 147-153
Citations number
37
Categorie Soggetti
Public, Environmental & Occupation Heath
ISSN journal
10559965
Volume
4
Issue
2
Year of publication
1995
Pages
147 - 153
Database
ISI
SICI code
1055-9965(1995)4:2<147:CMLIPT>2.0.ZU;2-M
Abstract
The human CYP1A1 gene codes for an inducible enzyme system involved in biotransformation of certain xenobiotics, including polycyclic aromat ic hydrocarbons; some of the metabolites are carcinogenic and mutageni c. Effects of environmental exposures (smoking, air pollution, and die t) on CYP1A1 gene induction in placental tissue and the modulation of induction by the CYP1A1 Mspl RFLP were evaluated in two groups from Po land: 70 mother-child pairs from Krakow, a city with elevated air poll ution; and 90 pairs from Limanowa, a less polluted area. Compared to p lacentas from nonsmoking women, CYP1A1 mRNA levels were significantly increased in placentas from current smokers (P < 0.001). Ex-smokers al so had significantly higher placental mRNA levels, including women who quit smoking prior to pregnancy (P < 0.01). A marginal increase in CY P1A1 mRNA with environmental tobacco smoke exposure was evident. Withi n Krakow, there was an increase in CYP1A1 mRNA with ambient pollution at the place of residence for each woman, which was significant among women who were not employed away from the home (P < 0.05 controlling f or smoking status, diet, and use of coal for heating). Significant inc reases in mRNA were associated with dietary consumption of smoked meat , cheese, and fish (P < 0.01). The CYP1A1 Mspl RFLP was not a signific ant determinant of CYP1A1 mRNA levels after controlling for smoking an d other variables. Human placenta provides a readily available and res ponsive system that can serve as a model for evaluating environmental and genetic determinants of CYP1A1 induction.