ORIGINAL ARTICLESThe absence of interaction between drug metabolizing enzyme genotypes and maternal lifestyle factors on glycophorin A somatic mutation frequency levels in newbornsNukui, Tomokoa; Day, Richard D.b; Gordish-Dressman, Heather A.c; Harger, Gaild; Bigbee, William L.c; Ness, Roberta B.d; Romkes, MarjorieaAuthor Information aCenter for Clinical Pharmacology, Department of Medicine, University of Pittsburgh, Pittsburgh and Departments of bBiostatistics cEnvironmental and Occupational Health dEpidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania, USA Correspondence and requests for reprints to Marjorie Romkes, Centre for Clinical Pharmacology, Department of Medicine, University of Pittsburgh, Suite 450, 100 Technology Drive, Pittsburgh, PA 15219, USA Tel: +1 412 383 8885; fax: +1 412 648 1837; e-mail: [email protected] Sponsorship: This study was supported by grants R01 HD33016 and R01 HD36880 from the National Institute of Child Health and Human Development, National Institutes of Health to W. L. Bigbee and M. Romkes, respectively. Received 29 July 2005 Accepted 19 September 2005 Pharmacogenetics and Genomics: February 2006 - Volume 16 - Issue 2 - p 129-138 doi: 10.1097/01.fpc.0000184954.08453.e1 Buy Metrics Abstract Prenatal exposure to carcinogens results in newborn DNA damage which in turn is associated with impaired health conditions in both childhood and adulthood. The present study aimed to evaluate whether phase I and II biotransformation enzyme genetic polymorphisms in combination with environmental exposures during pregnancy result in elevated levels of newborn DNA damage. Maternal peripheral and umbilical cord blood samples from 406 mother/newborn pairs were genotyped for a panel of phase I/II metabolic enzymes (CYP1A1, CYP2E1, GSTM1, GSTT1 and NAT2) responsible for the metabolism of tobacco and lifestyle-related mutagens and carcinogens. DNA damage was measured by somatic cell mutation frequency at the glycophorin A (GPA) locus in newborns. No association with elevated somatic cell mutation frequency was observed between the combination of maternal/newborn genotypes and cigarette smoke or lifestyle exposures. The observed variation in newborn GPA frequency might be due to either environmental factors not assessed in this study or inter-individual differences in alternative metabolic or DNA repair pathways. © 2006 Lippincott Williams & Wilkins, Inc.