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© 1997 Oxford University Press

other

Genetic Polymorphisms in Human Drug Metabolic Enzymes1

Mark Steven Miller*, Deborah Gail McCarver{dagger}, Douglas A. Bell{ddagger}, David L. Eaton§ and Joyce A. Goldstein

*Department of Cancer Biology, Bowman Gray School of Medicine, Comprehensive Cancer Center of Wake Forest University Winston-Salem, North Carolina 27157 {dagger}Department of Pediatrics and Pharmacology, Children's Hospital of Michigan, Wayne State University Detroit, Michigan 48201 {ddagger}Laboratory of Biochemical Risk Analysis P.O. Box 12233, Research Triangle Park North Carolina 27709 §Center for Ecogenetics and Environmental Health, Department of Environmental Health, University of Washington Seattle, Washington 98105-6099 ¶Human Metabolism Section, Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences P.O. Box 12233, Research Triangle Park North Carolina 27709

Received September 8, 1997; accepted September 11, 1997

Results obtained from both epidemiologic studies and experimental animal model systems have shown a wide range of phenotypic variation in the ability of individuals to metabolize drugs and environmental chemicals. Several studies have noted correlations between specific metabolic phenotypes and the incidence of disease, suggesting that certain allelic forms of drug metabolic enzymes can render the individual either more sensitive or resistant to the toxic or therapeutic effects of exogenous drugs and chemicals. While some of this variation can be attributed to different environmental exposures, it has become clear that genetic factors also play an important role in determining the response of the individual organism to exogenous agents. Recent advances in molecular biological techniques have begun to allow scientists to correlate observed phenotypic differences with the actual differences in genetic sequence at the gene level. This has allowed a correlation between gene structure and function, thus providing a mechanistic basis to explain the interaction between genetic background and individual response to environmental exposures. Results presented at this symposium discussed how genetic polymorphisms for both Phase I and Phase II metabolic enzymes in the human population modulate the response to environmental toxicants.


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