By Anna M. Fan;Fan
ISBN-10: 0824794907
ISBN-13: 9780824794903
Introduces the basic rules and present thoughts of toxicology and threat assessment--offering complete discussions on medical checking out, chance evaluation of chemical substances and dangerous fabrics, the applying of animal facts to human wellbeing and fitness threat overview, mathematical versions, statistical techniques, environmental legislation, info assets, and threat administration.
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Extra info for Toxicology and Risk Assessment: Principles, Methods, and Applications
Sample text
Although these polymorphisms are well-established, epidemiological data linking a particular phenotype to increased or decreased cancer risk are often lacking. An association between the extensive metabolizer phenotypeof debrisoquine-4-hydroxylase(CYP2D6) and increased lung cancer risk hasbeen reported, and the tobacco-specific nitrosamine, NNK, is a substratefor this enzyme. Associations between arylhydrocarbon hydroxylase inducibility(Cm1 Al)and lung andlaryngealcancerandbetweentheslow-acetylatorphenotype(N-acetyltransferase)and bladder cancer and the fast-acetylator phenotype and colon cancer have also been reported.
Whereasinitiation is generally considered to be an irreversible process, promotion is not, so repeated exposure to promoters may be required for tumorigenesis. Possible mechanismsof tumor promotion, which need not be mutually exclusive, include induction of cell proliferation; inhibition of intercellular communication, which relieves initiated cells from restraint normally exertedby surrounding normal tissue; and immunosuppression. I3 Carcinogenesis C. Progression The rate of conversion of papillomas to carcinomas, termed progression or malignant conversion, can be increasedby treatment with some agents.
D. Molecular Targets in Multistage Carcinogenesis Heritable alterations that leadto altered expressionor function of genes involved in regulation of proliferation and differentiation are important in carcinogenesis. Protooncogenes and tumor suppressor genes are two such gene classes. Protooncogenes are normal cellular genes that, when inappropriately activated by mutational events to oncogenes, alter regulation of growth and 1990). , differentiation (reviewed in Cooper, only one affected allele confers the mutant phenotype on the cell).