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Role of Biotransformation Reactions in Prenatal and Postnatal Chemical Toxicity

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Methods in Radioimmunoassay, Toxicology, and Related Areas

Part of the book series: Progress in Analytical Chemistry ((PAC))

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Abstract

Drugs and other chemicals may produce qualitatively and quantitatively different toxicologic effects in embryos, fetuses and newborns than in the adult of the same species. When such toxicity occurs during embryogenesis congenital malformations may result. On the other hand, agents which produce toxicity during late fetal development, or during the neonatal period, may impair development or produce toxicity qualitatively similar to that seen in the adult. During embryogenesis there are embryological and non-embryological factors which determine an organism’s susceptibility to an agent, such as the nature of the agent, the dose, and maternal physiology (Wilson, 1965). Agents which disrupt embryonic development may initially act at any of the processes essential for normal development, e.g., cell division, differential gene expression, changes in the surface properties and shapes of cells, or general cellular metabolism. Most organs have a period of particular susceptibility to teratogens which probably coincides with the early and critical developmental events for that organ. During the fetal and neonatal period, however, after differentiation of cells is largely completed, chemical toxicity may involve interference with cell growth.

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Gibson, J.E. (1974). Role of Biotransformation Reactions in Prenatal and Postnatal Chemical Toxicity. In: Simmons, I.L., Ewing, G.W. (eds) Methods in Radioimmunoassay, Toxicology, and Related Areas. Progress in Analytical Chemistry. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-3321-0_7

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  • DOI: https://doi.org/10.1007/978-1-4684-3321-0_7

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-3323-4

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