Physiologically-based pharmacokinetic model for pregnancy as a tool for investigation of developmental mechanisms.

J F Young
Author Information
  1. J F Young: Division of Reproductive and Developmental Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA. jyoung@nctr.fda.gov

Abstract

There is no known mechanism of teratogenesis! Although receptor occupancy has been implicated, associated and/or deemed necessary for some malformations in newborns (e.g. estrogen receptors, retinoic acid receptors), the upstream and downstream events from receptor occupancy that definitively tie a xenobiotic exposure with a resultant malformation are essentially unknown. One part of the puzzle that can be delineated is the xenobiotic target-tissue exposure curve. Physiologically-based pharmacokinetic (PBPK) models are designed to provide time-course exposure curves for organs, tissues and fluids of human or animal systems. In this context pregnancy requires special considerations in that the PBPK model must represent the dynamic growth of both the maternal and embryo/fetal systems.

MeSH Term

Abnormalities, Drug-Induced
Animals
Computer Simulation
Disease Models, Animal
Embryonic and Fetal Development
Female
Humans
Maternal Exposure
Maternal-Fetal Exchange
Models, Biological
Pregnancy
Prenatal Exposure Delayed Effects
Receptors, Drug
Reproducibility of Results
Rodentia
Teratogens
Time Factors
Xenobiotics

Chemicals

Receptors, Drug
Teratogens
Xenobiotics

Word Cloud

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