... citation for the above?

Receptor- and reactive intermediate-mediated mechanisms of
teratogenesis.
Drugs and environmental chemicals can adversely alter the development
of the fetus at critical periods during pregnancy, resulting in death,
or in structural and functional birth defects in the surviving
offspring. This process of teratogenesis may not be evident until a
decade or more after birth. Postnatal functional abnormalities include
deficits in brain function, a variety of metabolic diseases, and
cancer. Due to the high degree of fetal cellular division and
differentiation, and to differences from the adult in many biochemical
pathways, the fetus is highly susceptible to teratogens, typically at
low exposure levels that do not harm the mother. Insights into the
mechanisms of teratogenesis come primarily from animal models and in
vitro systems, and involve either receptor-mediated or reactive
intermediate-mediated processes. Receptor-mediated mechanisms
involving the reversible binding of xenobiotic substrates to a
specific receptor are exemplified herein by the interaction of the
environmental chemical 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or
"dioxin") with the cytosolic aryl hydrocarbon receptor (AHR), which
translocates to the nucleus and, in association with other proteins,
binds to AH-responsive elements (AHREs) in numerous genes, initiating
changes in gene transcription that can perturb development.
Alternatively, many xenobiotics are bioactivated by fetal enzymes like
the cytochromes P450 (CYPs) and prostaglandin H synthases (PHSs) to
highly unstable electrophilic or free radical reactive intermediates.
Electrophilic reactive intermediates can covalently (irreversibly)
bind to and alter the function of essential cellular macromolecules
(proteins, DNA), causing developmental anomalies. Free radical
reactive intermediates can enhance the formation of reactive oxygen
species (ROS), resulting in oxidative damage to cellular
macromolecules and/or altered signal transduction. The teratogenicity
of reactive intermediates is determined to a large extent by the
balance among embryonic and fetal pathways of xenobiotic
bioactivation, detoxification of the xenobiotic reactive intermediate,
detoxification of ROS, and repair of oxidative macromolecular damage.
PMID: 20020262