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Vol. 26, Issue 12, 1194-1198, December 1998
Division of Basic Sciences, National Cancer Institute (F.J.G.), and
Departamento de Bioquímica y Biología Molecular,
Facultad de Ciencias, Universidad de Extremadura (P.F.-S.)
The aryl hydrocarbon receptor (AHR) is believed to mediate the
toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin
(TCDD), polychlorinated biphenyls, and polycyclic aromatic
hydrocarbons. AHR is a member of the Per, ARNT,
Sim/basic-helix-loop-helix superfamily of ligand-activated
transcription factors that also harbors the transcription
factors involved in the hypoxia response, development of the
central nervous system, and day-night adaptations. To investigate the
role of AHR in chemical toxicity and carcinogenesis and to determine
any possible function in mammalian development and physiological homeostasis, AHR-null mice were developed. The AHR-null mice were resistant to the acute toxicity of TCDD and had an altered teratogenic response to this compound. These mice were found to have a number of
abnormal phenotypes, thus confirming that AHR plays an important developmental and physiological role. Among the most consistent phenotypes was an altered liver pathology that was associated with
accelerated rates of apoptosis. Evidence suggests that this may be
related to an abnormal accumulation of levels of hepatic retinoic acid
that cause an activation of transforming growth factor 
, resulting
in stimulation of apoptosis. AHR may directly or indirectly control
levels of a cytochrome P450 that is responsible for catabolizing
retinoic acid.
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