Dioxin toxicity in vivo results from an increase in the dioxin-independent transcriptional activity of the aryl hydrocarbon receptor.

ABSTRACT: The Aryl hydrocarbon receptor (Ahr) is the nuclear receptor mediating the toxicity of dioxins--widespread and persistent pollutants whose toxic effects include tumor promotion, teratogenesis, wasting syndrome and chloracne. Elimination of Ahr in mice eliminates dioxin toxicity but also produces adverse effects, some seemingly unrelated to dioxin. Thus the relationship between the toxic and dioxin-independent functions of Ahr is not clear, which hampers understanding and treatment of dioxin toxicity. Here we develop a Drosophila model to show that dioxin actually increases the in vivo dioxin-independent activity of Ahr. This hyperactivation resembles the effects caused by an increase in the amount of its dimerisation partner Ahr nuclear translocator (Arnt) and entails an increased transcrip

SUBMITTER: Cespedes MA 

PROVIDER: S-EPMC2975661 | biostudies-literature | 2010 Nov

REPOSITORIES: biostudies-literature