The aromatic hydrocarbon receptor, transcription, and endocrine aspects of dioxin action

Abstract

The widespread and persistent environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin elicits adaptive and adverse biological responses by inducing changes in gene transcription. Some of dioxin's effects reflect disruption of endocrine homeostasis. The aromatic hydrocarbon receptor protein, together with its heterodimerization partner, the aromatic hydrocarbon receptor nuclear translocator protein, mediates dioxin action. There are notable similarities between the mechanism of dioxin action and the mechanisms of steroid/retinoid/thyroid hormone action. Studies of dioxin action may provide insights into the regulation of hormone-responsive genes and endocrine physiology.