Over the last few decades, there have been numerous reports of adverse effects on the reproductive health of wildlife and laboratory
animals caused by exposure to endocrine disrupting chemicals (EDCs). The increasing trends in human male reproductive disorders
and the mounting evidence for causative environmental factors have therefore sparked growing interest in the health threat posed
to humans by EDCs, which are substances in our food, environment and consumer items that interfere with hormone action,
biosynthesis or metabolism, resulting in disrupted tissue homeostasis or reproductive function. The mechanisms of EDCs involve
a wide array of actions and pathways. Examples include the estrogenic, androgenic, thyroid and retinoid pathways, in which the
EDCs may act directly as agonists or antagonists, or indirectly via other nuclear receptors. Dioxins and dioxin-like EDCs exert their
biological and toxicological actions through activation of the aryl hydrocarbon-receptor, which besides inducing transcription of
detoxifying enzymes also regulates transcriptional activity of other nuclear receptors. There is increasing evidence that genetic
predispositions may modify the susceptibility to adverse effects of toxic chemicals. In this review, potential consequences of
hereditary predisposition and EDCs are discussed, with a special focus on the currently available publications on interactions
between dioxin and androgen signaling.

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