2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) is proposed to interfere with fetal growth via altered activity of the aryl hydrocarbon receptor (protein: AHR; gene: AHR) pathway which regulates diverse biological and developmental processes including xenobiotic metabolism. Genetic variation in AHR is an important driver of susceptibility to low birthweight in children exposed to prenatal smoking, but less is known about these genetic interactions with TCDD, AHR’s most potent xenobiotic ligand.

中文翻译：

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塞维索第二代健康研究中的 AHR 基因-二恶英相互作用和出生体重


2,3,7,8-四氯二苯并-对-二恶英 (TCDD) 被认为通过改变芳烃受体（蛋白质：AHR；基因： AHR ）途径的活性来干扰胎儿生长，该途径调节多种生物和发育过程，包括异生素代谢。 AHR的遗传变异是产前吸烟儿童易患低出生体重的重要驱动因素，但人们对这些与 AHR 最有效的异生配体 TCDD 的遗传相互作用知之甚少。