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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Seveso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）被提议通过改变芳烃受体（蛋白质：AHR；基因：AHR）途径的活动来干扰胎儿的生长，该途径调节包括异种生物在内的多种生物和发育过程代谢。AHR的遗传变异是暴露于产前吸烟儿童低出生体重的重要驱动因素，但对这些与AHR最有效的异源生物配体TCDD的遗传相互作用的了解还很少。