Polycyclic aromatic hydrocarbons (PAHs) are a risk factor for the occurrence of cardiac diseases. The present study was conducted to investigate the influence of prenatal exposure to a mixed PAHs on heart and the underlying mechanism. Pregnant mice were orally administered with a mixture of 8 kinds of PAHs (0, 5, 50, 500 μg/kg body weight) once every 2 days for a total of 8 dosages. The mixed PAHs contained naphthalene, acenaphthylene, phenanthrene, fluoranthene, pyrene, benzo[a]pyrene, dibenzo[a,h]anthracene and benzo[g,h,i]perylene at a weight ratio of 10: 10: 10: 10: 10: 1: 1: 1. The adult males, not females, showed significantly decreased heart/body weight ratio, which was attributed to the loss of cardiac fiber and the increase of cell apoptosis. The protein expression of transforming growth factor β1 and its downstream transcription factors, Smad3 and Smad4, was significantly downregulated, which caused the loss of cardiac fiber. The downregulated phosphatidylinositol 3-kinase and AKT led to increased expression of caspase3, caspase9, BAX and reduced expression of Bcl-2, which was responsible for the increased cell apoptosis. Different levels of aromatic hydrocarbon receptor and sex hormone receptors between males and females were associated with the distinct effect on heart.

多环芳烃（PAHs）是心脏病发生的危险因素。本研究旨在探讨产前暴露于混合多环芳烃对心脏的影响及其潜在机制。妊娠小鼠每 2 天口服 8 种多环芳烃混合物（0、5、50、500 μg/kg 体重），共 8 个剂量。混合多环芳烃含有萘、苊、菲、荧蒽、芘、苯并[ a ]芘、二苯并[ a , h ]蒽和苯并[ g , h , i]]苝的重量比为 10: 10: 10: 10: 10: 1: 1: 1。成年男性而非女性的心脏/体重比显着降低，这归因于心脏纤维的损失和细胞凋亡增加。转化生长因子β1及其下游转录因子Smad3和Smad4的蛋白表达显着下调，导致心肌纤维丢失。下调的磷脂酰肌醇 3-激酶和 AKT 导致 caspase3、caspase9、BAX 表达增加和 Bcl-2 表达减少，Bcl-2 是导致细胞凋亡增加的原因。男性和女性之间不同水平的芳香烃受体和性激素受体与对心脏的不同影响有关。