Toxic effects and relevant molecular mechanisms of polycyclic aromatic hydrocarbon exposure on female reproductive health
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Abstract
Polycyclic aromatic hydrocarbons (PAHs) are widespread persistent environmental toxicants. Their typical representative benzoapyrene (BaP), a human carcinogen, can pass through the placental barrier and be finally metabolized into benzoapyrene-7, 8-dihydrodiol-9, 10-epoxide (BPDE) and its DNA adducts, directly affecting female reproductive health. This article reviewed the toxic effects and mechanisms of PAHs on female reproductive health at various levels such as populations, animals, cells, and molecules. At population level, exposure to PAHs in pregnant women could lead to adverse pregnancy outcomes such as abortion, premature delivery, and embryo undevelopment, and also affect the normal growth and development of fetuses. At animal level, BaP could not only affect the reproductive health of female rats, but also cause adverse developmental outcomes in young rats. At cellular level, BaP or BPDE could inhibit the invasion, migration, and proliferation of human trophoblastic cells, and promote the apoptosis and death of trophoblastic cells. Epigenetic factors, such as DNA methylation, miRNA, and lncRNA, are directly involved in the BaP exposure relevant molecular processes leading to cell dysfunction. At present, this research field is still in its primary stage, and requires multidisciplinary cooperation and in-depth studies, aiming to provide a scientific basis and preventive approach for female reproductive health protection.
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