Reproductive toxicity of benzo[α]pyrene: Effects, mechanisms, and perspectives

Polycyclic aromatic hydrocarbons are pervasive environmental pollutants. Benzo[α]pyrene (B[α]P), a prototypical polycyclic aromatic hydrocarbon, elicits increasing apprehension due to its endocrine-disrupting properties and reproductive toxicity in animals; however, the toxicological effects and underlying mechanisms have not been thoroughly compiled and elucidated. This research delineates B[α]P toxicity in the reproductive systems of multiple species, including mammals, amphibians, fish, and invertebrates, alongside the relevant molecular and epigenetic evidence. In males, exposure to B[α]P causes testicular injury, promotes spermatogenic diseases, and diminishes sperm quality. The metabolism of B[α]P leads to oxidative damage and the creation of DNA adducts, compromising the blood-testis barrier, hindering testosterone synthesis, and inducing DNA damage and apoptosis. In females, B[α]P adversely affects ovarian structures and follicular maturation, compromises oocyte quality, and reduces embryo implantation rates, associated with key biological processes, including B[α]P metabolism, oxidative damage, epigenetic alterations, and endocrine disruptions. Moreover, the reproductive toxicity generated by B[α]P negatively impacts both the directly exposed individuals and their descendants through the inheritance of epigenetic modifications, hence jeopardizing reproductive health across multiple generations or possibly transgenerationally. While current studies have revealed the reprotoxicity of B[α]P, additional research is necessary to unravel its transgenerational effects and the molecular mechanisms involved. This knowledge will facilitate accurate environmental risk assessment, the development of biomarkers for early diagnosis, and the identification of molecular targets for intervention and prevention.