Maternal Exposure of SD Rats to Benzo[a]Pyrene Impairs Neurobehavior and Hippocampal Synaptic Ultrastructure in Offspring via Downregulating Synaptic-Associated Factors.

Benzo[a]pyrene (B[a]P) is a carcinogenic contaminant widely present in the environment. Recently, increasing studies have paid attention to the developmental neurotoxicity of B[a]P in offspring in their early life stages; however, the underlying molecular mechanisms have not been clearly elucidated. In this study, we aimed to evaluate the effects of prenatal B[a]P exposure on neurobehavior of pups during their brain growth spurt (BGS) period and also explore the potential underlying mechanisms.

Prenatal benzo[a]pyrene exposure impairs hippocampal synaptic plasticity and cognitive function in SD rat offspring during adolescence and adulthood via HDAC2-mediated histone deacetylation.

Benzo[a]pyrene (B[a]P) is a widespread carcinogenic pollutant in the environment. Although previous studies have demonstrated the neurodevelopmental toxicity of B[a]P, the precise mechanisms underlying the neurotoxic effects induced by prenatal B[a]P exposure remain largely unknown. In the present study, pregnant Sprague-Dawley (SD) rats were injected intraperitoneally with 0, 10, 20, or 40 mg/kg-bw of B[a]P for three consecutive days on embryonic days 17-19.