Exposure to Benzo[a]pyrene Decreases Noradrenergic and Serotonergic Axons in Hippocampus of Mouse Brain

Epidemiological studies showed the association between air pollution and dementia. A soluble fraction of particulate matters including polycyclic aromatic hydrocarbons (PAHs) is suspected to be involved with the adverse effects of air pollution on the central nervous system of humans. It is also reported that exposure to benzopyrene (B[a]P), which is one of the PAHs, caused deterioration of neurobehavioral performance in workers. The present study investigated the effect of B[a]P on noradrenergic and serotonergic axons in mouse brains. In total, 48 wild-type male mice (10 weeks of age) were allocated into 4 groups and exposed to B[a]P at 0, 2.88, 8.67 or 26.00 & mu;g/mice, which is approximately equivalent to 0.12, 0.37 and 1.12 mg/kg bw, respectively, by pharyngeal aspiration once/week for 4 weeks. The density of noradrenergic and serotonergic axons was evaluated by immunohistochemistry in the hippocampal CA1 and CA3 areas. Exposure to B[a]P at 2.88 & mu;g/mice or more decreased the density of noradrenergic or serotonergic axons in the CA1 area and the density of noradrenergic axons in the CA3 area in the hippocampus of mice. Furthermore, exposure to B[a]P dose-dependently upregulated Tnf & alpha; at 8.67 & mu;g/mice or more, as well as upregulating Il-1 & beta; at 26 & mu;g/mice, Il-18 at 2.88 and 26 & mu;g/mice and Nlrp3 at 2.88 & mu;g/mice. The results demonstrate that exposure to B[a]P induces degeneration of noradrenergic or serotonergic axons and suggest the involvement of proinflammatory or inflammation-related genes with B[a]P-induced neurodegeneration.

Automated summary

Epidemiological studies have shown a link between air pollution and dementia. This study focused on the effect of benzopyrene (B[a]P), a soluble fraction of particulate matters, on noradrenergic and serotonergic axons in mouse brains. The results demonstrated that exposure to B[a]P induced degeneration of these axons and suggested the involvement of proinflammatory or inflammation-related genes in B[a]P-induced neurodegeneration.