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Abd El Naby, Walaa Slouma Hamouda; Zong, Cai; Fergany, Alzahraa; Ekuban, Frederick Adams; Ahmed, Saleh; Reda, Yousra; Sato, Harue; Ichihara, Sahoko; Kubota, Natsuko; Yanagita, Shinya; Ichihara, Gaku
International journal of molecular sciences, 06/2023, Letnik: 24, Številka: 12Journal Article
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 (BaP), which is one of the PAHs, caused deterioration of neurobehavioral performance in workers. The present study investigated the effect of BaP 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 BaP at 0, 2.88, 8.67 or 26.00 µg/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 BaP at 2.88 µg/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 BaP dose-dependently upregulated at 8.67 µg/mice or more, as well as upregulating at 26 µg/mice, at 2.88 and 26 µg/mice and at 2.88 µg/mice. The results demonstrate that exposure to BaP induces degeneration of noradrenergic or serotonergic axons and suggest the involvement of proinflammatory or inflammation-related genes with BaP-induced neurodegeneration.
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