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 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 B[a]P 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 B[a]P dose-dependently upregulated Tnfα at 8.67 µg/mice or more, as well as upregulating Il-1ß at 26 µg/mice, Il-18 at 2.88 and 26 µg/mice and Nlrp3 at 2.88 µg/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.

Protective effects of zinc oxide nanoparticles against doxorubicin induced testicular toxicity and DNA damage in male rats.

The present study aims to investigate the protective effects of zinc oxide nanoparticles (ZnO NPs) on doxorubicin-induced testicular injury. Forty mature male rats were randomly allocated into four equal groups: G1 (control), G2 (3 mg per kg BW of zinc oxide nanoparticles was administered), G3 (6 mg per kg BW of doxorubicin was intraperitoneally injected), and G4 (doxorubicin + ZnO NPs). Some fertility parameters, antioxidant status, genotoxicity assay, and a histopathological examination were used for this investigation. The doxorubicin-treated group showed a significant decrease in the index weight of reproductive organs, epididymal sperm count, motility%, and live sperm% and a significant increase in sperm abnormalities. Moreover, GSH and CAT activities were significantly decreased, and MDA content was significantly increased in the doxorubicin-treated group. Interestingly, co-administration of ZnO NPs significantly reduced the doxorubicin-induced changes in the investigated parameters. In addition, ZnO NPs alone did not show any undesirable effects on the sperm parameters, testis or DNA. However, its administration improves the reproductive parameters and significantly increases the testosterone level. We concluded that the administration of ZnO NPs at 3 mg per kg BW ameliorated the testicular toxicity and genotoxicity caused by doxorubicin through its antioxidant and androgenic activity.