title: Diesel exhaust particle toxicity on spermatogenesis in the mouse is aryl hydrocarbon receptor dependent.
abstract: Diesel exhaust particles (DEPs) are particulate matter from diesel exhaust containing many toxic compounds, such as polyaromatic hydrocarbons (PAHs). Some toxicities of PAH are considered to express via aryl hydrocarbon receptor (AhR). We hypothesized that the male reproductive toxicity of DEPs may depend on PAHs. BALB/c male mice received 24.7, 74.0 or 220 microg/mouse DEP suspension or vehicle injected into the dorsal subcutaneous layer 10 times during 5 weeks. The mice were euthanized, and blood and organs were collected 2 weeks after the last treatment. The epididymis weights, relative epididymis weights per body weight and daily sperm productions and viabilities of the 74.0 and 220 microg/mouse DEP-treated groups decreased significantly compared with those of the vehicle group. The total incidence of sperm abnormalities in the 74.0 and 220 microg/mouse DEP-treated groups increased significantly compared with the vehicle group. The seminiferous epithelium area ratios of the 74.0 and 220 microg/mouse DEP-treated groups were significantly higher compared with the vehicle and 24.6 microg/mouse DEP-treated groups. The ratios of seminiferous tubules with elongated-type spermatids in the 74.0 and 220 microg/mouse DEP-treated groups were significantly decreased compared with the vehicle group. The testosterone level and hepatic ethoxyresorufin-O-deethylase (EROD) activity as an indirect index of AhR activity in the 74.0 microg/mouse DEP-treated group were significantly increased compared with those of the vehicle group. These results clearly demonstrated that DEPs suppress testicular function, especially spermatogenesis and sperm motility. These effects may be AhR dependent.
authors.affiliation: Division of Human Sciences, Faculty of Health Sciences, Aomori University of Health and Welfare, Aomori, Japan. h_izawa@auhw.ac.jp
authors.forename: Hiromi
authors.initials: H
authors.lastname: Izawa
authors.forename: Machiko
authors.initials: M
authors.lastname: Kohara
authors.forename: Gen
authors.initials: G
authors.lastname: Watanabe
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Taya
authors.forename: Masaru
authors.initials: M
authors.lastname: Sagai
mesh_terms: D000818:Animals; D001835:Body Weight / Q000187:drug effects; D019363:Cytochrome P-450 CYP1A1 / Q000032:analysis / Q000378:metabolism; D004822:Epididymis / Q000033:anatomy & histology / Q000187:drug effects; D008099:Liver / Q000201:enzymology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009929:Organ Size; D052638:Particulate Matter / Q000633:toxicity*; D018336:Receptors, Aryl Hydrocarbon / Q000378:metabolism*; D012670:Seminiferous Epithelium / Q000187:drug effects; D013091:Spermatogenesis / Q000187:drug effects*; D013094:Spermatozoa / Q000002:abnormalities / Q000187:drug effects; D013737:Testis / Q000033:anatomy & histology / Q000187:drug effects; D013739:Testosterone / Q000097:blood; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D052638:Particulate Matter; D018336:Receptors, Aryl Hydrocarbon; D001335:Vehicle Emissions; D013739:Testosterone; D019363:Cytochrome P-450 CYP1A1