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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 µg/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 µg/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 µg/mouse DEP-treated groups increased significantly compared with the vehicle group. The seminiferous epithelium area ratios of the 74.0 and 220µg/mouse DEP-treated groups were significantly higher compared with the vehicle and 24.6 µg/mouse DEP-treated groups. The ratios of seminiferous tubules with elongated-type spermatids in the 74.0 and 220 µg/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 µg/ 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. Key words: Aryl hydrocarbon receptor, Diesel exhaust particles, Epididymis, Sperm, Testis (J. Reprod. Dev. 53: [1069][1070][1071][1072][1073][1074][1075][1076][1077][1078] 2007) iesel exhaust particles (DEPs) are particulate matter from diesel exhaust (DE) containing many toxic compounds that can cause pulmonary cancer, allergic rhinitis and bronchial asthma [1,2]. It has also been reported that DEPs contain endoc r i n e d i s r u p t e r s , s u c h a s p o l y a r o m a t i c hydrocarbons (PAHs) [1], dioxin derivatives [3,4] and nitrophenols [5][6][7][8].The aryl hydrocarbon receptor (AhR) is involved in PAH toxicity [9]. When PAHs are incorporated into cells, they bind with AhR to form a PAH-AhR complex, which is transferred into the nucleus and combined with the AhR nuclear translocater. This

Abstract. Diesel exhaust particles (DEPs) contain polycyclic aromatic hydrocarbons (PAH) that bind to aryl hydrocarbon receptors (AhRs) and decrease sperm production. Since it is not clear if AhR mediates DEP toxicity, we investigated the effect of DEPs in four strains of mice that have different AhR responsiveness. We treated BALB/c, C57BL/6, ICR and DBA/2 mice with DEP suspensions and compared their toxicity in each strain. In both the vehicle-and DEP-treated groups, ethoxyresorufin-O-deethylase (EROD) activity, as an indirect index of AhR activity, was increased in the order of BALB/c > C57BL/6 > ICR > DBA/2. Only BALB/c and C57BL/6 mice had significantly lower daily sperm production (DSP) than vehicle-treated mice. All strains exhibited increased sperm abnormalities. In particular, the C57BL/6, ICR and DBA/2 mice exhibited significantly increased abnormalities. A significant correlation was found between EROD activity and DSP or incidence of morphologically abnormal sperm. These data suggest that DEP toxicity may affect the male reproductive system in an AhR-dependent manner. Key words: Cytochrome P450 1A1, Diesel exhaust particle, Epididymis, Sperm, Testis (J. Reprod. Dev. 53: [1191][1192][1193][1194][1195][1196][1197] 2007) iesel exhaust particles (DEPs) are particulate matter from diesel exhaust (DE) containing many toxic compounds that can cause pulmonary cancer, allergic rhinitis and bronchial asthma [1,2]. It has been reported that DEPs also contain endoc r i n e d i s r u p t e r s , s u c h a s p o l y a r o m a t i c hydrocarbons (PAHs) [1], dioxin derivatives [3,4] and nitrophenols [5][6][7][8][9].DEPs and DE have also been reported to cause male reproductive toxicity. DEPs decrease sperm production in mice [10] and rats [11], while DE increases serum concentrations of testosterone and the weight of the accessory glands in rats [12]. Furthermore, the number of sperm and Sertoli cells decreases in mature rats exposed to DE as fetuses [13]. We hypothesized that the male reproductive toxicity of DEPs may depend on PAHs. We previously reported that DEPs can activate aryl hydrocarbon receptors (AhR) in an in vitro system using an Ah-Immunoassay kit [14]. In addition, DEP-treated mice showed decreased daily sperm