ABSTRACT
Diesel exhaust particles (DEPs) are particulate matter from diesel exhaust that contain many toxic compounds, such as polyaromatic hydrocarbons (PAHs). Some toxicities of PAH are thought to be expressed via aryl hydrocarbon receptors (AhRs). The male reproductive toxicity of DEPs might depend on AhR activation induced by PAHs. We hypothesized that AhR antagonists protect against the male reproductive toxicity of DEPs. Quercetin is a flavonoid and a well-known AhR antagonist, while onion contains many flavonoids, including quercetin. Hence, we examined whether quercetin and onion have alleviative effects against the male reproductive toxicity induced by DEPs. BALB/c male mice were fed quercetin- or onion-containing diets and received 10 injections of DEP suspension or vehicle into the dorsal subcutaneous layer over 5 weeks. The mice were euthanized at 2 weeks, after the last treatment, and their organs were collected. Daily sperm production and total incidence of sperm abnormalities were significantly affected in the DEP groups as compared with the vehicle group, but the total incidence of sperm abnormalities in the quercetin + DEP-treated mice was significantly reduced as compared with the DEP-treated mice. The numbers of Sertoli cells were significantly decreased in DEP-treated mice as compared with the vehicle-treated mice, but, the numbers of Sertoli cells were significantly increased in the quercetin and the onion + DEP-treated mice as compared with the DEP-treated mice. These results clearly indicate alleviative effects of quercetin and onion against the male reproductive toxicity induced by DEP.
Subject(s)
Onions/chemistry , Particulate Matter/toxicity , Quercetin/pharmacology , Reproduction/drug effects , Vehicle Emissions/toxicity , Animals , Body Weight/drug effects , Male , Mice , Mice, Inbred BALB C , Organ Size/drug effects , Quercetin/metabolism , Receptors, Aryl Hydrocarbon/antagonists & inhibitors , Receptors, Aryl Hydrocarbon/metabolism , Sertoli Cells/drug effects , Spermatozoa/drug effects , Spermatozoa/metabolismABSTRACT
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.
Subject(s)
Epididymis/drug effects , Receptors, Aryl Hydrocarbon/metabolism , Spermatozoa/drug effects , Testis/drug effects , Vehicle Emissions/toxicity , Animals , Body Weight/drug effects , Cytochrome P-450 CYP1A1/metabolism , Epididymis/metabolism , Male , Mice , Mice, Inbred BALB C , Mice, Inbred C57BL , Mice, Inbred DBA , Mice, Inbred ICR , Species Specificity , Spermatozoa/metabolism , Spermatozoa/pathology , Testis/metabolismABSTRACT
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.
