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The effect of nanoparticle-rich diesel exhaust (NR-DE) on the testicular function and factors related with the biosynthesis of testosterone gene expression were investigated in mice. Male C57BL/Jcl mice were exposed to clean air, low-dose NR-DE (Low NR-DE), high-dose NR-DE (High NR-DE) or filtered diesel exhaust (F-DE) for 8 weeks. We found that the mice exposed to High NR-DE had significantly higher testosterone levels than those in the control and F-DE groups. To determine the effects of NR-DE on testicular testosterone production, interstitial cells dissected from the male mice which were exposed to NR-DE, F-DE, or clean air for 8 weeks were incubated with or without human chorionic gonadotropin (hCG; 0.1 IU/mL) for 4 h. The concentrations of testosterone in the culture media were measured. The testosterone production was significantly increased in with or without hCG of High NR-DE exposed group, and significantly decreased in both with or without hCG of F-DE exposed groups. Moreover, several genes, which is associated with testicular cholesterol synthesis, HMG-CoA, LDL-R, SR-B1, PBR, and P450scc, P450 17α, and 17β-HSD were determined in the testis of adult male mice. The results showed High NR-DE exposure significantly increased the expression of these genes. Whereas, the levels in the F-DE exposure group returned to those in the control group, implicating that the nanoparticles in DE contribute to the observed reproductive toxicity. We conclude that enhancement of testosterone biosynthesis by NR-DE exposure may be regulated by increasing testicular enzymes of testosterone biosynthesis. [ABSTRACT FROM AUTHOR]

Background: Nanoparticle-rich diesel exhaust (NR-DE) has potentially adverse effects on testicular steroidogenesis. However, it is unclear whether NR-DE influences steroidogenic systems in the brain. Objective: To investigate the effect of NR-DE on hippocampal steroidogenesis of adult male rats in comparison with its effect on the testis. Methods: F344 male rats (8-week-old) were randomly divided into four groups ( n = 8 or 9 per group) and exposed to clean air with 4.6 ± 3.2 μg/m3 in mass concentration, NR-DE with 38 ± 3 μg/m3 (a level nearly equivalent to the environmental standard in Japan (low NR-DE)), NR-DE with 149 ± 8 μg/m3 (high NR-DE), or filtered diesel exhaust with 3.1 ± 1.9 μg/m3 (F-DE), for 5 hours/day, 5 days/week, for 1, 2 or 3 months. F-DE was prepared by removing only particulate matters from high NR-DE with an HEPA filter. Results: Exposures to the high NR-DE for 1 month, and low NR-DE for 2 months, significantly increased or tended to increase plasma and testicular testosterone levels compared to clean air exposure, which might have resulted from the increased expression of mRNA of steroidogenic acute regulatory protein and its protein in the testes of rats. In the hippocampus, high NR-DE exposure for 1 month significantly increased the androstendione level compared to the clean air exposure, while no significant difference was observed in the steroidogenesis between fresh air exposure and any exposure to NR-DE or F-DE. Conclusion: NR-DE may influence steroidogenic enzymes in the testis, but not those in the hippocampus. [ABSTRACT FROM AUTHOR]

Exposure to air pollution containing diesel exhaust particles (DEP) is associated with an increase in mortality rate attributed to cardiovascular diseases, but the mechanisms by which DEP produces adverse cardiovascular effects at the cellular level are not elucidated. This study investigated the cytotoxic mechanisms underlying DEP-induced neonatal rat cardiac myocytes effects in vitro, focusing on the role of reactive oxygen species (ROS). DEP extracts (DEPE) damaged cells in a concentration- and a time-dependent manner. Lactate dehydrogenase activity leaked to medium was also increased in a concentration-dependent manner after 24 h of DEPE exposure. DEPE-induced cytotoxicity was markedly reduced by treatment with superoxide dismutase, catalase, and N -(2-mercaptopropionyl)-glycine. Furthermore, superoxide was produced from both DEPE and myocardial cells. These results suggest that ROS such as superoxide, hydrogen peroxide, and hydroxyl radical are involved in DEPE-induced cardiac cell damage. [ABSTRACT FROM AUTHOR]

To clarify the toxic effects of diesel exhaust (DE) on delivery in mice and on growth of young, C57Bl-strain females were exposed to 0.3, 1.0, or 3.0 mg diesel exhaust particles (DEP)/m[sup 3] or filtered clean air (control) for 4 mo (12 h/day, 7 days/wk). After exposure, some females from each group were examined by necropsy, and the remainders were mated with unexposed males. Estrous females for necropsy who had been exposed to 1.0 mg DEP/m[sup 3] had significantly lower uterine weights than the control estrous females. In the mated females, 9.1, 10.0, or 25.0% (0.3, 1.0, or 3.0 mg DEP/m[sup 3]) of the pregnancies resulted in abnormal deliveries (abortion and unable delivery), but this was not significant. The rate of good nest construction by delivered females exposed to 3.0 mg DEP/m[sup 3] was significantly lower. Young were weighed at 11, 14, and 21 days, and weekly from wk 4 to 9 after birth. Body weights of male young of dams exposed to 1.0 or 3.0 mg DEP/m[sup 3] were significantly lower at 6 and 8 wk of age. Body weights of female young of dams exposed to 1.0 or 3.0 mg DEP/m[sup 3] were also significantly lower at 6, 8, and 9 wk. Vaginal orifices of young female mice whose dams were exposed to 0.3 and 1.0 mg DEP/m[sup 3] opened significantly earlier. The young were killed at 30 or 70 days during deep anesthesia, and their body weights, organ weights, and body lengths were measured. Anogenital distance (AGD) of 30-day-old males whose dams were exposed to 0.3 mg DEP/m[sup 3] was significantly shorter than that of the controls. Weights of thymus and ovary in 30-day-old females whose dams were exposed to 3.0 mg DEP/m[sup 3] were significantly lower. In 70-day-old males of dams exposed to 3.0 mg DEP/m[sup 3], body weights were significantly lower and AGD was significantly shorter. Weights of adrenals, testes, and seminal vesicles in 70-day-old males with dams exposed to 1.0 mg DEP/m[sup 3] were significantly lower. In 70-day-old females with dams exposed to DE, body weights in the 3.0-mg DEP/m[sup 3] group were significantly lower, and weights of adrenals, liver, and thymus in the 1.0-mg DEP/m[sup 3] group were significantly lower. Thymus weights in 70-day-old females with dams exposed to 0.3 mg DEP/m[sup 3] were significantly lower. Crown–rump length (CR) in 70-day-old females with dams exposed to 1.0 or 3.0 mg DEP/m[sup 3] was significantly shorter. These results show that toxic substances in DE might cause abnormal delivery in mice, and that exposed females affected the growth and sexual maturation of their young. [ABSTRACT FROM AUTHOR]

The effects of diesel exhaust particles (DEP) on pulmonary functions and consequent diseases are well known, but there have been few reports concerning involvement of the cardiovascular system. In order to assess a direct action of DEP on cardiac tissue, the effects on blood pressure of intravenous administration of 12 or 120 mg/kg DEP to anesthetized rats were studied for a 15-min period. DEP (120 mg/kg) significantly lowered blood pressure for 25 s with no signs of arrhythmia or mortality, a phenomenon seen in guinea pigs. After 25 s blood pressure gradually returned to control levels and was maintained for 15 min. The 12-mg/kg DEP concentration did not markedly affect rat blood pressure. Pretreatment with atropine (24 mg/kg) blocked the DEP-induced fall in blood pressure, while pretreatment with propranolol (48 mg/kg) proved ineffective against DEP, suggesting involvement of the parasympathetic system. Data show that the rat is less sensitive to DEP-induced effects on blood pressure and may be a poor model to reflect cardiovascular changes. [ABSTRACT FROM AUTHOR]

To investigate the effects of diesel exhaust (DE) particles on the reproductive system, male Fischer 344 rats at 13 mo of age were exposed to clean air or DE at particle concentrations of 0.3, 1, or 3 mg/m[sup 3] for 8 mo. DE did not markedly affect testicular and body weights. However, DE at 0.3 mg/m[sup 3] significantly decreased prostate and coagulating gland weights, accompanied by a reduction in thymus and adrenal gland weight. In contrast, there was a significant rise in the weights of prostate, seminal vesicles, and coagulating glands in the 3 mg/m[sup 3] DE group. In rats exposed to 0.3 or 1 mg/m[sup 3] DE, serum luteinizing hormone (LH) and testosterone increased significantly, while a rise in testicular testosterone was noted with 3 mg/m[sup 3] DE. The concentrations of follicle-stimulating hormone (FSH) and inhibin as well as the sperm head counts were not markedly altered in any treatment group. Positive staining with inhibin-α subunit and 3β-hydroxysteroid dehydrogenase (3β-HSD) were observed in Sertoli cells and Leydig cells, respectively. Immunolocalization of inhibin-α subunit and 3β-HSD was not changed by exposure to DE. In conclusion, DE appears to exert greater effects on accessory glands than on testes in Fischer 344 rats, and the responsiveness of rats is less than that found in mice. [ABSTRACT FROM AUTHOR]