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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]

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]