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DIFFERENTIAL CARDIAC SUSCEPTIBILITY OF WISTAR KYOTO (WKY) AND SPONTANEOUSLY HYPERTENSIVE RATS (SHR) TO DIESEL EXHAUST EXPOSURE
Citation:
WALLENBORN, G., M. SCHLADWEILER, A. D. LEDBETTER, Q. T. KRANTZ, A. NYSKA, J. JOHNSON, W. P. LINAK, R. GOTTIPOLU, J. E. RICHARDS, AND U. P. KODAVANTI. DIFFERENTIAL CARDIAC SUSCEPTIBILITY OF WISTAR KYOTO (WKY) AND SPONTANEOUSLY HYPERTENSIVE RATS (SHR) TO DIESEL EXHAUST EXPOSURE. Presented at American Thoracic Society Annual Meeting, San Francisco, CA, May 18 - 23, 2007.
Description:
Exposure to diesel exhaust particles (DEP) is linked to increases in cardiovascular effects. This is enhanced in individuals with pre-existing disease. Animal models of cardiovascular disease are used to study this susceptibility. The heart is rich in mitochondria, which produce high levels of free radicals, leading to inactivation of tricarboxylic acid cycle enzymes. We hypothesized that a 4-wk DEP inhalation would result in strain-related structural impairment of cardiac mitochondria and changes in these enzyme activities in WKY and SHR. Male rats (12-14 wks age) were exposed whole body to air or 0.5 or 2.0 mg/m3 DEP for 6h/d, 5 d/wk for 4 wks. Neutrophilic influx was noted in the bronchoalveolar lavage fluid in both strains. A lower level of baseline cardiac mitochondrial aconitase activity was seen in SHR than WKY. Aconitase activity appeared to be decreased in an exposure related manner in both strains. Significantly higher baseline levels of cardiac cytosolic ferritin and aconitase activity were seen in the SHR than WKY. No exposure-related changes were noted in either of these measures. Mitochondrial succinate and isocitrate dehydrogenase activities were not changed following DEP exposure in either strain. Transmission electron microscopy images of the heart indicated abnormalities in cardiac mitochondria of control SHR but not control WKY. No exposure related structural changes were induced by DEP. In conclusion, strain differences in cardiac oxidative stress biomarkers and structure of mitochondria exist between SHR and WKY. DEP exposure results in small changes in cardiac mitochondrial and cytosolic markers of oxidative stress. (Abstract does not represent USEPA policy. Research supported in part by UNC/EPA CT829471.)