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THE ROLE OF OXIDATIVE STRESS AND MITOCHONDRIA IN PARTICULATE MATTER (PM)-INDUCED CARDIOPULMONARY INJURY IN STROKE PRONE SPONTANEOUSLY HYPERTENSIVE (SHRSP) AND WISTAR KYOTO (WKY) RATS
Citation:
WALLENBORN, G., M. SCHLADWEILER, A. D. LEDBETTER, R. THOMAS, R. H. JASKOT, J. E. RICHARDS, AND U. P. KODAVANTI. THE ROLE OF OXIDATIVE STRESS AND MITOCHONDRIA IN PARTICULATE MATTER (PM)-INDUCED CARDIOPULMONARY INJURY IN STROKE PRONE SPONTANEOUSLY HYPERTENSIVE (SHRSP) AND WISTAR KYOTO (WKY) RATS. Presented at American Thoracic Society Annual Meeting, San Diego, CA, May 19 - 24, 2006.
Description:
Epidemiological studies have associated PM exposure with cardiovascular mortality and morbidity, and this effect seems to be enhanced in populations with pre-existing cardiovascular disease. One hypothesis for this exacerbation is that the higher underlying level of oxidative stress present in diseased individuals facilitates a greater response to PM exposure. Measuring the activities of cellular antioxidants and mitochondrial enzymes involved in the tricarboxylic acid cycle is a method of monitoring oxidative stress. Here, comparison of enzyme activity levels in the lung and heart of SHRSP to WKY rats is used to investigate the interplay of underlying cardiovascular disease and PM exposure. Male rats (12-15 wks age) were intratracheally instilled with saline or 1.11, 3.33 or 8.33 mg/kg of oil combustion PM. Responses were analyzed 24h later. Mitochondrial and cytosolic fractions were isolated from heart and lung tissues, and the purity of these fractions was confirmed by measurements of glutamate dehydrogenase (GDH) and lactate dehydrogenase (LDH) activities. Upon PM exposure, cytosolic superoxide dismutase activity decreased in the lungs and increased in the hearts of SHRSP. Baseline levels of cardiac cytosolic glutathione peroxidase were higher in control SHRSP than WKY rats. Mitochondrial ferritin levels and GDH activity decreased in the hearts of PM exposed SHRSP but not WKY rats. These data suggest that a single acute exposure to PM induces oxidative stress in the hearts of SHRSP but not WKY rats. Furthermore, within cardiomyocytes, mitochondria may be the target of PM-induced oxidative stress. (Abstract does not represent USEPA policy. This research was supported in part by UNC/EPA CT829471.)