You are here:
OXIDATIVE STRESS PARTICIPATES IN PARTICULATE MATTER (PM) INDUCED LUNG INJURY
Citation:
Roberts, E. S., J. E. Richards, AND K L. Dreher. OXIDATIVE STRESS PARTICIPATES IN PARTICULATE MATTER (PM) INDUCED LUNG INJURY. Presented at Experimental Cell Biology (FASEB), New Orleans, Louisiana, April 20-24, 2002.
Description:
Oxidative stress participates in particulate matter (PM) induced acute lung injury.
Elizabeth S. Roberts1, Judy L. Richards2, Kevin L. Dreher2. 1College of Veterinary Medicine, NC State University, Raleigh, NC, 2US Environmental Protection Agency, NHEERL, RTP, NC.
Epidemiological reports suggest that PM is associated with increases in cardiopulmonary-related morbidity and mortality. In vitro studies have provided insights into the mechanism of cellular injury caused by PM, however in vivo data correlations require further assessment. This study examines the effects of residual oil fly ash (ROFA) on pulmonary gene induction. Male Sprague Dawley rats were pre-treated with either an intraperitoneal (IP) injection of 500 mg/kg dimethlythiourea (DMTU) or saline, thirty minutes prior to instillation with 0.5 mg/rat ROFA or saline. Bronchoalveolar lavage fluid (BALF) was obtained at 24h for determination of cytotoxicity and inflammation. Gene profiling analysis was performed on total RNA recovered from lungs of control and exposed rats at 1h, 3h, and 24h. ROFA increased BALF lactate dehydrogenase and induced neutrophilia at 24h post-exposure. IP pre-treatment with DMTU inhibited the ROFA-induced cytotoxicity and inflammation, as well as, IL6, TNFa and MCP1 gene induction. These results demonstrate that oxidative stress is critical to lung injury induced by air pollution particles such as ROFA. (This abstract does not reflect EPA policy.)