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INHALATION OF OZONE AND DIESEL EXHAUST PARTICLES (DEP) INDUCES ACUTE AND REVERSIBLE CARDIAC GENE EXPRESSION CHANGES
Citation:
KODAVANTI, U. P., B. VALLANAT, M. SCHLADWEILER, AND A. D. LEDBETTER. INHALATION OF OZONE AND DIESEL EXHAUST PARTICLES (DEP) INDUCES ACUTE AND REVERSIBLE CARDIAC GENE EXPRESSION CHANGES. Presented at Society of Toxicology (SOT) Annual Meeting, Washington, DC, March 06 - 10, 2011.
Impact/Purpose:
This Abstract examined the effect of ozone and diesel exhaust particles on cardiac gene expression pattern and provides the evidence that cardiac transcriptional changes are reversible upon termmation of ex osure.
Description:
We have recently shown that episodic but not acute exposure to ozone or DEP induces vascular effects that are associated with the loss of cardiac mitochondrial phospholipid fatty acids (DEP 2.0 mg/m3 > ozone, 0.4 ppm). In this study we determined ozone and DEP-induced cardiac gene expression changes following acute and episodic exposures. Male WKY rats were exposed nose-only to air, ozone (0.4 ppm), resuspended DEP (2.0 mg/m3), or ozone+DEP, 5 h/d, 1 d/wk for 16 wk; or air, ozone (0.5 ppm), or DEP (2.0 mg/m3), 5h/d for 2 d. Left ventricular tissues were analyzed for gene expression using Affymetrix rat 2.0 arrays (n=4-6) 1 d after acute and 2 d after 16 wk exposure. Surprisingly, only minimal alterations were noted in rats episodically exposed for 16 wk (ozone, 38; DEP, 165 and ozone+DEP, 26 genes). Notable exposure-related effects were observed in rats in the acute exposure protocol (ozone, 1421 and DEP, 1517 genes; p<0.05), suggesting that cardiac gene expression changes were reversible and/or exhibited adaptation upon repeat exposures as generally seen in functional analysis. Most gene changes in both exposures involved regulators of cell signaling, ion channels, oxidation/reduction reactions and immune function. More ion channel genes were affected by ozone than DEP suggesting greater physiological impact of ozone at concentrations used. Remarkable similarities existed in the direction of change (increase or decrease) between ozone and DEP. Few genes were differentially affected, however those genes are deemed critical in cardiac injury; e.g., sarcolipin induced by ozone but inhibited by DEP. Critical genes induced by ozone but not DEP included Apo E, PGD2, aldolase, epoxide hydrolase and adenosine monophosphate deaminase. More genes were inhibited by DEP when compared to ozone. These data provide mechanistic insights into the commonalities of air pollutant induced cardiovascular effects that may reflect acute and reversible physiological changes observed after exposure. (This abstract does not represent USEPA policy