The effect of chronic ozone exposure to ischemia reperfusion (I/R) injury in isolated perfused rat hearts was previously demonstrated. The present study tested our hypothesis that chronic ozone exposure led to attenuation of polyamines in the heart, which may limit sensitivity to I/R. Sprague Dawley rats were continuously exposed for 8 hrs/day for 28 days to filtered air or 0.8 ppm ozone. Isolated hearts were previously subjected to 0.5 hour of global ischemia followed by 1 hour of reperfusion after which global polyamine content was examined between the two groups. Spermidine production was significantly increased in the experimental group compared to control group (of I/R hearts). These results suggest that ozone-induced sensitivity to chronic I/R injury activates myocardial polyamine stress response characterized by increased enzymatic activities and accumulation of spermidine. Collectively, these results suggest that I/R possibly disturbs polyamine metabolism, and increased oxidative stress and concomitant reduced myocardial cell viability.
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