413-419Reperfusion following an ischemic period represents an increased risk factor for cardiovascular morbidity and mortality. Heart reperfusion is characterized, mainly, by ventricular tachycardia, arrhythmias and a drop in blood pressure. The aim of this study was to explore the effect of the aldehyde dehydrogenase-2 agonist (ALDA-1), an inducer of the expression of the mitochondrial aldehyde dehydrogenase enzyme, on heart reperfusion damage; this is plausibly caused by the accumulation of aldehydes in the myocardium, as well as by mitochondrial permeability transition. Oxidative stress caused inhibition of cis-aconitase, increased generation of TBARs and disruption of mitochondrial DNA These adverse effects were avoided with ALDA-1 treatment
