ALDA-1 protects myocardium from reperfusion damage due to its inhibitory action on mitochondrial permeability transition

Reperfusion 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.