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RESEARCH PRODUCT

Early reductive stress followed by a late onset oxidative stress in acute myocardial infarction

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Introduction The idea that the cells might suffer from reductive rather than oxidative stress and that such stress may be relevant in pathophysiology has gained momentum. Aim We aimed at studying markers of oxidative stress and damage as well as the expression of antioxidant enzymes in a swine model of acute myocardial infarction (AMI) followed by reperfusion. Results and Discussion We found an increase in the GSH to GSSG ratio, a decrease in protein glutathionylation and a decrease in p38 MAPK phosphorylation after 90 minutes of ischaemia in heart samples. It was accompanied by an increase in the expression of Thioredoxin (TrX) and Peroxiredoxin (PrX) and a decrease in the expression of Glutathione Peroxidase (Gpx). One week after reperfusion an increase in lipid peroxidation, protein glutathionylation and protein carbonylation was accompanied by a massive increase in the expression of TrX, PrX, GPx, Glutathione Reductase (GR) and Glucose 6 Phosphate Dehydrogenase (G6PD). These increments seemed to be Nrf-2 independent and most of them were maintained in the heart samples one month after reperfusion. Conclusion We have found an early reductive stress followed by a late onset oxidative stress in AMI followed by reperfusion.