Oxidative Stress in Aortic Valves Associated with Infective Endocarditis: A Report on Three Cases

<b>Background/Objectives:</b> Infective endocarditis (IE) most commonly results from infections by Gram-positive bacteria, and, in this condition, the redox homeostasis is lost due to the overproduction of H₂O₂, leading to the overstimulation of the immune system and the upregulation of the production of proinflammatory cytokines. The aim of this study was to evaluate the levels of oxidative biomarkers and the enzymatic and non-enzymatic antioxidant systems in subjects with IE. <b>Methods:</b> The study included three cases with IE that had undergone aortic valve replacement (AVR) surgery that was complicated by IE, comparing them with subjects with AVR without IE. We determined the malondialdehyde (MDA), total antioxidant capacity (TAC), carbonyl group concentration, glutathione (GSH), thiols and the nitrate/nitrite ratio (NO₃^-/NO₂^-) in homogenized tissue from the cardiac valves. We also measured the activity of glutathione-S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GR) and thioredoxin reductase (TrxR). The superoxide dismutase (SOD) isoforms and peroxidase activity were determined using native gels. <b>Results:</b> There were increases in the activity of antioxidant enzymes such as GST, SOD isoforms and peroxidases (<i>p</i> ≤ 0.01) and decreases in oxidative stress markers such as GSH (<i>p</i> = 0.05); meanwhile, MDA and carbonylation were increased (<i>p</i> ≤ 0.05). <b>Conclusions:</b> The results suggest that bacterial infections favor oxidative stress in the aortic valves, which increases the SOD isoforms and peroxidase activity. This contributes to the loss of the intricate redox homeostasis system in patients with IE, causing a positive feedback loop in the oxidative background that results in damage to the heart, likely leading to a fatal outcome.