Oxidative Stress and Lipid Peroxidation in Experimental Myocardial Infarction: Biochemical Evaluation in Cardiac and Hepatic Tissue

<i>Introduction</i>: Myocardial infarction (MI) remains one of the most common and life-threatening cardiovascular diseases worldwide. Experimental models of MI are essential for understanding its pathophysiology and evaluating therapeutic interventions. <i>Objective</i>: The aim of this study was to evaluate lipid peroxidation and antioxidant defense during experimental MI in rats. <i>Methods</i>: MI was induced in adult male rats by ligation of the left coronary artery. On the third day after MI, cardiac and liver tissues were collected. Heart and liver homogenates, as well as mitochondrial (MF) and microsomal (MSF) fractions of the liver, were analyzed for malondialdehyde (MDA) concentration and superoxide dismutase (SOD) activity. <i>Results</i>: Compared with the control group, MDA concentration increased fivefold in cardiac homogenates and 6.1-fold in liver MF, while MSF showed the most pronounced increase (28.2-fold). SOD activity was significantly reduced: by 31.5% in MF and by 73.1% in MF. <i>Conclusion</i>: Experimental MI induces pronounced oxidative stress, characterized by excessive lipid peroxidation and suppression of antioxidant defenses. This model represents a valuable tool for investigating cardioprotective strategies and antioxidant therapy.

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