Myocardial infarction (MI) is a serious medical condition that usually occurs when blood flow to a portion of the heart muscle is reduced or interrupted due to blockage of a coronary artery. The resulting oxygen deprivation disrupts energy production in cardiac cells and may lead to cellular injury and death. Free radicals and reactive oxygen species (ROS) play an important role in the development of cardiac injury, particularly during ischemia and reperfusion. When the production of these reactive species exceeds the body's antioxidant defense capacity, a condition known as oxidative stress develops. How Do Free Radicals Affect the Heart Muscle? Reactive oxygen species are generated by several cellular sources, including mitochondria and NADPH oxidase enzymes. Inflammatory cells also contribute to ROS production following tissue injury. When these species accumulate excessively, they can cause several harmful effects, including: Lipid peroxidation: Damage to the lipids that form cell membranes, compromising cellular integrity and function. Protein oxidation: Changes in the structure and activity of proteins and enzymes, disrupting essential biochemical processes in cardiac cells. DNA damage: Injury to genetic material, which may contribute to cellular dysfunction. Mitochondrial dysfunction: Reduced efficiency of adenosine triphosphate (ATP) production and an increased likelihood of cardiac cell death. Increased inflammation: Exacerbation of tissue injury in and around the affected area. These processes are particularly important during reperfusion, when blood flow is restored to previously ischemic tissue. Although reperfusion is essential for saving the heart muscle, it may also be accompanied by increased ROS production, contributing to a phenomenon known as ischemia–reperfusion injury. The Role of Antioxidants and Biomarkers The human body possesses several antioxidant defense systems that help limit oxidative damage. These include the enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), as well as the antioxidant molecule glutathione (GSH). Together, these systems help maintain cellular redox homeostasis. From a research perspective, oxidative stress can be investigated using biomarkers such as malondialdehyde (MDA), which is associated with lipid peroxidation, and total antioxidant capacity (TAC), which reflects the overall antioxidant capacity of a sample according to the measurement method used. Cardiac troponin, on the other hand, is a key biomarker of myocardial injury and is used alongside clinical assessment and other investigations in the diagnosis of myocardial infarction. It is important to emphasize that oxidative stress biomarkers cannot replace cardiac troponin or clinical evaluation, and their changes alone do not establish a diagnosis of myocardial infarction. Oxidative stress contributes to the mechanisms responsible for cardiac cell injury during myocardial infarction, particularly in the context of ischemia and reperfusion. Understanding these mechanisms is an important aspect of biochemistry because it connects molecular reactions within cells to pathological changes in the heart. It also supports research into cardiac biomarkers and potential strategies for protecting cardiac cells. Al-Mustaqbal University – The First University in Iraq