## 4 Discussion
This balance might indicate better cellular functioning and an optimal response to the post-MI oxidative challenge. However, as we ascend the right side of the J-curve, characterized by high uric acid levels, we again observe an increase in AOPP levels. In this situation, the excessive concentration of uric acid may shift its role from being an antioxidant to a pro-oxidant. High uric acid levels can contribute to the production of ROS, increasing protein damage, as reflected by higher AOPP levels [33; 34]. Elevated uric acid can induce inflammation and endothelial dysfunction, further contributing to the OS and the subsequent increase in AOPP levels [35; 36]. In summary, the J-curve relationship between uric acid and AOPP post-MI reflects the complex balance between uric acid's protective and harmful effects in oxidative stress. This interplay is crucial in understanding the pathophysiology of myocardial infarction and highlights the importance of maintaining an optimal level of uric acid for the best post-MI outcomes. Elevated range of AOPP may potentially identify a group of people at high risk of death from cardiovascular causes [11]. However, recently, the relationship between the increase of uric acid by diuretics and the risk of ischemic heart disease was demonstrated [37]. Inflammation and OS are established risk factors for the formation of atherosclerosis. Some studies show that AOPP can accelerate the progression of atherosclerosis through OS and inflammation [38] by inhibiting high-density lipoprotein (HDL) receptor scavenger receptor class B type I-mediated HDL cholesterol reverse transport, leading to metabolic disturbances [39]. Some studies have suggested that AOPP can be involved in cardiovascular diseases (CVD) [40; 41]. AOPP are capable of triggering oxidative responses in neutrophils, amplifying the generation of ROS, and facilitating the secretion of cytokines, which can contribute to the acceleration of damage to endothelial cells [42; 43]. It has also been observed that AOPP can harm cardiomyocytes by increasing the expression of TRAF3 Interacting Protein 2 (TRAF3 IP2), which plays a crucial role in activating signaling pathways associated with the apoptosis of heart cells [44]. According to our results in healthy people and patients after MI (serum uric acid \(<\) 8 mg/dL), uric acid is an antioxidant, which is confirmed by low AOPP levels. [PERSON] et al. [45] proposed the antioxidant properties of uric acid; they demonstrated in their in vitro experiments that uric acid is a potent scavenger of peroxyl radicals, hydroxyl radicals, and singlet oxygen. Increasing the synthesis of serum uric acid is also associated with forming oxygen free radicals, which damage the heart's structure. The consequence of growing the free radicals is an increase in damaged proteins. The rise in AOPP and uric acid in studied MI patients may have clinical significance because the decrease in OS or the serum uric acid level could probably improve the state of patients after MI. Uric acid contributes to vascular damage through a series of complex interactions. Key among these is its role in promoting oxidative stress and inflammation within the vascular system. This process involves the generation of ROS, which in turn triggers inflammation and proliferation in both endothelial and vascular smooth muscle cells [46]. Previous studies reported that exposure to serum uric acid in cells can lead to generation of ROS [47; 48]. Uric acid can also impact vascular endothelial function significantly, largely through the downregulation of nitric oxide (NO) production [49]. This reduction in NO, a critical molecule for maintaining vascular health, can contribute to thrombosis [50]. A study designed by [PERSON] et al. [51] shows that the role of uric acid depends on its concentration by assessing the relation between serum uric acid level and in-hospital and short-term mortality rates. Patients were divided into four groups according to gender and serum uric acid level.