## 4 Discussion  
Our study elucidates the connection between uric acid levels and AOPP in patients with MI, revealing significant insights into the oxidative stress mechanisms underlying cardiovascular diseases. Notably, we observed that AOPP levels are elevated in MI patients compared to healthy subjects, with a pronounced increase in individuals presenting high concentrations of serum uric acid. However, the crux of our investigation extends beyond comparing AOPP levels between healthy individuals and MI patients; it delves into the intricate dynamics of the relationship between uric acid and AOPP. To precisely examine the relationship between uric acid and AOPP, we established a control group of younger individuals without coexisting diseases. This strategic decision aimed to minimize confounding variables, such as age-related changes and unrelated health conditions that could influence uric acid and AOPP levels, potentially masking the specific interaction we sought to examine. Studying the relationship between uric acid and AOPP in healthy individuals is essential, as it could provide valuable data that will aid in interpreting results post-MI. This methodological choice was informed by the need to establish a clear baseline for the SUA-AOPP interaction in a relatively homogeneous group. While it is well acknowledged that a subset of post-MI patients presents elevated uric acid levels and AOPP due to the influence of coexisting diseases and other factors, these increments are generally more pronounced as a direct result of the MI itself [28; 29; 30]. Nonetheless, we recognize the need for further investigation to substantiate this presumption and differentiate the specific impacts of MI on uric acid and AOPP levels from those attributed to coexisting conditions. To ensure the observed changes in uric acid were primarily associated with MI rather than other health conditions or medication use, we diligently strived to exclude patients with elevated uric acid due to pre-existing diseases or drug intake. However, it is essential to acknowledge that despite our rigorous approach, the  
Figure 3: Advanced oxidative protein products in dependence on serum uric acid for healthy people (**A**) and myocardial infarction patients (**B**); MI: myocardial infarction; AOPP: advanced oxidation protein products; SUA: serum uric acid. possibility remains that some illnesses influencing uric acid levels may have evaded detection. Moreover, the challenge of identifying uric acid as an independent risk factor for MI is compounded by the variety of confounding factors, such as hypertension, dyslipidemia, smoking, and alcohol consumption, which can all independently affect the risk and outcomes of heart attacks [31; 32]. This acknowledgment underscores the complexity of disentangling the multifaceted influences on uric acid levels in the context of our study. The relationship between uric acid levels and AOPP after MI appears to assume a J-curve form (Figure 3B), which can be explained by the dual role of uric acid as both an antioxidant and a pro-oxidant, depending on its concentration [33]. At the left side of the J-curve, where uric acid levels are low, we often observe high AOPP levels. This reflects an insufficient antioxidant defense due to the lower availability of uric acid. At physiological levels, uric acid is a scavenger of free radicals, protecting tissues from oxidative damage. Thus, its lower levels might lead to an inadequate response to the heightened oxidative stress that typically follows MI, resulting in increased oxidative protein damage indicated by elevated AOPP levels. Moving towards the bottom of the J-curve, where uric acid levels are moderate, there tends to be a correlation with lower or middle AOPP levels. This part of the curve suggests a balanced state where the antioxidant properties of uric acid are optimally utilized. In this state, uric acid effectively neutralizes free radicals, reducing OS and lowering AOPP levels.