Introduction
Chronic kidney disease (CKD) represents one of the most pressing public health challenges of modern societies, imposing an increasing burden on healthcare systems and national economies, in addition to its profound impact on human quality of life. Recent scientific evidence indicates that oxidative stress is a pivotal factor in the progression and complications of CKD. The imbalance between the excessive production of reactive oxygen species (ROS) and the weakening of the body’s antioxidant defense mechanisms leads to the accumulation of molecular damage in renal cells and tissues.
Among the key enzymes involved in the antioxidant defense system are superoxide dismutase (SOD2) and glutathione peroxidase (GPX1). The former catalyzes the conversion of superoxide radicals into hydrogen peroxide, while the latter detoxifies hydrogen peroxide using glutathione as a major cofactor, thereby maintaining redox balance within the cell. Molecular studies have demonstrated that genetic polymorphisms in these genes may reduce enzymatic activity, consequently increasing susceptibility to CKD due to the buildup of oxidative products and the body’s reduced ability to counteract oxidative damage.
Studying the relationship between genetic variations in SOD2 and GPX1 and the levels of oxidative stress biomarkers represents a significant step toward a deeper understanding of the molecular mechanisms underlying chronic kidney diseases. Such investigations may also contribute to developing gene-based diagnostic tools and targeted therapeutic strategies aimed at enhancing antioxidant balance and minimizing cellular damage. Accordingly, this study seeks to analyze the association between genetic polymorphisms of these two enzymes and oxidative stress indicators in patients with chronic kidney failure, with the goal of identifying the genetic–biochemical correlations that may explain variations in disease susceptibility and progression.
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Conclusion
The findings revealed that polymorphisms in antioxidant genes—particularly SOD2 and GPX1—play a critical role in increasing the risk of chronic kidney disease by weakening the cellular defense mechanisms against reactive oxygen species, thereby exacerbating oxidative damage in renal tissues. The resulting decrease in enzymatic activity leads to elevated levels of oxidative markers such as malondialdehyde (MDA) and nitrotyrosine, which contribute to the progressive deterioration of kidney function.
These results underscore the importance of employing personalized genetic analysis for early assessment of CKD risk and adopting precision medicine approaches as a future direction in both diagnosis and treatment. They also highlight the need to strengthen antioxidant defense strategies through nutritional supplementation, pharmacological interventions, and lifestyle or environmental modifications.
In conclusion, understanding the relationship between genetic variations in SOD2 and GPX1 and oxidative stress markers is not merely an academic achievement but also a solid scientific foundation for developing more accurate and effective preventive and therapeutic policies. Such advancements aim to reduce the health and economic burden of chronic kidney disease and improve patients’ quality of life through targeted and integrated medical interventions.
Al-Mustaqbal University – The First University in Iraq