Examining the Function of Oxidative Stress Management in Autoimmune Thyroid Disease: An Analysis of GPX Gene Variants

Abstract

Background: Autoimmune thyroid dysfunction, especially autoimmune thyroiditis (AIT), is so common and has multi-systemic implication, it poses a serious threat to world health. In order to test the hypothesis that oxidative stress pathways may play a role in the pathophysiology of the illness, this study examined the relationship between glutathione peroxidase (GPx) gene polymorphisms and autoimmune thyroid dysfunction.

Methods: This age- and sex-matched case-control study comprised 100 thyroid disease patients and 100 healthy controls. Every participant had a comprehensive evaluation, which comprised: Genetic examination of GPx polymorphisms by PCR-RFLP Thyroid function testing (FT3, FT4, TSH) evaluation of autoantibodies (anti-TPO, anti-TG).
The statistical analysis, which included t-tests, Pearson correlation, and chi-square testing, was conducted using SPSS v20.

Results: Thyroid antibody levels were significantly higher in patients than in controls (p < 0.001). Finding certain variants in the GPx gene linked to an increased risk of illness (p = 0.003). Strong association between antibody levels and specific GPx variations (r = 0.45, p < 0.01)

Conclusion: These findings underscore the critical role that oxidative stress plays in the development of autoimmune thyroid dysfunction by showing that GPx gene polymorphisms may operate as genetic markers for the condition. Although further study is required to clarify the underlying processes, the findings point to possible clinical implications in risk assessment and antioxidant-based therapy techniques.