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Published on: June 21, 2018
Association of the GPx-3 + 1494 A/G gene polymorphism with serum trace elements in psoriasis vulgaris
Fulya Yukcu1, Mustafa Yildiz2, Raziye Akcilar3
1Faculty of Medicine, Department of Biophysics, Kutahya Health Sciences University, Kutahya, 43100, Türkiye. fulya.yukcu@ksbu.edu.tr.
Background:
Psoriasis vulgaris (PV) is a chronic inflammatory skin disorder in which oxidative stress, redox imbalance, and genetic susceptibility play crucial roles. Glutathione peroxidase-3 (GPx-3), a selenium-dependent antioxidant enzyme, regulates redox homeostasis by detoxifying reactive oxygen species. Variants in the GPx-3 gene may alter antioxidant defense and trace element metabolism, thereby contributing to PV pathogenesis.
Aim:
This case-control study investigated the association between the GPx-3 +1494A/G polymorphism and serum trace element levels in PV.
Methods:
A total of 71 patients with PV and 71 age- and sex-matched healthy controls were genotyped using allele-specific polymerase chain reaction (AS-PCR) followed by agarose gel electrophoresis. Serum zinc (Zn), copper (Cu), and iron (Fe) concentrations were measured by atomic absorption spectrometry. Statistical analyses were performed using chi-square (χ²) and Mann-Whitney U tests.
Results:
The AG genotype was significantly more prevalent in PV patients than in controls (88.7% vs. 50.6%, p = 0.002). Among AG carriers, PV patients exhibited higher Zn levels (p < 0.001), lower Fe concentrations (p = 0.037), and a reduced Cu/Zn ratio (p = 0.025). Additionally, the AG genotype was associated with increased body mass index (p = 0.049).
Conclusion:
This study demonstrates a significant association between the GPx-3 +1494A/G polymorphism and serum trace element levels in PV. The AG genotype was more prevalent among patients and accompanied by elevated Zn, reduced Fe and a lower Cu/Zn ratio, suggesting genotype-related alterations in trace element balance. These findings indicate that the +1494A/G variant may contribute to psoriasis susceptibility by modulating oxidative stress and redox homeostasis.
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