ArticleIrish journal of medical science2026
Association of the GPx-3 + 1494 A/G gene polymorphism with serum trace elements in psoriasis vulgaris.
Article in Irish journal of medical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPsoriasis 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.
aimThis case-control study investigated the association between the GPx-3 +1494A/G polymorphism and serum trace element levels in PV.
methodsA 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.
resultsThe 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).
conclusionThis 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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