Investigation of the Effects of SOD1 +35A/C and GPx-3 +1494A/G Gene Polymorphisms in Patients With Acne Vulgaris
1Department of Biophysics, Kutahya Health Sciences University Faculty of Medicine, Kutahya, Türkiye
2Department of Physiology, Kutahya Health Sciences University Faculty of Medicine, Kutahya, Türkiye
3Department of Dermatology, Kutahya Health Sciences University Faculty of Medicine, Kutahya, Türkiye
J Clin Pract Res 2024; 46(2): 161-170 DOI: 10.14744/cpr.2024.55197
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Abstract

Objective: Acne vulgaris (AV) is a common skin disorder. Genotypic variations of antioxidant-related genes may directly influence the function of AV-related genes by mitigating the risk of oxidative stress. This study aimed to investigate the impact of SOD1 +35A/C and GPx-3 +1494A/G gene polymorphisms in patients with AV.
Materials and Methods: The study comprised 81 healthy controls and 81 AV patients. The GPx-3 +1494A/G genotype was evaluated using Allele-Specific Polymerase Chain Reaction (AS-PCR), while the SOD1 +35A/C genotype was analyzed through the Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) technique.
Results: Genotype and allele frequencies of the SOD1 +35A/C gene polymorphism differed significantly between the AV patients and the control group (χ2=13.9, df=2, p=0.001 and χ2=13.1, df=1, p=0.001, respectively). Individuals with the AA genotype, compared to those with the AC genotype, showed an increased incidence of AV (Odds Ratio [OR]=4.81, 95% Confidence Interval [CI]=1.94–11.9, p=0.001). Individuals carrying the A allele were at a higher risk of AV compared to those with the C allele (OR=4.43, 95% CI=1.87–10.4, p=0.001). The AC genotype and C allele were associated with a protective effect in the control group (OR=0.21, 95% CI=0.08–0.52, p=0.001 and OR=0.23, 95% CI=0.10–0.54, p=0.001). However, no significant differences were observed in the GPx-3 +1494A/G genotype and allele frequencies between both groups.
Conclusion: The findings of this study indicate a correlation between the SOD1 +35A/C polymorphism and an increased incidence of AV.