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<p>The oxidative stress and impaired antioxidant defence play a critical role in the pathogenesis of diabetic nephropathy (DN) in type 2 diabetes mellitus (T2DM). Genetic polymorphisms in antioxidant enzyme genes may alter enzyme activity and increase susceptibility to oxidative damage. The case-control study evaluated the polymorphisms in + 35&#xa0;A/C SOD1, − 198&#xa0;C/T GPx1, C−262T CAT polymorphism to assess the risk of nephropathy in T2DM patients. A total of 150 participants, including T2DM patients with DN and healthy controls, were enrolled. Genotyping of the selected SNPs, SOD1 (rs2234694), GPx1 (rs1050450), and CAT (rs1001179), was performed using pre-validated TaqMan assays with Real-Time PCR. Antioxidant enzyme activities in red blood cells were assessed using enzyme-linked immunosorbent assay (ELISA). Patients with DN showed significantly reduced GPx (<i>P</i> = 0.001) and SOD (<i>P</i> = 0.003) activities compared to controls. The CC genotype of SOD1 (OR = 3.9, <i>P</i> = 0.002) and TT genotype of GPx1 (OR = 2.6, <i>P</i> = 0.019) was associated with an increased risk of nephropathy. The T and C allele in both genes conferred higher susceptibility. CT + TT genotypes of CAT were linked to macroalbuminuria. The TTC haplotype and a high genetic risk score were significantly associated with DN (<i>P</i> = 0.002). Polymorphisms in SOD1 and GPx1genes and a higher genetic risk score are significantly associated with DN in T2DM, likely through reduced antioxidant enzyme activity.</p>

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Antioxidant Gene Polymorphisms (GPx1, SOD1, CAT), Enzyme Activity and Genetic Risk Score in Type 2 Diabetic Patients with Nephropathy

  • 期刊论文

  • 发表日期：

    2026年6月23日

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  • Nachimuthu Maithilikarpagaselvi,
  • Kanwar Tanu,
  • Bajpai Kumar Nitin,
  • Banerjee Mithu

摘要

The oxidative stress and impaired antioxidant defence play a critical role in the pathogenesis of diabetic nephropathy (DN) in type 2 diabetes mellitus (T2DM). Genetic polymorphisms in antioxidant enzyme genes may alter enzyme activity and increase susceptibility to oxidative damage. The case-control study evaluated the polymorphisms in + 35 A/C SOD1, − 198 C/T GPx1, C−262T CAT polymorphism to assess the risk of nephropathy in T2DM patients. A total of 150 participants, including T2DM patients with DN and healthy controls, were enrolled. Genotyping of the selected SNPs, SOD1 (rs2234694), GPx1 (rs1050450), and CAT (rs1001179), was performed using pre-validated TaqMan assays with Real-Time PCR. Antioxidant enzyme activities in red blood cells were assessed using enzyme-linked immunosorbent assay (ELISA). Patients with DN showed significantly reduced GPx (P = 0.001) and SOD (P = 0.003) activities compared to controls. The CC genotype of SOD1 (OR = 3.9, P = 0.002) and TT genotype of GPx1 (OR = 2.6, P = 0.019) was associated with an increased risk of nephropathy. The T and C allele in both genes conferred higher susceptibility. CT + TT genotypes of CAT were linked to macroalbuminuria. The TTC haplotype and a high genetic risk score were significantly associated with DN (P = 0.002). Polymorphisms in SOD1 and GPx1genes and a higher genetic risk score are significantly associated with DN in T2DM, likely through reduced antioxidant enzyme activity.