Allelic disparities in the extra cellular–super oxide dismutase (EC-SOD) gene and risk of ischemic heart diseases
Abstract Background Superoxide dismutase enzymes (SOD) mainly the extracellular (EC-SOD) are considered prime antioxidants against superoxide anions (O2 •−). EC-SOD R213G mutation has a deleterious effect that disrupts its vascular displacement and allows atherogenesis. Data regarding the EC-SOD gen...
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| Format: | Article |
| Language: | English |
| Published: |
SpringerOpen
2025-05-01
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| Series: | The Egyptian Journal of Internal Medicine |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s43162-025-00452-7 |
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| Summary: | Abstract Background Superoxide dismutase enzymes (SOD) mainly the extracellular (EC-SOD) are considered prime antioxidants against superoxide anions (O2 •−). EC-SOD R213G mutation has a deleterious effect that disrupts its vascular displacement and allows atherogenesis. Data regarding the EC-SOD gene with cardiovascular diseases (CVD) and ischemic heart disease (IHD) are scarce. The study aimed to clarify the role of EC-SOD-R213G polymorphism and allelic disparities on its levels as an indicator of arterial wall antioxidant status and vascular integrity to provide insights on its role in IHD among Egyptian patients. A case–control study included eighty subjects categorized into four groups: Group I: 20 controls. Group II:20 with chronic angina. Group III:20 with myocardial infarction (MI) without hypertension (HTN). Group IV:20 MI patients with HTN. Restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) and ELISA techniques were applied. Results A significant association of EC-SOD + 213G genotype and allele frequencies in all patient groups when compared to controls (G allele frequency was 42%, 52%, 57%, and 10%, respectively, P < 0.05) with an odds ratio (OR) of 95% CI = 6.0 (1.6–24.43), 9.0 (2.42–36.47), and 12.18 (3.26–49.7), respectively (P < 0.05). The R and RR genotype frequencies were significantly lower in groups II, III, and IV than in controls (R allele 58%, 48%, 43%, and 90%, respectively, P < 0.05). Plasma EC-SOD levels were significantly increased in IHD patients than in controls, with a nonsignificant change between the two MI patient groups (t = 1.51, P = 0.147). Notably, EC-SOD levels recorded variant values with different R213G allelic variants in all IHD groups (P < 0.01), with a higher increase in GG and RG than RR carriers. Conclusion The EC-SOD gene Arg (213) Gly substitution was associated with an increased risk of IHDs among Egyptian patients. The EC-SOD + 213 R allele was significantly associated with protection from IHDs compared to the G allele. In addition, the EC-SOD heterozygous RG and the homozygous GG carriers were detected to have higher plasma EC-SOD levels with decreased arterial wall concentrations than in noncarriers, which reduces the anti-oxidative protection and increases atherogenic risk, increasing the susceptibility of IHD among Egyptian patients. |
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| ISSN: | 2090-9098 |