Oxidative stress is a sophisticated situation that orignates from the accumulation of reactive free radicals within cellular compartments. The antioxidant mechanism of the MnSOD enzyme facilitates the removal of these lethal oxygen species from cellular components. The main goal of this pertained work is to study the contribution of the SOD2 (rs4880; p.Val16Ala) variant to the development of bronchial asthma among children. The study’s design was carried out based on a total of 254 participants including 127 asthmatic children (91 atopic and 36 non-atopic) along with 127 unrelated healthy controls. Allelic discrimination analysis was executed using the T-ARMS-PCR protocol. This potential variant conferred a significant association with decreased risk of bronchial asthmatic children under allelic (OR = 0.56, P-value = 0.002), recessive (OR = 0.32, P-value = 0.011), and dominant (OR = 0.51, P-value = 0.040) models. Additionally, atopic and non-atopic asthmatic children indicated a protection against bronchial asthma development under allelic, and dominant models (p-value < 0.05). Our findings suggested that the SOD2*rs4880 variant was correlated with decreased risk of childhood bronchial asthma.

氧化应激是一种复杂的情况，源于细胞内活性自由基的积累。 MnSOD 酶的抗氧化机制有助于从细胞成分中去除这些致命的氧物质。这项相关工作的主要目标是研究SOD2 (rs4880; p.Val16Ala)变异对儿童支气管哮喘发展的贡献。该研究的设计基于总共 254 名参与者，其中包括 127 名哮喘儿童（91 名特应性儿童和 36 名非特应性儿童）以及 127 名不相关的健康对照者。使用T-ARMS-PCR方案进行等位基因区分分析。这种潜在的变异与等位基因（OR = 0.56，P值 = 0.002）、隐性（OR = 0.32，P值 = 0.011）和显性（OR = 0.51，P值）的支气管哮喘儿童风险降低显着相关。值 = 0.040) 模型。此外，特应性和非特应性哮喘儿童在等位基因和显性模型下显示出对支气管哮喘发展的保护作用（p值 <0.05）。我们的研究结果表明，SOD2*rs4880变异与儿童支气管哮喘风险降低相关。