Anber Nahla H, Ahmed Shahin Hanaa Elsayed, Badawy Heba K, Oraby Enas A, Mohammed Sameh A, Shaaban Esraa Ibrahim A, Attia Zeinab Rizk, Mohamed Shereen, Shabana Mona Farag, El-Eshmawy Mohamed Adel, Elsayed Riham, Elsaid Afaf M, Alalawy Adel I, Elshazli Rami M
Department of Biochemistry, Emergency Hospital, Mansoura University, Mansoura, Egypt.
Nursing Department, College of Applied Medial Sciences, Jouf University, ElQurayyat, Saudi Arabia.
Biochem Genet. 2025 Feb;63(1):789-816. doi: 10.1007/s10528-024-10742-4. Epub 2024 Mar 24.
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,它源于细胞内活性自由基的积累。锰超氧化物歧化酶(MnSOD)的抗氧化机制有助于从细胞成分中清除这些致命的氧物种。这项相关工作的主要目标是研究SOD2(rs4880;p.Val16Ala)变体对儿童支气管哮喘发病的影响。该研究共纳入254名参与者,其中包括127名哮喘儿童(91名特应性和36名非特应性)以及127名无亲缘关系的健康对照。采用T-ARMS-PCR方案进行等位基因鉴别分析。在等位基因(OR = 0.56,P值 = 0.002)、隐性(OR = 0.32,P值 = 0.011)和显性(OR = 0.51,P值 = 0.040)模型下,这种潜在变体与支气管哮喘儿童风险降低显著相关。此外,在等位基因和显性模型下,特应性和非特应性哮喘儿童显示出对支气管哮喘发病的保护作用(p值 < 0.05)。我们的研究结果表明,SOD2*rs4880变体与儿童支气管哮喘风险降低相关。