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GSTO1、GSTO2、GSTP1、GPX1 和 SOD2 多态性与原发性开角型青光眼的关联。

Association of GSTO1, GSTO2, GSTP1, GPX1 and SOD2 polymorphism with primary open angle glaucoma.

机构信息

Eye Clinic, University Clinical Center of Serbia, Pasterova 2, Belgrade, Serbia.

University Eye Clinic, Medical Center Zvezdara, D. Tucovica 161, Belgrade, Serbia; Faculty of Special Education and Rehabilitation, University of Belgrade, Belgrade, Serbia.

出版信息

Exp Eye Res. 2022 Jan;214:108863. doi: 10.1016/j.exer.2021.108863. Epub 2021 Nov 24.

Abstract

It is becoming increasingly evident that oxidative stress has a supporting role in pathophysiology and progression of primary open angle glaucoma (POAG). The aim of our study was to assess the association between polymorphisms in genes encoding enzymes involved in redox homeostasis, mitochondrial superoxide dismutase (SOD2), glutathione peroxidase (GPX1) and glutathione transferases (GSTs) with susceptibility to POAG. Single nucleotide polymorphisms in GST omega (GSTO1rs4925, GSTO2 rs156697), pi 1 (GSTP1 rs1695), as well as GPX1 (rs1050450) and SOD2 (rs4880) were determined by quantitative polymerase chain reaction (qPCR) in 102 POAG patients and 302 respective controls. The risk for POAG development was noted in carriers of both GSTO2GG and GSTO1AA variant genotypes (OR = 8.21, p = 0.002). Individuals who carried GPX1TT and SOD2CC genotypes had also an increased risk of POAG development but without significance after Bonferroni multiple test correction (OR = 6.66, p = 0.005). The present study supports the hypothesis that in combination, GSTO1/GSTO2, modulate the risk of primary open angle glaucoma.

摘要

氧化应激在原发性开角型青光眼(POAG)的病理生理学和进展中起着支持作用,这一点越来越明显。我们的研究目的是评估参与氧化还原平衡的酶基因(编码线粒体超氧化物歧化酶(SOD2)、谷胱甘肽过氧化物酶(GPX1)和谷胱甘肽转移酶(GSTs)的多态性与 POAG 易感性之间的关联。通过定量聚合酶链反应(qPCR)在 102 名 POAG 患者和 302 名相应对照中确定 GST omega(GSTO1 rs4925、GSTO2 rs156697)、pi 1(GSTP1 rs1695)以及 GPX1(rs1050450)和 SOD2(rs4880)的单核苷酸多态性。在 GSTO2GG 和 GSTO1AA 变体基因型携带者中注意到 POAG 发展的风险(OR=8.21,p=0.002)。携带 GPX1TT 和 SOD2CC 基因型的个体也有 POAG 发展的风险增加,但在 Bonferroni 多重检验校正后没有统计学意义(OR=6.66,p=0.005)。本研究支持 GSTO1/GSTO2 联合调节原发性开角型青光眼风险的假设。

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