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Growth Factors, Oxidative Damage, and Inflammation in Exfoliation Syndrome.细胞生长因子、氧化损伤与剥脱综合征的炎症反应。
J Glaucoma. 2018 Jul;27 Suppl 1(Suppl 1):S54-S60. doi: 10.1097/IJG.0000000000000904.
2
Oxidative Stress.氧化应激。
Annu Rev Biochem. 2017 Jun 20;86:715-748. doi: 10.1146/annurev-biochem-061516-045037. Epub 2017 Apr 24.
3
Oxidative and Anti-Oxidative Stress Markers in Chronic Glaucoma: A Systematic Review and Meta-Analysis.慢性青光眼的氧化和抗氧化应激标志物:系统评价与荟萃分析
PLoS One. 2016 Dec 1;11(12):e0166915. doi: 10.1371/journal.pone.0166915. eCollection 2016.
4
Serum prolidase activity and oxidative stress in patients with pseudoexfoliation syndrome.假性剥脱综合征患者的血清脯氨酰肽酶活性与氧化应激
Graefes Arch Clin Exp Ophthalmol. 2016 Jul;254(7):1339-43. doi: 10.1007/s00417-016-3338-6. Epub 2016 Apr 15.
5
Total oxidative stress, paraoxonase and arylesterase levels at patients with pseudoexfoliation syndrome and pseudoexfoliative glaucoma.假性剥脱综合征和假性剥脱性青光眼患者的总氧化应激、对氧磷酶和芳基酯酶水平。
Int J Ophthalmol. 2015 Oct 18;8(5):985-90. doi: 10.3980/j.issn.2222-3959.2015.05.24. eCollection 2015.
6
Serum and aqueous xanthine oxidase levels, and mRNA expression in anterior lens epithelial cells in pseudoexfoliation.假性剥脱综合征中血清和房水黄嘌呤氧化酶水平以及晶状体前囊上皮细胞中的mRNA表达。
Graefes Arch Clin Exp Ophthalmol. 2015 Jul;253(7):1161-7. doi: 10.1007/s00417-015-3043-x. Epub 2015 May 10.
7
Prospects for gene-environment interactions in exfoliation syndrome.剥脱综合征中基因-环境相互作用的前景。
J Glaucoma. 2014 Oct-Nov;23(8 Suppl 1):S64-7. doi: 10.1097/IJG.0000000000000113.
8
Evaluation of oxidative stress and paraoxonase phenotypes in pseudoexfoliation syndrome and pseudoexfoliation glaucoma.假性剥脱综合征和假性剥脱性青光眼中氧化应激和对氧磷酶表型的评估。
Clin Lab. 2014;60(1):79-86. doi: 10.7754/clin.lab.2013.121229.
9
[New pathogenetic insights into pseudoexfoliation syndrome/glaucoma. Therapeutically relevant?].[假性剥脱综合征/青光眼的新发病机制见解。与治疗相关吗?]
Ophthalmologe. 2012 Oct;109(10):944-51. doi: 10.1007/s00347-012-2531-1.
10
Decreased total antioxidants status in the plasma of patients with pseudoexfoliation glaucoma.假性剥脱性青光眼患者血浆中总抗氧化剂水平降低。
Mol Vis. 2011;17:2769-75. Epub 2011 Oct 25.

氧化应激在假性剥脱综合征和假性剥脱性青光眼中的作用。

Role of Oxidative Stress in Pseudoexfoliation Syndrome and Pseudoexfoliation Glaucoma.

作者信息

Aydın Yaz Yasemin, Yıldırım Nilgün, Yaz Yetkin, Tekin Neslihan, İnal Mine, Şahin Fezan Mutlu

机构信息

Eskişehir State Hospital, Ophthalmology Clinic, Eskişehir, Turkey

Eskişehir Osmangazi University Faculty of Medicine, Department of Ophthalmology, Eskişehir, Turkey

出版信息

Turk J Ophthalmol. 2019 Apr 30;49(2):61-67. doi: 10.4274/tjo.galenos.2018.10734.

DOI:10.4274/tjo.galenos.2018.10734
PMID:31055889
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6517849/
Abstract

OBJECTIVES

To investigate the role of oxidative stress on pseudoexfoliation formation and progression from pseudoexfoliation syndrome (XFS) to pseudoexfoliation glaucoma (XFG).

MATERIALS AND METHODS

This study investigated oxidative stress biomarkers in blood samples from 58 patients with XFG, 47 patients with XFS, and 134 healthy age- and sex-matched controls.

RESULTS

The highest serum malondialdehyde (MDA) levels were measured in XFG patients (p<0.001), and MDA level was higher in XFS patients than controls (p<0.001). Superoxide dismutase (SOD) and catalase (CAT) enzyme activities were significantly lower in XFS and XFG patients than in the control group, whereas a significant increase was observed in glutathione (GSH) levels (p<0.001 for all). However, levels of these three biomarkers did not differ significantly between XFS and XFG patients (p=0.188, p=0.185, and p=0.733, respectively). Nitric oxide (NO) concentration was significantly lower in XFG patients compared to XFS patients and controls (p<0.001) but did not differ between XFS patients and controls (p=0.476).

CONCLUSION

Elevated MDA levels suggest that lipid peroxidation is important in XFS and XFG development and progression from XFS to XFG. In addition, reduction in SOD and CAT enzyme activities is considered a deficiency in the enzymatic antioxidant protection system. Furthermore, GSH values may be evaluated as a compensatory response to oxidative stress in XFS and XFG. Alterations in NO indicate the role of a vascular regulatory factor in the progression from XFS to glaucoma.

摘要

目的

探讨氧化应激在假性剥脱形成以及从假性剥脱综合征(XFS)进展为假性剥脱性青光眼(XFG)过程中的作用。

材料与方法

本研究检测了58例XFG患者、47例XFS患者以及134例年龄和性别匹配的健康对照者血样中的氧化应激生物标志物。

结果

XFG患者血清丙二醛(MDA)水平最高(p<0.001),XFS患者的MDA水平高于对照组(p<0.001)。XFS和XFG患者超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的酶活性显著低于对照组,而谷胱甘肽(GSH)水平显著升高(均p<0.001)。然而,这三种生物标志物的水平在XFS和XFG患者之间无显著差异(分别为p=0.188、p=0.185和p=0.733)。与XFS患者和对照组相比,XFG患者的一氧化氮(NO)浓度显著降低(p<0.001),但XFS患者与对照组之间无差异(p=0.476)。

结论

MDA水平升高表明脂质过氧化在XFS和XFG的发生发展以及从XFS进展为XFG过程中起重要作用。此外,SOD和CAT酶活性降低被认为是酶促抗氧化保护系统的缺陷。此外,GSH值可被视为XFS和XFG中对氧化应激的一种代偿反应。NO的变化表明血管调节因子在从XFS进展为青光眼过程中的作用。