López-Contreras Ana Karen, Arévalo-Simental Diana Esperanza, Pacheco-Moisés Fermín Paúl, Martínez-Ruíz María Guadalupe, Olvera-Montaño Cecilia, Robles-Rivera Ricardo Raúl, Sifuentes-Franco Sonia, Campos-Bayardo Tannia Isabel, Huerta-Olvera Selene Guadalupe, Rodríguez-Carrizalez Adolfo Daniel
Institute of Clinical and Experimental Therapeutics, Department of Physiology, Health Sciences University Center, University of Guadalajara, Guadalajara 44340, Jalisco, Mexico.
Department of Ophthalmology, Hospital Civil de Guadalajara "Fray Antonio Alcalde", Guadalajara 44280, Jalisco, Mexico.
Life (Basel). 2024 Dec 2;14(12):1588. doi: 10.3390/life14121588.
Proliferative diabetic retinopathy (PDR) is the most severe complication of chronic hyperglycaemi stimulates oxidative stress that changes the retinal basement membrane function and provokes neovascularization, macular edema and retinal detachment. But an oxidative-antioxidant biomarker assessment in ocular matrices, such as aqueous humor (AH) and vitreous, might show the oxidative stress (OS) status in the posterior segment. Here, we show a cross-sectional analytical study of 39 patients who had a vitrectomy and assess the levels of different oxidative-antioxidant biomarkers in blood, aqueous and vitreous humor in three groups: diabetes mellitus 2 (DM2) with PDR [DM(+)PDR(+)] ( =13), DM2 without PDR [DM(+)PDR(-)] ( = 13) and non-DM2 non-PDR [DM(-)PDR(-)] as the control group ( = 13). Our finding suggests the presence of oxidative stress in diabetic retinopathy, as evidenced by increased levels of 8-isoprostanes and decreased levels of total antioxidant capacity from stages before the development of diabetic retinopathy. Our results reveal a notable increment in catalase levels in the DM(+)PDR(+) group in blood and vitreous humor. Likewise, we identified that the DM(+)PDR(-) group presents significant levels in 8-IP and SOD in vitreous humor and blood versus aqueous humor. These finding suggest the role of antioxidant enzymes in compensating oxidative stress mechanisms in PDR development.
增殖性糖尿病视网膜病变(PDR)是慢性高血糖最严重的并发症,其刺激氧化应激,改变视网膜基底膜功能并引发新生血管形成、黄斑水肿和视网膜脱离。但是,对眼内基质(如房水(AH)和玻璃体)中的氧化 - 抗氧化生物标志物进行评估,可能会显示眼后段的氧化应激(OS)状态。在此,我们展示了一项对39例行玻璃体切除术患者的横断面分析研究,并评估了三组患者血液、房水和玻璃体中不同氧化 - 抗氧化生物标志物的水平:患有PDR的2型糖尿病(DM2)[DM(+)PDR(+)](n = 13)、无PDR的DM2 [DM(+)PDR(-)](n = 13)以及作为对照组的非DM2非PDR [DM(-)PDR(-)](n = 13)。我们的研究结果表明糖尿病视网膜病变中存在氧化应激,这可通过糖尿病视网膜病变发展前阶段8 - 异前列腺素水平升高和总抗氧化能力水平降低得到证明。我们的结果显示,在DM(+)PDR(+)组的血液和玻璃体中过氧化氢酶水平显著升高。同样,我们发现DM(+)PDR(-)组在玻璃体和血液中的8 - IP和SOD水平相对于房水有显著差异。这些发现表明抗氧化酶在PDR发展过程中补偿氧化应激机制的作用。