Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Singapore National Eye Centre, Singapore, Singapore.
Acta Ophthalmol. 2018 Jun;96(4):e412-e420. doi: 10.1111/aos.13526. Epub 2017 Aug 21.
Dry eye, an age-related condition, is a multifactorial disease of the tears and ocular surface that results in symptoms of discomfort, visual disturbance and tear film instability. Environmental factors are also often implicated in dry eye including exposure to pollutants, ultraviolet (UV) radiation and ozone as well as the chronic use of preserved eyedrops such as in the treatment of glaucoma. These factors increase oxidative stress and ocular surface inflammation. Here, we reviewed the cellular, animal and clinical studies that point to the role of oxidative stress in dry eye disease. The biomarkers used to indicate oxidative damage in ocular surface tissues include 8-hydroxy-2 deoxyguanosine (8-OHdG), 4-hydroxynonenal (HNE) and malondialdehyde (MDD). Antioxidative defences in the ocular surface occur in the form of tear proteins such as lactoferrin and S100A proteins, and enzymes such as superoxide dismutase (SOD), peroxidase, catalase and mitochondrial oxidative enzymes. An imbalance between the level of reactive oxygen species (ROS) and the action of protective enzymes will lead to oxidative damage, and possibly inflammation. A small number of interventional studies suggest that oxidative stress may be directly targeted in topical therapy of dry eye treatment. For example, in vitro studies suggest that L-carnitine and pterostilbene, a blueberry component may reduce oxidative stress, and in animal studies, alpha-lipoic acid (ALP) and selenoprotein P may be helpful. Examples of treatments used in clinical trials include vitamin B12 eyedrops and iodide iontophoresis. With recent emphasis on ageing medicine and preventive holistic health, as well as the role of environmental science, research on oxidative stress in the ocular surface is likely to have increasing impact in the coming years.
干眼症是一种与年龄相关的疾病,是一种多因素的泪液和眼表面疾病,可导致不适、视觉障碍和泪膜不稳定等症状。环境因素也常与干眼症有关,包括接触污染物、紫外线(UV)辐射和臭氧,以及长期使用含防腐剂的眼药水,如治疗青光眼。这些因素会增加氧化应激和眼表面炎症。在这里,我们回顾了表明氧化应激在干眼症中的作用的细胞、动物和临床研究。用于指示眼表面组织氧化损伤的生物标志物包括 8-羟基-2-脱氧鸟苷(8-OHdG)、4-羟基壬烯醛(HNE)和丙二醛(MDA)。眼表面的抗氧化防御以泪液蛋白的形式存在,如乳铁蛋白和 S100A 蛋白,以及酶,如超氧化物歧化酶(SOD)、过氧化物酶、过氧化氢酶和线粒体氧化酶。活性氧(ROS)的水平与保护酶的作用之间的失衡将导致氧化损伤,并可能导致炎症。少数干预性研究表明,氧化应激可能是干眼症治疗的局部治疗的直接靶点。例如,体外研究表明,左旋肉碱和蓝莓成分白藜芦醇可能会降低氧化应激,在动物研究中,α-硫辛酸(ALP)和硒蛋白 P 可能会有帮助。临床试验中使用的治疗方法包括维生素 B12 眼药水和碘离子导入。随着近年来对衰老医学和预防整体健康以及环境科学的重视,眼表面氧化应激的研究在未来几年可能会产生越来越大的影响。