Saccà Sergio C, Roszkowska Anna Maria, Izzotti Alberto
Department of Head/Neck Pathologies, St Martino Hospital, Ophthalmology unit, Genoa, Italy.
Department of Specialized Surgery, University Hospital, Ophthalmology Unit, Messina, Italy.
Mutat Res. 2013 Apr-Jun;752(2):153-171. doi: 10.1016/j.mrrev.2013.01.001. Epub 2013 Jan 19.
The human eye is constantly exposed to sunlight and artificial lighting. Exogenous sources of reactive oxygen species (ROS) such as UV light, visible light, ionizing radiation, chemotherapeutics, and environmental toxins contribute to oxidative damage in ocular tissues. Long-term exposure to these insults places the aging eye at considerable risk for pathological consequences of oxidative stress. Furthermore, in eye tissues, mitochondria are an important endogenous source of ROS. Over time, all ocular structures, from the tear film to the retina, undergo oxidative stress, and therefore, the antioxidant defenses of each tissue assume the role of a safeguard against degenerative ocular pathologies. The ocular surface and cornea protect the other ocular tissues and are significantly exposed to oxidative stress of environmental origin. Overwhelming of antioxidant defenses in these tissues clinically manifests as pathologies including pterygium, corneal dystrophies, and endothelial Fuch's dystrophy. The crystalline lens is highly susceptible to oxidative damage in aging because its cells and their intracellular proteins are not turned over or replaced, thus providing the basis for cataractogenesis. The trabecular meshwork, which is the anterior chamber tissue devoted to aqueous humor drainage, has a particular susceptibility to mitochondrial oxidative injury that affects its endothelium and leads to an intraocular pressure increase that marks the beginning of glaucoma. Photo-oxidative stress can cause acute or chronic retinal damage. The pathogenesis of age-related macular degeneration involves oxidative stress and death of the retinal pigment epithelium followed by death of the overlying photoreceptors. Accordingly, converging evidence indicates that mutagenic mechanisms of environmental and endogenous sources play a fundamental pathogenic role in degenerative eye diseases.
人眼持续暴露于阳光和人工照明下。紫外线、可见光、电离辐射、化疗药物和环境毒素等外源性活性氧（ROS）来源会导致眼组织的氧化损伤。长期暴露于这些损伤因素会使衰老的眼睛面临氧化应激病理后果的巨大风险。此外，在眼组织中，线粒体是ROS的重要内源性来源。随着时间的推移，从泪膜到视网膜的所有眼部结构都会受到氧化应激的影响，因此，每个组织的抗氧化防御机制都起着抵御眼部退行性病变的保护作用。眼表和角膜保护其他眼组织，并显著暴露于环境来源的氧化应激中。这些组织中抗氧化防御能力的压倒性下降在临床上表现为包括翼状胬肉、角膜营养不良和内皮性富克斯角膜营养不良等病理状况。晶状体在衰老过程中极易受到氧化损伤，因为其细胞及其细胞内蛋白质不会更新或替换，从而为白内障的形成提供了基础。小梁网是负责房水引流的前房组织，特别容易受到线粒体氧化损伤的影响，这种损伤会影响其内皮细胞，并导致眼压升高，这标志着青光眼的开始。光氧化应激可导致急性或慢性视网膜损伤。年龄相关性黄斑变性的发病机制涉及氧化应激和视网膜色素上皮细胞的死亡，随后是上方光感受器的死亡。因此，越来越多的证据表明，环境和内源性来源的诱变机制在退行性眼病中起着基本的致病作用。
