Oxidative Stress Implication in Retinal Diseases-A Review

Abstract

Oxidative stress (OS) refers to an imbalance between free radicals (FRs), namely highly reactive molecules normally generated in our body by several pathways, and intrinsic antioxidant capacity. When FR levels overwhelm intrinsic antioxidant defenses, OS occurs, inducing a series of downstream chemical reactions. Both reactive oxygen species (ROS) and reactive nitrogen species (RNS) are produced by numerous chemical reactions that take place in tissues and organs and are then eliminated by antioxidant molecules. In particular, the scientific literature focuses more on ROS participation in the pathogenesis of diseases than on the role played by RNS. By its very nature, the eye is highly exposed to ultraviolet radiation (UVR), which is directly responsible for increased OS. In this review, we aimed to focus on the retinal damage caused by ROS/RNS and the related retinal pathologies. A deeper understanding of the role of oxidative and nitrosative stress in retinal damage is needed in order to develop targeted therapeutic interventions to slow these pathologies.

Keywords: Eales’ disease; Stargardt disease; age-related macular degeneration; diabetic retinopathy; macular diseases; neurodegeneration; nitrosative stress; oxidative stress; reactive oxygen species; retinitis pigmentosa; retinopathy of prematurity.

Figure 1

En face (upper panel) and structural B-scan (bottom panel) images of spectral domain-optical coherence tomography (SD-OCT) of a right eye. Patient affected by wet age-related macular degeneration (AMD) with exudative retinal detachment (ERD) in the foveal area. Numerous drusen deposits as hyperfluorescent dots (yellow arrows) are under retinal pigment epithelium (RPE) (white lines).

Figure 2

Optical coherence tomography angiography (OCTA) in right eye. Images of a patient suffering from wet age-related macular degeneration (AMD) characterized by a phenomenon of abnormal vascular proliferation in the choriocapillaris layer and consecutive choroidal neovascular membrane (CNV) development in the macular region, clearly evident in the last image at the top right.

Figure 3

Fluorescein angiography of a patient with proliferative diabetic retinopathy (DR) in left eye. Posterior pole in the left image. Presence of numerous microaneurysms as hyperfluorescent dots (orange arrow heads), bleeding as irregular black spots (red arrow heads), and initial macular edema (ME) as retinal foveal hyperfluorescence. Retinal nasal quadrant in the right image. Presence of large dark areas without terminal vessels due to retinal ischemia (white arrows). In both images, some hyperfluorescent spots on the optic disc and along the nasal and temporal vascular arches are highlighted, due to proliferation of new blood vessels (red circles).

Figure 4

Spectral domain-optical coherence tomography (SD-OCT) of a patient with retinitis pigmentosa (RP). In right eye, it is possible to notice the absence of photoreceptors (PRs) (blue arrows) and a retinal pigment epithelium (RPE) degeneration (white line) beyond the perifoveal area. Thinned ganglion cell complex (GCC thickness map). Outside normal retinal thickness distribution was established by the normative database reference map (NDB reference map).

Figure 5

Optical coherence tomography angiography (OCTA) in a patient with retinitis pigmentosa (RP). In right eye, it is possible to notice the absence of photoreceptors (PRs) (blue arrows) and a retinal pigment epithelium (RPE) degeneration (white arrows) beyond the perifoveal area. The vascular plexus is reduced (upper left image). Moreover, an epiretinal membrane (ERM) is detected in the enface image (upper right image) and structural image (bottom right panel) forming some retinal folds.