The Eye, Oxidative Damage and Polyunsaturated Fatty Acids

Abstract

Polyunsaturated fatty acids (PUFA) are known to have numerous beneficial effects, owing to their anti-inflammatory and antioxidant properties. From a metabolic standpoint, the mitochondria play a fundamental role in cellular homeostasis, and oxidative stress can affect their functioning. Indeed, the mitochondria are the main source of ROS, and an imbalance between ROS and antioxidant defenses leads to oxidative stress. In addition, aging, the decline of cellular functions, and continual exposure to light underlie many diseases, particularly those of the eye. Long-term exposure to insults, such as UV light, visible light, ionizing radiation, chemotherapeutics, and environmental toxins, contribute to oxidative damage in ocular tissues and expose the aging eye to considerable risk of pathological consequences of oxidative stress. Ample antioxidant defenses responsible for scavenging free radicals are essential for redox homeostasis in the eye, indeed, eye tissues, starting from the tear film, which normally are exposed to high oxygen levels, have strong antioxidant defenses that are efficient for protecting against ROS-related injuries. On the contrary, instead, the trabecular meshwork is not directly exposed to light and its endothelial cells are poorly equipped with antioxidant defenses. All this makes the eye a target organ of oxidative damage. This review focuses on the role of the polyunsaturated fatty acids in the human eye, particularly in such pathologies as dry eye, glaucoma, and macular degeneration, in which dietary PUFA supplementation can be a valid therapeutic aid.

Keywords: GSTM1; POAG; glaucoma epidemiology; oxidative damage; primary open angle glaucoma.

Figure 1

The human eye is constantly exposed to sunlight and artificial light. Exogenous sources of ROS, such as UV rays, visible light, ionizing radiations, chemotherapeutics, and environmental toxins, contribute to oxidative damage in the ocular tissues. In the long-term, such injuries expose the aged eye to considerable risk of the pathological consequences of oxidative stress. While this affects practically all organs and apparatuses, it has a heavy impact in diseases such as glaucoma, dry eye and age-related macular degeneration.

Figure 2

By interacting with genetic and environmental factors, oxidative stress results in DNA damage, alterations of gene expression and of the protein profile and, finally, disease.

Figure 3

Dry-eye syndrome is a multifactorial disease of the ocular surface in which oxidative stress is greatly involved. Affected patents suffer from symptoms of discomfort and tear film instability, and visual quality is reduced proportionally to the severity of the disease. The Figure 3 shows an example of corneal epithelium injuries in a patient affected by dry-eye syndrome, as detected by means of Lissamine green staining. Diffuse corneal epithelium alterations appear as green dots in the frame-shift of the inferior cornea surface.

Figure 4

Normal optic nerve (left eye). (A) Normal visual field represented by the grayscale map. Darker areas indicate lower sensitivities, while higher sensitivities are represented by a lighter tone. This graphical representation allows easy interpretation of visual field loss, and is usually used to demonstrate vision changes to the patient; (B) Normal optic disc with a healthy neuroretinal rim; Glaucomatous optic nerve (right eye). (C) Dense glaucomatous arcuate scotoma; (D) Glaucomatous optic disc with evident narrowing of the superotemporal and inferotemporal neuroretinal rim.

Figure 5

Exudative age-related macular degeneration with parafoveal neovascular component localized inferiorly in the area of intraretinal hemorrhage. The area of atrophy of the retinal pigment epithelium in the macular and superior paramacular sites. The exact pathological mechanisms leading to the different forms of AMD are still unclear. Oxidative stress and inflammation seem to play a major role in both AMD and aging, leading to the formation of abnormal extracellular matrix. This event results in altered behavior of RPE choriocapillaries, ultimately leading to atrophy of the retina, RPE, and choriocapillaries, which is paralleled by neovascularization of the choroid.