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.

The Role of Nutrition and Nutritional Supplements in Ocular Surface Diseases

“…Furthermore, ageing is an established risk factor for oxidative stress, as the concentration of endogenous antioxidant species significantly decreases with increasing age, while reactive oxygen species production increases [11]. Indeed, physiological processes progressively lose their efficacy and, as a result of such condition, the senescent cell up-regulates the expression of genes encoding a variety of proteins including inflammatory mediators and matrix-remodeling factors, which disrupt the local homeostasis, leading to the creation and maintenance of oxidative stress [12].…”

Activation of the Notch‑Nox4‑reactive oxygen species signaling pathway induces cell death in high glucose‑treated human retinal endothelial cells

“…In cultured bovine retinal pericytes, the application of methylglyoxal induced apoptosis via increases in ROS levels (6); however, the potential molecular mechanisms underlying increased ROS production in the pathogenesis of DR remain unclear. Mitochondria are the major source of superoxide production and are subject to direct attack by ROS (7). In diabetes, the dysfunction of retinal mitochondria has been reported, and overexpression of mitochondrial superoxide dismutase was observed to protect retinal and vascular cells against high glucose (HG)-induced increases in oxidative stress and DNA damage (8).…”

Extracellular Vesicles Mediate Anti-Oxidative Response—In Vitro Study in the Ocular Drainage System

“…Continuous exposure to UV light leads to excessive production of ROS that was attributed to cataracts [ 3 ] and primary open-angle glaucoma (POAG) [ 4 ]. The outer segment is partially protected by antioxidant enzymes and low molecular weight antioxidant presented in the AqH and in the ocular drainage tissues [ 5 , 6 , 7 ]. Changes in the AqH reducing capacity were reported in a rabbit model of POAG [ 8 , 9 ].…”