The Eye, Oxidative Damage and Polyunsaturated Fatty Acids.

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.

[Open angle glaucoma: epidemiology, pathogenesis and prevention]. / Glaucoma: epidemiologia molecolare, patogenesi, prevenzione.

There is growing evidence that reactive oxygen species (ROS) play a key role in the pathogenesis of primary open angle glaucoma (POAG). The occurrence of oxidative DNA damage in trabecular meshwork (TM) has been demonstrated by measuring the increase of 8-hydroxy-2'-deoxyguanosine, the most abundant DNA oxidative alteration, which is significantly increased in glaucoma-bearing subjects as compared with unaffected controls. Several lines of evidence support the hypothesis that ROS play a fundamental pathogenic role, including the following: (a) outflow resistance in the anterior chamber increases in the presence of high levels of hydrogen peroxide; (b) TM possesses abundant antioxidant activities; (c) significant increases in superoxide dismutase and glutathione peroxidase activities were detected in the aqueous humour of glaucoma patients; (d) hydrogen peroxide compromises TM integrity. The existence of a significant correlation between oxidative DNA damage and intraocular pressure in glaucoma patients has been reported. POAG patients appear to have a genetic predisposition rendering them susceptible to ROS-induced damage because of a more frequent deletion, as compared to controls, of the gene encoding for glutathione-S-transferase M1, a pivotal anti-oxidant activity. Furthermore, oxidative stress, occurring not only in TM but also in retinal cells, appears to be involved in the neuronal cell death that characterizes POAG. These considerations could bear relevance for POAG prevention and suggest that genetic analyses and the use of drugs or dietary measures attenuating the effects of ROS, if validated in future studies, could be useful tools contributing to the control of this disease.