The trabecular meshwork represents the “key” region in glaucoma pathogenesis, its alterations resulting in increased resistance of the outflow system.¹ In the primate eye, approximately 75% of the resistance to aqueous humor outflow resides in the tissues between the anterior chamber and the lumen of the Schlemm canal.¹ In particular, the human trabecular meshwork (HTM) is a specialized eye tissue that regulates the aqueous humor outflow and controls intraocular pressure (IOP). The HTM has been interpreted as a biological filter to be transited by the aqueous humor to reach the Schlemm canal.² More recently, it has been established that HTM cells are essential for maintenance of the whole outflow system homeostasis,³ thus recognizing the possible importance of HTM cell damage in the pathogenesis of glaucoma. Although many researchers suggest that glaucoma is the consequence of an ischemic injury,⁴ it is recognized that IOP has a pathogenetic role toward glaucomatous neuropathy, possibly by inducing the formation of oxidative free radicals.⁵ A previous study⁶ in patients with open-angle glaucoma provided evidence of the increased oxidative DNA damage in patients with glaucoma and its relationship to the lack of the GSTM1 gene, which catalyzes the neutralization of free radicals by their conjugation with glutathione.

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.