Antioxidant Defenses in the ocular surface

Abstract

The human eye is subjected constantly to oxidative stress due to daily exposure to sunlight, high metabolic activities, and oxygen tension. Reactive oxygen species generated from environmental insults and pathological conditions render the human eye particularly vulnerable to oxidative damage. The ocular surface composed of the tear film, the cornea, and the aqueous humor forms the first physical and biochemical barrier of the eye and plays a pivotal role in combating free radicals. These ocular compartments are enriched in certain antioxidants in the form of metabolic enzymes or small molecules. Such an antioxidant defense system in the ocular surface is essential for the maintenance of redox homeostasis in the eye and protection against oxidative damage. Herein, we review the properties and functions of key constituent antioxidants of the ocular surface.

Aldehyde Dehydrogenase Inhibitors: a Comprehensive Review of the Pharmacology, Mechanism of Action, Substrate Specificity, and Clinical Application

“…In this context, ALDH1A1 and ALDH3A1 (also respectively referred to as lens and corneal crystallins) are the isozymes that defend ocular surface tissues from reactive oxygen species (Estey et al, 2007;Chen et al, 2009). In addition, they maintain the integrity of the lens and cornea through nonenzymatic activities, including direct absorption of harmful UV radiation or serving as chaperones to prevent aggregation of misfolded proteins .…”

“…Increased ALDH activity, however, has been found to interfere with certain chemotherapeutic treatments (Slá dek, 1999;Jelski et al, 2007;Tanei et al, 2009;Deng et al, 2010). In addition, ALDHs can act as esterases (Blackwell et al, 1983;Yoshida et al, 1998) and also perform nonenzymatic functions, such as reducing osmotic stress in plants, binding to macromolecules (such as androgen and cholesterol) and protecting the mammalian cornea from UV exposure (Estey et al, 2007;Chen et al, 2009). Genetic polymorphisms of ALDH isozymes that result in diminished enzymatic activity are associated with several clinical disease states, including Sjögren-Larsson syndrome, Type 2 hyperprolinemia, pyridoxine-dependent seizures, hyperammonemia, ␥-hydroxybutyric aciduria, and alcoholic liver disease (Marchitti et al, 2008).…”

Synthetische Tränen – Ein Schritt näher der menschlichen Tränenflüssigkeit

“…Bei einem Überschuss an Oxidantien ist die Kapazität allerdings erschöpft, und die Schutzfunktion kann nicht aufrecht erhalten werden [13,14]. Man vermutet, dass dadurch zahlreiche Erkrankungen des Sehapparats, wie Katarakt, altersbedingte Makuladegeneration, aber auch das Trockene Auge ausgelöst werden können [15][16][17][18].…”

Evaluation of the Effect ofN-Acetylcysteine on Protein Deposition on Contact Lenses in Patients with the Boston Keratoprosthesis Type I

“…Oxidative mechanisms contribute to the development of many visionimpairing conditions of the ocular surface. 40,41 Studies on mucus have shown the mechanism of action of NAC is the reduction of disulfide bonds (S -S) to sulfhydryl bonds (-SH) 42 within the glycoprotein mucin, in turn disrupting crosslinking between monomers. 41 Similarly, we postulate that the use of an antioxidant that reduces mucin oligomerization will have a downstream effect on protein deposition on the contact lens.…”

“…40,41 Studies on mucus have shown the mechanism of action of NAC is the reduction of disulfide bonds (S -S) to sulfhydryl bonds (-SH) 42 within the glycoprotein mucin, in turn disrupting crosslinking between monomers. 41 Similarly, we postulate that the use of an antioxidant that reduces mucin oligomerization will have a downstream effect on protein deposition on the contact lens. Furthermore, this study demonstrates that the use of topical NAC can be linked to the improvement in protein deposit-related symptoms, such as decreased visual acuity and comfort.…”