Clinical and experimental evidence supports that chronic oxidative stress is a primary contributing factor to numerous retinal degenerative diseases, such as age-related macular degeneration (AMD).
Potential of melatonin to treat or prevent age-related macular degeneration through stimulation of telomerase activity
I suggest that melatonin therapy as pharmacologic agents and/or melatonin-rich foods, especially in AMD patients with measured low serum melatonin levels or high risk patients would be possibly an alternative approach to prevent and/or treat AMD.
Melatonin Metabolites Protect Human Retinal Pigment Epithelial Cells from Death Caused by Oxidative Stress
“It was concluded that these melatonin metabolites might be useful in treating many retinal conditions linked to the oxidative stress-induced damage.”
Melatonin cytoprotective properties may have practical implications in the treatment of ocular diseases, like glaucoma and age-related macular degeneration.
Melatonin, being an efficient antioxidant with antinitridergic properties, has a promising role in the treatment and management of glaucoma.
Mitochondrial complex I defect induces ROS release and degeneration in trabecular meshwork cells of POAG patients: protection by antioxidants
The authors present strong evidence that mitochondrial complex I defects are the major source of oxidative stress in TM cells of patients with POAG. Antioxidants such as Vit E and NAC are likely candidates to reduce ROS production and as complementary agents in the treatment of glaucoma.
Current evidence suggests that melatonin may act as a protective agent in ocular conditions such as photo-keratitis, cataract, glaucoma and retinopathy.
The role of free radical-induced lipid oxidation in the development of cataracts in human and canine eyes
Free radical-induced lipid oxidation causes accumulation of lenticular lipid peroxidation (LPO) products. Lens opacity correlates with the level of the LPO accumulation. Oxidation of lens proteins is due to a decreased glutathione concentration in the lens.
Treatment with 1% N-acetylcarnosine (NAC) protects telomeres to prevent and dissolve mature cataracts in dogs.
Cataracts in small animals are caused by oxidative stress on lens epithelial cells. Treatment with 1% N-acetylcarnosine (NAC) releases L-carnosine ophthalmically, stabilizing telomeres to help prevent and dissolve mature cataracts in dogs.
The majority had reduced pathologic macular changes. We conclude that the daily use of 3 mg melatonin seems to protect the retina and to delay macular degeneration. No significant side effects were observed…
Oxidative stress in the human trabecular meshwork clinically correlated with primary open-angle glaucoma
Study evaluated intensity of oxidative molecular damage and its clinical correlation to intraocular pressure. It found that oxidative stress could induce human trabecular meshwork degeneration, favoring an increase in IOP, leading to Glaucoma…
N-alpha-Acetylcarnosine is proposed for treatment of ocular disorders that have a component of oxidative stress in their genesis
Nalpha-acetylcarnosine is proposed as a prodrug of L-carnosine that is resistant to enzymatic hydrolysis by carnosinase with ability to give efficient protection against oxidative stress both in the lipid phase of biological membranes and in aqueous environments.