Dietary Antioxidants in Age-Related Macular Degeneration and Glaucoma

Abstract

Age-related macular degeneration (AMD) and glaucoma are ophthalmic neurodegenerative diseases responsible for irreversible vision loss in the world population. Only a few therapies can be used to slow down the progression of these diseases and there are no available treatment strategies for reversing the degeneration of the neural retina. In AMD, the pathological process causes the malfunction and damage of the retinal pigmented epithelium and photoreceptors in the macula. In glaucoma, damage of the retinal ganglion cells and their axons is observed and treatment strategies are limited to intraocular pressure lowering. Therefore, other prophylactic and/or therapeutic methods are needed. Oxidative stress is involved in the neurodegenerative process accompanying both AMD and glaucoma; therefore, the use of antioxidant agents would clearly be beneficial, which is supported by the decreased prevalence and progression of AMD in patients adherent to a diet naturally rich in antioxidants. Dietary antioxidants are easily available and their use is based on the natural route of administration. Many preclinical studies both in vitro and using animal models of retinal degeneration showed the efficacy of dietary antioxidants, which was further proved in clinical trials. Resveratrol is beneficial both in AMD and glaucoma animal models, but confirmed only among AMD patients. For AMD, carotenoids and omega-3 fatty acids were also proved to be sufficient in preventing neurodegeneration. For glaucoma, coenzyme Q10 and alpha-lipoic acid showed efficacy for decreasing retinal ganglion cell loss and inhibiting the accompanying destructive processes. Interestingly, the benefits of vitamins, especially vitamin E was not confirmed, neither in preclinical nor in clinical studies.

Fingertip-Measured Skin Carotenoids and Advanced Glycation End Product Levels in Glaucoma

“…Dietary intake of carotenoids would be involved in modifying AGE accumulation in the body. The formation process of AGEs includes oxidative reactions [ 38 ]; therefore, the antioxidant effect of carotenoids suppressed these oxidation steps to reduce the production of AGEs accordingly [ 13 ]. This was supported by a report that administration of chestnut ( Tarpa bispinosa Roxb.)…”

“…Antioxidants suppress inflammation caused by ROS and improve RGCs in experimental glaucoma [ 12 ]. Neurodegeneration caused by ROS is considered a modifiable factor of glaucoma onset and progression [ 13 , 14 ]. ROS is mainly generated by the metabolism of the mitochondria and neutralized by antioxidants [ 15 ].…”

Nutraceutical Approach for the Treatment of Retinal Inflammation after Infections

“…It is well known that retinal degeneration can be induced by several factors, including genetic mutations, oxidative stress, and inflammation. Several treatments employing natural molecules, with antioxidant and/or anti-inflammatory actions, have shown efficacy in slowing the progression of retinal degeneration (e.g., AMD) [46].…”

α‐Lipoic acid up‐regulates gene expression but reduces protein levels of fibroblast growth factor 21 in HepG2 cells

“…ALA is a dithiol compound and functions as a cofactor of mitochondrial enzymes including pyruvate dehydrogenase and a‐ketoglutarate dehydrogenase, which are critical in fuel metabolism 14 . Meanwhile, ALA exerts anti‐oxidant actions owing to its dithiolane ring, 14–16 with the ability to quench free radicals and recycle other antioxidants, and therefore, it possesses beneficial effects on oxidative stress‐related diseases to some extent 17–20 . However, ALA in high dose interferes with the cellular redox state and suppresses cell growth 21–24 .…”

“…14 Meanwhile, ALA exerts anti-oxidant actions owing to its dithiolane ring, [14][15][16] with the ability to quench free radicals and recycle other antioxidants, and therefore, it possesses beneficial effects on oxidative stress-related diseases to some extent. [17][18][19][20] However, ALA in high dose interferes with the cellular redox state and suppresses cell growth. [21][22][23][24] It has been reported that ALA inhibits growth and induces apoptosis of various tumour cells including lung cancer cells, colorectal cancer cells, breast cancer cells, T-lymphoma cells and HepG2 hepatoma cells via the induction of oxidative stress and ER stress.…”