Effects of an Antioxidant Protective Topical Formulation on Eye Exposed to Ultraviolet-Irradiation: a Study in Rabbit Animal Model

Abstract

Ultraviolet-radiation exerts a well-known role in the development of various ocular diseases and may contribute to the progress of age-related macular degeneration. Therefore, the use of compounds able to protect the eyes from UV-induced cellular damage is challenging. The aim of this study has been to test the protective effects of an antioxidant topical formulation against UV-induced damage in rabbit eyes. Twelve male rabbits were used. Animals were divided into 4 groups of 3 animals each. Control group (CG) did not receive any irradiation and/or eye drop. The other three experimental groups were treated as follows: the first group received only UVR irradiation for 30 min, without eye drop supplementation (Irradiation group, IG), the second (G30) and the third (G60) groups received UV irradiation for 30’ and 60’, respectively, and eye drop supplementation (riboflavin, d-α-tocopheryl polyethylene glycol, proline, glycine, lysine and leucine solution) every 15 min for three hours. In the IG group a significant increase of oxidized glutathione (GSSG) and hydrogen peroxide (H2O2) was recorded in the aqueous humor, whereas ascorbic acid levels were significantly lower when compared to control eyes. In the groups exposed to UVR rays for 30 min, and treated with the topical antioxidant formulation, the GSSG, H2O2 and ascorbic acid levels were similar to those recorded in controls, whereas in the G60 group the three markers significantly differ from control group. In the lens, a significant decrease of alpha tocopherol and total antioxidant capacity (TAC) was recorded in IG-animals as compared to control group, whereas malondialdehyde (MDA) levels were significantly higher in UV-induced eye than in control eyes. In the G30 groups the alpha tocopherol, MDA and TAC levels do not significantly differ from those recorded in controls, whereas in the G60 group these three markers significantly differ from control group. Present findings demonstrate that topical treatment with the antioxidant formulation used herein protects ocular structures from oxidative stress induced by UV exposure in in vivo animal model.

Corneal UV Protective Effects Of A Topical Antioxidant Formulation: A Pilot Study On In Vivo Rabbits

“…Vizzari et al showed that topical application of the antioxidant and shielding solution significantly counteracts the UV-induced oxidative stress in both aqueous humor and lens of exposed rabbits [40]. Furthermore, riboflavin shows an indirect antioxidant capacity because it has a shielding action (limits the damage caused by the UV-A irradiation) as demonstrated in our studies on cross linking [52][53][54].…”

“…The peculiar position and function of the eye makes the cornea constantly exposed to UV [38] and the UV light at wavelengths of 270-290 nm or less is totally absorbed by the cornea epithelium and Bowman's membrane [39]. Lipid peroxidation of cellular membranes, oxidative changes in proteins, direct oxidative damage to DNA [40][41][42], decreasing mitochondrial functions and antioxidant protective mechanism, induce apoptosis in corneal tissue [8,43]. The related histologic finding is represented by micropapillary changes and membrane detachment occurred in our experiments.…”

Corneal UV Protective Effects of a Topical Antioxidant Formulation: A Pilot Study on In Vivo Rabbits

“…Lipid peroxidation of cellular membranes, oxidative changes in proteins, direct oxidative damage to DNA [31][32][33], decreasing mitochondrial functions and antioxidant protective mechanisms, lead to apoptosis in corneal tissue [7,34]. The related histologic finding is represented by micropapillary changes and membrane detachment, as occurred in our experiments.…”

Protective Effect of Vitamin C against Infancy Rat Corneal Injury Caused by Acute UVB Irradiation

“…Vitamin C could reduce oxidative stress production and inflammation to achieve protective effects. Researches showed that vitamin C could suppress UVB-induced cell death, apoptosis, ROS production, and the inflammatory response by downregulating tumor necrosis factor-α (TNF-α) expression [14,15]. Moreover, UVB irradiation of vitamin-deficient animals resulted in severe corneal injury and -inflammatory response [16].…”