SAN2020

During the development of neurodegenerative ocular diseases, such as glaucoma, macular degeneration, or other retinopathies, oxidative stress is the main cause of cell damage. The increase in reactive oxygen and nitrogen species can overwhelm the cell’s natural defense mechanisms, with possible effects including the production of endogenous antioxidants and activation of pathways that lead to cell death such as apoptosis, necrosis, or autophagy. Furthermore, produce damages the structure and function of the axons that compose neuronal cells of the retina. This project describes the development and evaluation of a long-term model of retinal degeneration (RD) in rabbits through the co-administration of oxidant agents as glutamate (GLUT) and L-buthionine-S, R-sulfoximine (BSO) that trigger apoptosis by cytotoxicity and oxidative stress of retinal cells, mainly RGCs. The RD model in rabbits was evaluated by in vivo studies of optical coherence tomography (OCT) in time and histological studies in sections of retina for 18 days. Results showed progressive deterioration of retina in presence of oxidizing agents at 18 days. OCT studies evidenced a remarkable decrease in the thickness of the retina over time respect of the control. Histological studies showed notable disruption of layers of retina together with migration and reduction of cells, mainly RGCs. Results are encouraging for developing a long-term in vivo model of retinal degeneration for future neuroprotective drug testing.