Sodium iodate (NaIO3) has been shown to cause severe oxidative stress damage to retinal pigment epithelium cells. This results in the indirect death of photoreceptors, leading to a loss of visual capabilities. The aim of this work is the morphological and functional characterization of the retina and the visual pathway of an animal model of retinal neurodegeneration induced by oxidative stress. Following a single intraperitoneal dose of NaIO3 (65 mg/kg) to C57BL/6J mice with a mutation in the Opn4 gene (Opn4-/-), behavioral and electroretinographic tests were performed up to 42 days after administration, as well as retinal immunohistochemistry at day 57. A near total loss of the pupillary reflex was observed at 3 days, as well as an early deterioration of visual acuity. Behavioral tests showed a late loss of light sensitivity. Full-field electroretinogram recordings displayed a progressive and marked decrease in wave amplitude, disappearing completely at 14 days. A reduction in the amplitude of the visual evoked potentials was observed, but not their total disappearance. Immunohistochemistry showed structural alterations in the outer retinal layers. Our results show that NaIO3 causes severe structural and functional damage to the retina. Therefore, the current model can be presented as a powerful tool for the study of new therapies for the prevention or treatment of retinal pathologies mediated by oxidative stress.
Keywords: Opn4; neurodegeneration; oxidative stress; sodium iodate.