Exposure to a solar eclipse causes neuronal death in the retina

Background: A solar eclipse was observed in Europe on 11 August 1999. Sever al individuals suffered from transient or persisting retinal damage, caused by gazing at the eclipse without adequate eye protection. Retinal damage i s the most serious hazard of exposure to light, but the mechanisms by which this type of exposure produces retinal damage and its cellular correlates are not yet established. We used an animal model to monitor the mechanisms of retinal damage following excessive light exposure, and in particular to study whether observation of the eclipse induces death of retinal cells. Me thods: In the geographic area where the experiment was conducted, a partial (90%) solar eclipse was observed. Experimental albino rats were exposed to these eclipse conditions, and control rats were exposed to normal sunlight . Another group of control animals was exposed to the same conditions, but was provided with protective light filters of the type recommended for huma n use. The DNA fragmentation in retinal sections of the various groups was analysed by terminal deoxynucleotidyl-transferase-mediated dUTP nick-end la belling. This analysis revealed that exposure to both normal sunlight and t o the eclipse resulted in neuronal apoptosis. Immunohistochemical technique s were used to evaluate possible glial-vascular alterations. Results: Dying cells could first be detected 24 It after exposure, the largest number of which were found 6 days later in the photoreceptor layer. Control levels we re attained 14 days after the exposure. Retinal ganglion cells underwent ap optosis in both groups (normal sunlight and eclipse exposure). whereas i n the neuroglial cells there was an up-regulation of the intermediate filamen t content. The number of dying cells in both groups was greater in animals whose pupils had been dilated pharmacologically during exposure. On the oth er hand, the protective filters were effective in preserving the rat retina l cells from apoptosis. Conclusions: These result,, show, for the first tim e, that the cellular correlates of solar retinopathy are neuronal apoptosis accompanied by glio-vascular responses. Cellular apoptosis is an irreversi ble process, which could manifest itself as permanent visual impairment. Th e activation of non-neuronal cells, such as glial and endothelial cells, co uld be responsible for the more transient clinical symptoms.