Saenz-de-Viteri Manuel, Heras-Mulero Henar, Fernández-Robredo Patricia, Recalde Sergio, Hernández María, Reiter Nicholas, Moreno-Orduña Maite, García-Layana Alfredo
Experimental Ophthalmology Laboratory, School of Medicine, University of Navarra, 1 Irunlarrea Street, 31008 Pamplona, Spain ; Department of Ophthalmology, Clínica Universidad de Navarra, School of Medicine, University of Navarra, 36 Pio XII Avenue, 31008 Pamplona, Spain.
Experimental Ophthalmology Laboratory, School of Medicine, University of Navarra, 1 Irunlarrea Street, 31008 Pamplona, Spain.
Oxid Med Cell Longev. 2014;2014:637137. doi: 10.1155/2014/637137. Epub 2014 May 27.
Photochemical damage occurs after an exposure to high energy radiation within the visible spectrum of light, causing morphological changes in the retina and the formation of superoxide anion. In this study we created a model of phototoxicity in rabbits. Animals were exposed to a light source for 120 minutes and were sacrificed immediately or one week after exposure. Outer nuclear layer and neurosensory retina thickness measurements and photoreceptor counting were performed. Caspase-1 and caspase-3 were assessed by immunohistochemistry. Dihydroethidium was used to evaluate in situ generation of superoxide and thiobarbituric acid reactive substances were measured in retinal homogenates as indicators of lipid peroxidation. The total antioxidant capacity and oxidative ratio were also determined. Retinas from rabbits exposed to light showed higher levels of lipid peroxidation than the unexposed animals and a decrease in outer nuclear layer and neurosensory retina thickness. Our study demonstrates that light damage produces an increase in retinal oxidative stress immediately after light exposure that decreases one week after exposure. However, some morphological alterations appear days after light exposure including apoptotic phenomena. This model may be useful in the future to study the protective effect of antioxidant substances or new intraocular lenses with yellow filters.
光化学损伤发生在暴露于可见光谱范围内的高能辐射后,会导致视网膜形态变化并形成超氧阴离子。在本研究中,我们建立了兔光毒性模型。将动物暴露于光源下120分钟,然后立即处死或在暴露后一周处死。进行了外核层和神经感觉视网膜厚度测量以及光感受器计数。通过免疫组织化学评估半胱天冬酶-1和半胱天冬酶-3。使用二氢乙锭评估超氧的原位生成,并在视网膜匀浆中测量硫代巴比妥酸反应性物质作为脂质过氧化的指标。还测定了总抗氧化能力和氧化率。暴露于光的兔视网膜显示出比未暴露动物更高的脂质过氧化水平,并且外核层和神经感觉视网膜厚度降低。我们的研究表明,光损伤在光照后立即导致视网膜氧化应激增加,在暴露一周后降低。然而,一些形态学改变在光照几天后出现,包括凋亡现象。该模型未来可能有助于研究抗氧化物质或带有黄色滤光片的新型人工晶状体的保护作用。