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Oxidative Stress and Histological Changes in a Model of Retinal Phototoxicity in Rabbits

机译:兔视网膜光毒性模型中的氧化应激和组织学变化

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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.
机译:暴露于可见光谱内的高能辐射后会发生光化学损伤,从而引起视网膜的形态变化和超氧阴离子的形成。在这项研究中,我们创建了兔子的光毒性模型。将动物暴露于光源120分钟,并立即或暴露后一周将其处死。进行了外核层和神经感觉视网膜厚度的测量以及感光细胞的计数。通过免疫组织化学评估Caspase-1和caspase-3。使用二氢乙啶来评估超氧化物的原位生成,并在视网膜匀浆中测量硫代巴比妥酸的反应性物质,作为脂质过氧化的指标。还确定了总抗氧化剂容量和氧化比。兔子的视网膜暴露于光下比未暴露的动物表现出更高的脂质过氧化水平,外核层和神经感觉视网膜厚度减少。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,而在暴露后一周减少。但是,某些形态变化会在光照后几天出现,包括凋亡现象。该模型将来可能用于研究抗氧化剂或具有黄色滤光片的新型人工晶状体的保护作用。

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