Department of Anatomy, All India Institute of Medical Sciences, New Delhi, 110029, India.
Mol Cell Biochem. 2021 Sep;476(9):3483-3495. doi: 10.1007/s11010-021-04175-5. Epub 2021 May 13.
Iron is implicated in ocular diseases such as in age-related macular degeneration. Light is also considered as a pathological factor in this disease. Earlier, two studies reported the influence of constant light environment on the pattern of expressions of iron-handling proteins. Here, we aimed to see the influence of light in 12-h light-12-h dark (12L:12D) cycles on the expression of iron-handling proteins in chick retina. Chicks were exposed to 400 lx (control) and 5000 lx (experimental) light at 12L:12D cycles and sacrificed at variable timepoints. Retinal ferrous ion (Fe) level, ultrastructural changes, lipid peroxidation level, immunolocalization and expression patterns of iron-handling proteins were analysed after light exposure. Both total Fe level (p = 0.0004) and lipid peroxidation (p = 0.002) significantly increased at 12-, 48- and 168-h timepoint (for Fe) and 48- and 168-h timepoint (for lipid peroxidation), and there were degenerative retinal changes after 168 h of light exposure. Intense light exposure led to an increase in the levels of transferrin and transferrin receptor-1 (at 168-h) and ferroportin-1, whereas the levels of ferritins, hephaestin, (at 24-, 48- and 168-h timepoint) and ceruloplasmin (at 168-h timepoint) were decreased. These changes in iron-handling proteins after light exposure are likely due to a disturbance in the iron storage pool evident from decreased ferritin levels, which would result in increased intracellular Fe levels. To counteract this, Fe is released into the extracellular space, an observation supported by increased expression of ferroportin-1. Ceruloplasmin was able to convert Fe into Fe until 48 h of light exposure, but its decreased expression with time (at 168-h timepoint) resulted in increased extracellular Fe that might have caused oxidative stress and retinal cell damage.
铁与年龄相关性黄斑变性等眼部疾病有关。光也被认为是这种疾病的一种病理性因素。早些时候，有两项研究报道了持续光照环境对铁处理蛋白表达模式的影响。在这里，我们旨在观察 12 小时光照-12 小时黑暗（12L:12D）循环中的光对小鸡视网膜中铁处理蛋白表达的影响。小鸡暴露在 400 lx（对照）和 5000 lx（实验）的光下，并在不同时间点处死。暴露于光后分析视网膜亚铁离子（Fe）水平、超微结构变化、脂质过氧化水平、铁处理蛋白的免疫定位和表达模式。Fe 的总水平（p=0.0004）和脂质过氧化（p=0.002）在 12、48 和 168 小时时显著增加（Fe）和 48 和 168 小时时显著增加（脂质过氧化），并且在光暴露 168 小时后出现退行性视网膜变化。强光照射导致转铁蛋白和转铁蛋白受体-1（在 168 小时）和铁蛋白-1水平升高，而铁蛋白、赫菲斯蒂因（在 24、48 和 168 小时时）和铜蓝蛋白（在 168 小时时）水平降低。这些铁处理蛋白在光照后的变化可能是由于铁储存池的紊乱导致铁蛋白水平降低，从而导致细胞内 Fe 水平升高。为了对抗这种情况，Fe 被释放到细胞外空间，这一观察结果得到了铁蛋白-1表达增加的支持。铜蓝蛋白能够将 Fe 转化为 Fe，直到光照 48 小时，但随着时间的推移（在 168 小时时）其表达减少导致细胞外 Fe 增加，这可能导致氧化应激和视网膜细胞损伤。
