氧化应激
脂质过氧化
程序性细胞死亡
GPX4
视网膜变性
活性氧
细胞生物学
视网膜
视网膜
光污染
化学
生物
生物化学
过氧化氢酶
神经科学
细胞凋亡
光学
谷胱甘肽过氧化物酶
物理
作者
Xuan Li,Sen Zhu,Qisheng Feng
标识
DOI:10.1016/j.jphotobiol.2022.112617
摘要
With the development of technology and electronic products, the problem of light pollution is becoming more and more serious. Blue light, the most energetic light in visible light, is the main culprit of teenage vision problems in the modern environment. As the tissue with the highest oxygen consumption, the retina is vulnerable to oxidative stress. However, the exact way in which blue light-triggered reactive oxygen species (ROS) cause retinal cell death remains unclear. Ferroptosis is a newly defined cell death pathway, whose core molecular mechanism is cell death caused by excessive lipid peroxidation. In this study, the results indicated that blue light-triggered ROS burst in retinal cells, in the meantime, intracellular Fe2+ levels were also significantly up-regulated. Further, deferoxamine (DFO) significantly improved blue light-triggered lipid peroxidation and cell death in ARPE-19 cells, and ferrostatin-1 (Fer-1) alleviated retinal oxidative stress and degeneration in rats. Furthermore, the GSH-GPX4 and FSP1-CoQ10-NADH systems served as key systems for cellular defense against ferroptosis, and interestingly, our results demonstrated that blue light triggered imbalance of the GSH-GPX4 and FSP1-CoQ10-NADH systems in retinal cells. Taken together, these pieces of evidence suggest that ferroptosis may be a crucial pathway for blue light-induced retinal damage and degeneration, which helps us to understand exactly why blue light pollution causes visual impairment in adolescents.
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