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Sodium Iodate-Induced Ferroptosis in Photoreceptor-Derived 661W Cells Through the Depletion of GSH

文献类型: 外文期刊

作者: Chen, Chao 1 ; Wang, Han 1 ; Yang, Jiuyu 1 ; Zhao, Bi 2 ; Lei, Yutian 1 ; Li, Hanqiao 3 ; Yang, Kunhuan 3 ; Liu, Benying 2 ; Diao, Yong 1 ;

作者机构: 1.Huaqiao Univ, Inst Genom, Sch Med, 668 Jimei Rd, Xiamen 361021, Peoples R China

2.Yunnan Acad Agr Sci, Tea Res Inst, Yunnan Key Lab Tea Sci, Kunming 650201, Peoples R China

3.Xiamen Univ, Sch Med, Xiamen 361000, Peoples R China

关键词: sodium iodate; photoreceptor; ferroptosis; GSH

期刊名称:INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES ( 影响因子:4.9; 五年影响因子:5.7 )

ISSN: 1661-6596

年卷期: 2025 年 26 卷 5 期

页码:

收录情况: SCI

摘要: Oxidative stress-induced photoreceptor cell death is closely associated with the etiology of age-related macular degeneration (AMD), and sodium iodate (SI) has been widely used as an oxidant stimulus in AMD models to induce retinal pigment epithelium (RPE) and photoreceptor cell death. However, the mechanism underlying SI-induced photoreceptor cell death remains controversial and unclear. In this study, we elucidate that ferroptosis is a critical form of cell death induced by SI in photoreceptor-derived 661W cells. SI disrupts system Xc-, leading to glutathione (GSH) depletion and triggering lipid peroxidation, thereby promoting ferroptosis in photoreceptor-derived 661W cells. Additionally, SI enhances intracellular Fe2+ levels, which further facilitates reactive oxygen species (ROS) accumulation, making the 661W cells more susceptible to ferroptosis. Exogenous GSH, as well as specific inhibitors of ferroptosis such as Fer-1 and antioxidants like NAC, significantly attenuate SI-induced ferroptosis in photoreceptor-derived 661W cells. These findings provide new insights into the mechanisms of ferroptosis as a key pathway in SI-induced photoreceptor-derived 661W cell death.

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