Zhang Qing, Chen Dezhi, Liu Xiaomeng, Deng Zhewen, Li Jiaqi, Zhu Senqiang, Ma Bo, Liu Rui, Zhu Hongjun
School of Chemistry and Molecular Engineering, Nanjing Tech University, Nanjing, 211816, China.
School of Pharmaceutical Sciences, Nanjing Tech University, Nanjing, 211816, China.
Small. 2025 Apr;21(16):e2403165. doi: 10.1002/smll.202403165. Epub 2024 Sep 9.
The development of small molecule photosensitizers based on iridium complex is limited by the mismatch between therapeutic effect and systemic toxicity, as well as the incomplete understanding of the molecular mechanism underlying cell death induction. Herein, a small molecule iridium complex IrC with high photocytotoxicity is synthesized, with half maximal inhibitory concentration as low as 91 nm, demonstrating excellent anti-tumor, relief of splenomegaly, and negligible side effects. Starting from the factors of effective photosensitizers, the in-depth theoretical analysis on photon absorption efficiency, energy transfer level matching, and properties of the triplet excited state of IrC is conducted. This also elucidates the feasibility of generating the high singlet oxygen quantum yield. In addition, the death mechanism induced by IrC is focused, innovatively utilizing GPX4-overexpression and GPX4-knockout cells via CRISPR/Cas9 technique to comprehensively verify ferroptosis and its further molecular mechanism. The generation of ROS mediated by IrC, along with the direct inhibition of GPX4 and glutathione, synergistically increased cellular oxidative stress and the level of lipid peroxidation. This study provides an effective approach for small molecule complexes to induce GPX4-dependent ferroptosis at low-dose photodynamic therapy.
基于铱配合物的小分子光敏剂的发展受到治疗效果与全身毒性不匹配以及对细胞死亡诱导潜在分子机制理解不完整的限制。在此,合成了一种具有高光细胞毒性的小分子铱配合物IrC,其半数抑制浓度低至91纳米,显示出优异的抗肿瘤、脾肿大缓解作用且副作用可忽略不计。从有效光敏剂的因素出发,对IrC的光子吸收效率、能量转移能级匹配以及三重激发态性质进行了深入的理论分析。这也阐明了产生高单线态氧量子产率的可行性。此外,聚焦于IrC诱导的死亡机制,通过CRISPR/Cas9技术创新性地利用GPX4过表达和GPX4敲除细胞全面验证铁死亡及其进一步的分子机制。由IrC介导的ROS生成,连同对GPX4和谷胱甘肽的直接抑制,协同增加细胞氧化应激和脂质过氧化水平。本研究为小分子配合物在低剂量光动力疗法中诱导GPX4依赖性铁死亡提供了一种有效方法。