Five inorganic monoiron(Ⅱ) carbonyl salts 1-5, fac-M[Fe(CO)₃I₃]_n (Mⁿ⁺=Na⁺ (1), K⁺ (2), Mg²⁺ (3), Ca²⁺ (4), NH₄⁺ (5)) were prepared from the reactions of cis-[Fe(CO)₄I₂] precursor with the iodo salts (MI_n), and developed as CO-releasing molecules (CORMs) for CO therapy of cancer. The decomposition of salts 1-5 with CO-release in DMSO, D₂O, saline, and phosphonate buffer solution was investigated by the Fourier transform infrared (FTIR) spectroscopic monitoring. The corresponding kinetics for the decomposing of these salts were estimated by abiding by a first-order model. Cytotoxicity of the five salts was assessed on a bladder cancer cell line (RT112) by the methyl thiazolyl tetrazolium (MTT) assays for 24 h, with the half maximal inhibitory concentration (IC₅₀) values of 25-43 μmol·L^-1. Notably, varying a counter ion of fac-[Fe(CO)₃I₃]^- anion from an organic aminium to an inorganic cation unambiguously affects its stability and thus the cytotoxicity. Moreover, a mechanistic probing into the cytotoxicity of fac-[Fe(CO)₃I₃]^- anion was paved. Interestingly, not only the produced iodine radicals but also the gaseous CO from the decomposition contributed to its cytotoxicity. Particularly, it was found that, with the treatment of the anion, the reactive oxygen species (ROS) level in the mitochondria significantly enhanced, and the mitochondria-related protein expression of Parkin was extremely upregulated. The ferroptosis inhibitor assays of Ferrostatin‑1 and Liproxstatin-1 confirmed that these complexes evoked a ferroptosis-involved pathway to contribute to their cytotoxicity. Therefore, a mechanistic understanding of the cytotoxicity of fac-[Fe(CO)₃I₃]^- anion is proposed, which is stimulated by the decomposing of the anion, and thus manufactures the mitochondria-relevant activities such as fission, energy metabolism, and mitophagy, and evokes a pathway of ferroptosis, to lead severe cellular damage even death.

采用一步合成法，以喹啉-2-甲醛、卤代苯胺和五羰基溴化锰为原料，合成了3个锰羰基配合物[Mn(CO)₃(quino(CH=N)phX)Br]，其中X=Cl (1)、Br (2)、I (3)。通过核磁共振、单晶X射线衍射、红外光谱及紫外可见光谱等技术对其结构进行了系统表征。研究表明，该系列配合物在避光条件下具有良好的稳定性，而在LED红光(λ=622~770 nm)照射下可快速分解并释放一氧化碳(CO)，展现出低能量光响应特性。动力学研究显示，配合物释放CO过程符合一级动力学模型，且卤素取代基(Cl/Br/I)电子效应对反应速率具有显著调控作用。肌红蛋白实验进一步证实了配合物3在光照下可生成CO气体。生物相容性结果表明，该类配合物对癌细胞表现出显著的细胞毒性(IC₅₀=2~13 μmol·L^-1)。