铁死亡是由细胞环境中的氧化还原失衡引起的细胞死亡过程。然而，细胞死亡通路被证明在抗癌治疗中有益，因此正在寻找诱导铁死亡的化合物。本论文介绍了一种新合成的铁络合物FeT，由亚铁氰酸盐和酒石酸组成，似乎满足这些期望。它相对稳定，易溶于水，能过氧化不饱和脂肪酸。模型细胞采用T24膀胱细胞。初步研究证明，该化合物对细胞增殖具有强烈的抑制作用。评估了FeT的细胞毒性。独立地，它启动了caspase活性，表明该化合物具有复杂的细胞影响。这种效果是由于FeT渗透进入细胞内部，可能直接损伤线粒体，从而解释了凋亡参与细胞死亡的原因。同时，在渗透进入细胞后，它引起活性氧自由基（ROS）的增加，脂质过氧化和还原型谷胱甘肽的降低，被解释为引起铁死亡的原因。反过来，降低线粒体电势可能表明铁死亡和内部途径的凋亡。

Ferroptosis is a cell death process caused by redox imbalance in the cell environment. However, the cell death pathway proves beneficial in anticancer therapy, so compounds inducing ferroptosis are sought. The paper presents a newly synthesized iron complex named FeT, composed of ferricyanide and tartrate, which seems to meet these expectations. It is relatively stable, easily soluble in water and capable of peroxidating unsaturated fatty acids. T24 bladder cells were used as model cells. Preliminary studies demonstrated a strong inhibitory effect of this compound on cell proliferation. The cytotoxicity of FeT was assessed. Independently, it initiates caspase activity, indicating the complex cellular impact of this compound. This effect is compellingly the result of FeT penetration into the cell's interior with possible direct damage to mitochondria, thus explaining the involvement of apoptosis in cell death. At the same time, after penetrating into the cell, it causes an increase in reactive oxygen species (ROS), lipid peroxidation and a decrease in reduced glutathione, which is interpreted as to cause ferroptosis. In turn, reducing mitochondrial potential may indicate both ferroptosis and an internal pathway to apoptosis.