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Diiron Hexacarbonyl Complex Induces Site-SpecificRelease of Carbon Monoxide in Cancer Cells Triggered by EndogenousGlutathione

机译:Diiron六羰基配合物诱导特定位点一氧化碳在内源性触发的癌细胞中的释放谷胱甘肽

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摘要

In this study, we have evaluated a water-soluble, nontarget reagent and a carrier-free diiron hexacarbonyl complex, [Fe2{μ-SCH2CH(OH)CH2(OH)}2(CO)6] (>TG-FeCORM), that can induce the site-specific release of carbon monoxide (CO) in cancer cells triggered by endogenous glutathione (GSH). The releasing rate of CO was dependent on the amount of endogenous GSH. Being the amount of endogenous GSH higher in cancer cells than in normal cells, the CO-releasing rate resulted faster in cancer cells. Moreover, the anti-inflammatory properties related to the intracellular CO release of >TG-FeCORM were also confirmed in the living HeLa cells.
机译:在这项研究中,我们评估了水溶性非目标试剂和无载体的二铁六羰基二铁配合物[Fe2 {μ-SCH2CH(OH)CH2(OH)} 2(CO)6](> TG-FeCORM ),可以诱导内源性谷胱甘肽(GSH)触发癌细胞中一氧化碳(CO)的定点释放。 CO的释放速率取决于内源性GSH的量。由于癌细胞中内源性GSH的含量高于正常细胞,因此CO释放速率导致癌细胞中的CO释放速率更快。此外,在活着的HeLa细胞中也证实了与> TG-FeCORM 的细胞内CO释放有关的抗炎特性。

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