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Diiron Hexacarbonyl Complex Induces Site-Specific Release of Carbon Monoxide in Cancer Cells Triggered by Endogenous Glutathione

[Image: see text] In this study, we have evaluated a water-soluble, nontarget reagent and a carrier-free diiron hexacarbonyl complex, [Fe(2){μ-SCH(2)CH(OH)CH(2)(OH)}(2)(CO)(6)] (TG-FeCORM), that can induce the site-specific release of carbon monoxide (CO) in cancer cells triggered by endogenous glut...

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Detalles Bibliográficos
Autores principales: Gao, Cunji, Liang, Xiaohua, Guo, Zhengxi, Jiang, Bang-Ping, Liu, Xiaoming, Shen, Xing-Can
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Chemical Society 2018
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6044757/
https://www.ncbi.nlm.nih.gov/pubmed/30023846
http://dx.doi.org/10.1021/acsomega.8b00052
Descripción
Sumario:[Image: see text] In this study, we have evaluated a water-soluble, nontarget reagent and a carrier-free diiron hexacarbonyl complex, [Fe(2){μ-SCH(2)CH(OH)CH(2)(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.