AI Article Synopsis
- Electrophilic iron(II)-clathrochelates show notable cytotoxicity in human promyelocytic leukemia cells, with an IC50 value of 6.5±4.6μM.
- The treatment leads to a dramatic increase in intracellular oxidative stress, evidenced by a 17-fold rise compared to control cells.
- The mechanism behind this cytotoxicity appears to involve alkylation of glutathione, disrupting the cellular antioxidative system and catalyzing the production of reactive oxygen species.
Article Abstract
We observed that electrophilic iron(II)-clathrochelates exhibit significant cytotoxicity in human promyelocytic leukemia cells (IC50=6.5±4.6μM), which correlates with the enhancement of intracellular oxidative stress (17-fold increase with respect to the cells treated with the solvent only). Based on in vitro studies we suggested that this effect is caused by alkylation of glutathione leading to inhibition of the cellular antioxidative system and by catalytic generation of reactive oxygen species by products of the alkylation reaction.
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| http://dx.doi.org/10.1016/j.bmcl.2015.11.060 | DOI Listing |
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