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Published November 11, 2008 | Accepted Version
Journal Article Open

Mechanism of cellular uptake of a ruthenium polypyridyl complex


Transition metal complexes provide a promising avenue for the design of therapeutic and diagnostic agents, but the limited understanding of their cellular uptake is a roadblock to their effective application. Here, we examine the mechanism of cellular entry of a luminescent ruthenium(II) polypyridyl complex, Ru(DIP)2dppz2+ (where DIP = 4,7-diphenyl-1,10-phenanthroline and dppz = dipyridophenazine), into HeLa cells, with the extent of uptake measured by flow cytometry. No diminution of cellular uptake is observed under metabolic inhibition with deoxyglucose and oligomycin, indicating an energy-independent mode of entry. The presence of organic cation transporter inhibitors also does not significantly alter uptake. However, the cellular internalization of Ru(DIP)2dppz2+ is sensitive to the membrane potential. Uptake decreases when cells are depolarized with high potassium buffer and increases when cells are hyperpolarized with valinomycin. These results support passive diffusion of Ru(DIP)2dppz2+ into the cell.

Additional Information

© 2008 American Chemical Society. Received May 9, 2008; Revised manuscript received September 4, 2008. We are grateful to the Caltech Flow Cytometry Facility for expert assistance and facilities. Financial support for this work from the National Institutes of Health (Grant GM33309 to J.K.B.) is acknowledged.

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