The lipophilic vs. hydrophilic properties of three protic ruthenium compounds were studied as a function of pH. Specifically, we measured Log(Do/w) values for [(N,N)2Ru(6,6'-dhbp)]2+ complexes (where N,N = 2,2'-bipyridine (1A), 1,10-phenanthroline (2A), 2,3-dihydro-[1,4]dioxino[2,3-f][1,10]phenanthroline (3A) and 6,6'-dhbp is the diprotic 6,6'-dihydroxy-2,2'-bipyridine ligand) from pH 4.0 to 8.0. This study allowed us to demonstrate that as the ligand is deprotonated at higher pH values the resulting neutral charge on the complex improves its lipophilic properties. Thus, improved uptake by passive diffusion is expected with protic ligands on Ru(II). Furthermore, cellular studies have demonstrated that passive diffusion is the dominant pathway for cellular uptake. However, metabolic inhibition has also shown that energy dependent efflux reduces the amount of the ruthenium complex (as measured by mean fluorescence intensity) in the cells. These compounds have been shown by fluorescence microscopy to accumulate in the nuclei of cancer cells (MCF7, MDA-MB-231, and HeLa). Taken together, this data shows that uptake is required for toxicity but uptake alone is not sufficient. The greatest light activated toxicity appears to occur in breast cancer cell lines with relatively moderate uptake (MCF7 and MDA-MB-231) rather than the cell line with the greatest uptake of complex 3A (normal breast cell line MCF-10A).