Photoactivation is a promising approach for modulating the biological activity of RuII compounds. In this work, RuII flavonolato compounds, [Ru(η6-p-cymene)(L)(3-Hfl)]OTf (8; 3-Hfl = monoanion of 3-hydroxyflavone; L = solvent) and [Ru(η6-p-cymene)Cl(3-Hfl-X)] (3a–3c; 3-Hfl-X = p-H, -Cl, or -F on the flavonolato phenyl substituent), have been evaluated for photoinduced reactivity within the flavonolato unit upon irradiation with UV (300 nm) or visible (419 nm) light under aerobic conditions. For each compound, irradiation in CH3CN was found to result in the loss of the p-cymene ligand and the formation of products resulting from oxidative ring opening of the flavonolato ligand in a dioxygenase-type reaction. This reaction also results in the release of carbon monoxide. The RuII products generated in these reactions are [RuII(solvent)(carboxylato)]+ and [Ru(CO)(solvent)(carboxylato)]+ (carboxylato = O-benzoylsalicylato or benzoato) species, as determined by ESI-MS. The amount of free CO generated depends on the wavelength of irradiation, with 300 nm light giving a higher amount of free CO. Evaluation of the photoinduced reactivity of 8 in DMSO/H2O (10:90) at 300 nm showed similar reactivity to that found in organic solvent, although the reaction occurs more slowly. The products of the photoreactions of 8 and 3a at 419 nm are nontoxic toward human T-lymphocyte (Jurkat) and non-small-cell lung carcinoma (A549) cells. This lack of toxicity versus the starting compounds is likely due to differences in interactions of the [RuII(solvent)(carboxylato)]+ and [RuII(CO)(solvent)(carboxylato)]+ species with biomolecules (e.g., serum proteins), thus resulting in reduced bioavailabilty. 1H NMR studies provide evidence that the photoreaction products coordinate to biologically relevant donors such as histidine and 5′-GMP in d 6-DMSO/D2O (10:90) and exhibit reactivity with these small molecules that is distinctly different from that exhibited by the starting compounds. Overall, the photoreactivity of 8 and 3a–3c may represent an approach toward altering the biological chemistry of these compounds.

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Aliphatic oxidative carbon-carbon bond cleavage reactions involving Cu(II) catalysts and O2 as the terminal oxidant are of significant current interest. However, little is currently known regarding how the nature of the Cu(II) catalyst, including the anions present, influence the reaction with O2. In previous work, we found that exposure of the Cu(II) chlorodiketonate complex [(6-Ph2TPA)Cu(PhC(O)CClC(O)Ph)]ClO4 (1) to O2 results in oxidative aliphatic carbon-carbon bond cleavage within the diketonate unit, leading to the formation of benzoic acid, benzoic anhydride, benzil, and 1,3-diphenylpropanedione as organic products. Kinetic studies of this reaction revealed a slow induction phase followed by a rapid decay of the absorption features of 1. Notably, the induction phase is not present when the reaction is performed in the presence of a catalytic amount of chloride anion. In the studies presented herein, a combination of spectroscopic (UV-vis, EPR) and density functional theory (DFT) methods have been used to examine the chloride and benzoate ion binding properties of 1 under anaerobic conditions. These studies provide evidence that each anion coordinates in an axial position of the Cu(II) center. DFT studies reveal that the presence of the anion in the Cu(II) coordination sphere decreases the barrier for O2 activation and the formation of a Cu(II)-peroxo species. Notably, the chloride anion more effectively lowers the barrier associated with O-O bond cleavage. Thus, the nature of the anion plays an important role in determining the rate of reaction of the diketonate complex with O2. The same type of anion effects were observed in the O2 reactivity of the simple Cu(II)-bipyridine complex [(bpy)Cu(PhC(O)C(Cl)C(O)Ph)ClO4] (3).