Visible Light Driven Nanosecond Bromide Oxidation by a Ru Complex with Subsequent Br-Br Bond Formation.

Visible light excitation of [Ru(deeb)(bpz)2](2+) (deeb = 4,4'-diethylester-2,2'-bipyridine; bpz = 2,2'-bipyrazine), in Br(-) acetone solutions, led to the formation of Br-Br bonds in the form of dibromide, Br2(•-). This light reactivity stores ∼1.65 eV of free energy for milliseconds. Combined (1)H NMR, UV-vis and photoluminescence measurements revealed two distinct mechanisms. The first involves diffusional quenching of the excited state by Br(-) with a rate constant of (8.1 ± 0.1) × 10(10) M(-1) s(-1). At high Br(-) concentrations, an inner-sphere pathway is dominant that involves the association of Br(-), most likely with the 3,3'-H atoms of a bpz ligand, before electron transfer from Br(-) to the excited state, ket = (2.5 ± 0.3) × 10(7) s(-1). In both mechanisms, the direct photoproduct Br(•) subsequently reacts with Br(-) to yield dibromide, Br(•) + Br(-) → Br2(•-). Under pseudo-first-order conditions, this occurs with a rate constant of (1.1 ± 0.4) × 10(10) M(-1) s(-1) that was, within experimental error, the same as that measured when Br(•) were generated with ultraviolet light. Application of Marcus theory to the sensitized reaction provided an estimate of the Br(•) formal reduction potential E(Br(•)/Br(-)) = 1.22 V vs SCE in acetone, which is about 460 mV less positive than the accepted value in H2O. The results demonstrate that Br(-) oxidation by molecular excited states can be rapid and useful for solar energy conversion.

Genotoxic effect of ethacrynic acid and impact of antioxidants.

It is known that ethacrynic acid (EA) decreases the intracellular levels of glutathione. Whether the anticipated oxidative stress affects the structural integrity of DNA is unknown. Therefore, DNA damage was assessed in EA-treated HCT116 cells, and the impact of several antioxidants was also determined. EA caused both concentration-dependent and time-dependent DNA damage that eventually resulted in cell death. Unexpectedly, the DNA damage caused by EA was intensified by either ascorbic acid or trolox. In contrast, EA-induced DNA damage was reduced by N-acetylcysteine and by the iron chelator, deferoxamine. In elucidating the DNA damage, it was determined that EA increased the production of reactive oxygen species, which was inhibited by N-acetylcysteine and deferoxamine but not by ascorbic acid and trolox. Also, EA decreased glutathione levels, which were inhibited by N-acetylcysteine. But, ascorbic acid, trolox, and deferoxamine neither inhibited nor enhanced the capacity of EA to decrease glutathione. Interestingly, the glutathione synthesis inhibitor, buthionine sulfoxime, lowered glutathione to a similar degree as EA, but no noticeable DNA damage was found. Nevertheless, buthionine sulfoxime potentiated the glutathione-lowering effect of EA and intensified the DNA damage caused by EA. Additionally, in examining redox-sensitive stress gene expression, it was found that EA increased HO-1, GADD153, and p21mRNA expression, in association with increased nuclear localization of Nrf-2 and p53 proteins. In contrast to ascorbic acid, trolox, and deferoxamine, N-acetylcysteine suppressed the EA-induced upregulation of GADD153, although not of HO-1. Overall, it is concluded that EA has genotoxic properties that can be amplified by certain antioxidants.

Effect of antioxidants on the genotoxicity of phenethyl isothiocyanate.

Isothiocyanates are plant-derived compounds that may be beneficial in the prevention of certain chronic diseases. Yet, by stimulating the production of reactive oxygen species (ROS), isothiocyanates can be genotoxic. Whether antioxidants influence isothiocyanate-induced genotoxicity is unclear, but this situation was clarified appreciably herein. In HCT116 cells, phenethyl isothiocyanate (PEITC) increased ROS production, which was inhibited by N-acetylcysteine (NAC) and deferoxamine (DFO) but not by ascorbic acid (ASC) and trolox (TRX) that were found to be more potent radical scavengers. Surprisingly, ASC and TRX each intensified the DNA damage that was caused by PEITC, but neither ASC nor TRX by themselves caused any DNA damage. In contrast, NAC and DFO each not only attenuated PEITC-induced DNA damage but also attenuated the antioxidant-intensified, PEITC-induced DNA damage. To determine if the DNA damage could be related to possible changes in the major antioxidant defence system, glutathione (GSH) was investigated. PEITC lowered GSH levels, which was prevented by NAC, whereas ASC, TRX and DFO neither inhibited nor enhanced the GSH-lowering effect of PEITC. The GSH synthesis inhibitor, buthionine sulphoxime, intensified PEITC-induced DNA damage, although by itself buthionine sulphoxime did not directly cause DNA damage. The principal findings suggest that ASC and TRX make PEITC more genotoxic, which might be exploited in killing cancer cells as one approach in killing cancer cells is to extensively damage their DNA so as to initiate apoptosis.

Chloride ion-pairing with Ru(II) polypyridyl compounds in dichloromethane.

Chloride ion-pairing with a series of four dicationic Ru(II) polypyridyl compounds of the general form [Ru(bpy)3-x(deeb)x](PF6)2, where bpy is 2,2'-bipyridine and deeb is 4,4'-diethylester-2,2'-bipyridine, was observed in dichloromethane solution. The heteroleptic compounds [Ru(bpy)2(deeb)](2+) and [Ru(bpy)(deeb)2](2+) were found to be far less sensitive to ligand loss photochemistry than were the homoleptic compounds [Ru(bpy)3](2+) and [Ru(deeb)3](2+) and were thus quantified in most detail. X-ray crystal structure and (1)H NMR analysis showed that, when present, the C-3/C-3' position of bpy was the preferred site for adduct formation with chloride. Ion-pairing was manifest in UV-visible absorption spectral changes observed during titrations with TBACl, where TBA is tetrabutyl ammonium. A modified Benesi-Hildebrand analysis yielded equilibrium constants for ion-pairing that ranged from 13 700 to 64 000 M(-1) and increased with the number of deeb ligands present. A Job plot indicated a 2:1 chloride-to-ruthenium complex ratio in the ion-paired state. The chloride ion was found to decrease both the excited state lifetime and the quantum yield for photoluminescence. Nonlinear Stern-Volmer plots were observed that plateaued at high chloride concentrations. The radiative rate constants decreased and the nonradiative rate constants increased with chloride concentration in a manner consistent with theory for radiative rate constants and the energy gap law. Equilibrium constants for excited state ion-pairing abstracted from such data were found to be significantly larger than that measured for the ground state. Photophysical studies of hydroxide and bromide ion-pairing with [Ru(bpy)2(deeb)](2+) are also reported.

Flash-quench studies on the one-electron reduction of triiodide.

The one-electron reduction of triiodide (I(3)(-)) by a series of reduced ruthenium polypyridyl compounds was studied in an acetonitrile solution at room temperature using the flash-quench technique. Reductive quenching of the metal-to-ligand charge-transfer excited state of [Ru(bpy)(2)(deeb)](2+), [Ru(deeb)(2)(bpy)](2+), or [Ru(deeb)(3)](2+), where bpy is 2,2'-bipyridine and deeb is 4,4'-(CO(2)CH(2)CH(3))(2)-2,2'-bipyridine, by iodide generated the reduced ruthenium compounds and diiodide (I(2)(•-)). Charge recombination of the reduced ruthenium compounds and I(2)(•-) occurred with rate constants near the calculated diffusion limit of 2.6 × 10(10) M(-1) s(-1). The reaction of the reduced ruthenium compounds with I(3)(-) was characterized spectroscopically through the addition of I(3)(-) into the experimental solution prior to the laser flash. Transient absorption data indicated that I(2)(•-) was a reaction product of I(3)(-) reduction and appeared with an average second-order rate constant of (5.0 ± 0.6) × 10(9) M(-1) s(-1) for all three compounds. The insensitivity of the rate constants for I(3)(-) reduction over an 80 meV change in the driving force was unexpected. The relevance of these findings to solar energy conversion within dye-sensitized solar cells is discussed.