Fluorescence yields and lifetimes of solutions of europium and terbium salts in solution are greatly enhanced by using deuterated solvents. The magnitude of increase varies from an 18-fold enhancement in yield and lifetime for an aqueous solution of europium nitrate to a twofold enhancement for europium ethylenediaminetetra-acetate dissolved in methanol. The enhancement is proportional to the fraction of deuterated solvent present. Results lead to conclusions that the dominant mode of radiationless deactivation of a rare-earth ion in solution is via loss of energy to hydrogen vibrations. Further, such loss is proportional to the number of hydrogen vibrations in the local rare-earth environment. Values for the rate constant for radiationless loss of energy to hydrogen vibrations are determined for the salts studied. The influence upon radiationless processes of complexing between the rare earth and anion is discussed. Likewise the dependence of the enhancement factor upon the rare-earth ion is considered. There is no evidence that the lifetime from the 5D1 level of europium nitrate is enhanced by deuterium substitution. This lifetime is ≤5 μsec in both D2O and H2O solutions.
Fluorescence yields of solutions of several chelates of europium and terbium have been measured: (a) upon excitation in the ligand absorption bands and (b) upon selective excitation to individual upper levels of the rare-earth ion. Yields with upper-ion-level excitation are lower than when the emitting level is excited directly and yields with ligand excitation are lower still. Efficiencies of energy transfer to the emitting level from upper ion levels and from the ligands, for the solutions studied, are calculated from the data.
The fluorescence yield observed when the emitting level is excited directly, together with the fluorescence lifetime, allows both radiative and radiationless rate constants for deactivation of the emitting level to be calculated. The enhanced fluorescence yields of chelates compared to unchelated rare-earth ions are found to be due primarily to the enhancement of the radiative transition by the chelate environment rather than to a protective influence against quenching provided by the ligands.
For terbium chelates the strong temperature dependence of the fluorescence intensity is explained in terms of quenching of the emitting level via thermal excitation to the lowest triplet state of the ligand. This is indicated by the agreement between the activation energy for quenching and the energy difference between the emitting level and the triplet state.
A method has been developed using the intensities of delayed fluorescence and of phosphorescence of coronene which permits calculation of the rate constant for crossing to S1 from isoenergetic triplet levels (ke') as well as the S1-T1 gap. For these calculations, measurements of the fluorescence yield and the temperature dependence of both the phosphorescence lifetime and the ratio of delayed fluorescence to phosphorescence were made using poly(methy1 methacrylate) specimens containing coronene-h12 and coronene-dl2. The calculated S1-T1 gap of 3930 cm-l agrees with the value obtained from the 0,O bands of the fluorescence and phosphorescence spectra. Values of ks' of coronene-d12 and coronene-h12 are equal to within the experimental error and are similar to k3, the rate constant for the reverse. intersystem crossing from S1 to TI. The delayed fluorescence accounts for only a small fraction of the total radiationless deactivation of triplet coronene. The temperature-dependent part of the rate constant for deactivation of triplet coronene is larger for ordinary coronene than for deuterated coronene.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.