ABSTRACT
A complete Th(1-x)U(x)(C(2)O(4))(2).2H(2)O solid solution was prepared by mild hydrothermal synthesis from a mixture of hydrochloric solutions containing cations and oxalic acid. The crystal structure has been solved from twinned single crystals for x = 0, 0.5, and 1 with monoclinic symmetry, space group C2/c, leading to unit cell parameters of a approximately 10.5 A, b approximately 8.5 A, and c approximately 9.6 A. The crystal structure consists of a two-dimensional arrangement of actinide centers connected through bis-bidentate oxalate ions forming squares. The actinide metal is coordinated by eight oxygen atoms from four oxalate entities and two water oxygen atoms forming a bicapped square antiprism. The connection between the layers is assumed by hydrogen bonds between the water molecules and the oxygen of oxalate of an adjacent layer. Under these conditions, the unit cell contains two independent oxalate ions. From high-temperature mu-Raman and X-ray diffraction studies, the compounds were found to undergo a transition to an orthorhombic form (space group Ccca). The major differences in the structural arrangement concern the symmetry of uranium, which decreases from C2 to D2, leading to a unique oxalate group. Consequently, the nu(s)(C-O) double band observed in the Raman spectra recorded at room temperature turned into a singlet. This transformation was then used to make the phase transition temperature more precise as a function of the uranium content of the sample.
ABSTRACT
After environmental contamination, U accumulates in the kidneys and in bones, where it causes visible damage. Recent in vitro data prove that the occurrence of citrate increases U bioavailability without changing its speciation. Two hypotheses can explain the role of citrate: it either modifies the U intracellular metabolization pathway, or it acts on the transport of U through cell membrane. To understand which mechanisms lead to increased bioavailability, we studied the speciation of U after accumulation in NRK-52E kidney cells. U speciation was first identified in various exposure media, containing citrate or not, in which U was supplied as U carbonate. The influence of serum proteins was analyzed in order to detect the formation of macromolecular complexes of U. Transmission electron microscopy (TEM) was employed to follow the evolution of the U species distribution among precipitated and soluble forms. Finally, extended X-ray absorption fine structure spectroscopy (EXAFS) enabled the precipitates observed to be identified as U-phosphate. It also demonstrated that the intracellular soluble form of U is U carbonate. These results suggest that citrate does not change U metabolization but rather plays a role in the intracellular accumulation pathway. U speciation inside cells was directly and clearly identified for the first time. These results elucidate the role of U speciation in terms of its bioavailability and consequent health effects.
