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At least 91 records · Page 5Linked to original sources
PubMed2000

Magnetic-octupole order in neptunium dioxide?

The phase transition occurring at 25 K in NpO2, discovered almost 50 years ago, is the most long-lasting mystery in the physics of actinide compounds. Theories based on magnetic or electric-quadrupole order lead inevitably to fundamental, qualitative inconsistencies with observations. We show that the phenomenology of NpO2 can be understood if the order parameter is assumed to be a magnetic octupole of gamma(2) ( xyz) symmetry. NpO2 is the first compound for which indications of an octupolar phase transition have been found.

Journal Article↗
PubMed1995

Intranuclear sites of Np 237 in mammalian cells: a study using electron microscopy and electron probe microanalysis.

Two methods, electron microscopy and wavelength dispersive electron probe microanalysis, were used to determine the intracellular sites and chemical form of concentrations of neptunium nitrate 237 after chronic intoxication by the intraperitoneal route in two organs in the rat known to concentrate this element (kidney, liver). Abnormal intranuclear formations in the form of clusters of dense granules containing neptunium, phosphorus, sulphur, and calcium were found in the nuclei of kidney proximal tubule cells and hepatocytes. These formations had a maximum diameter of the order of 2 microns and were located in the central part of the nucleus, away from the nucleolus and peripheral chromatin. Serious nuclear and cytoplasmic ultrastructural lesions are often associated in cells containing neptunium inclusions. The absorbed doses in the kidney and the liver were very low. A relationship between these abnormal intranuclear structures and the carcinogenic effect of neptunium remains to be clarified. This effect is related more probably to the chemical toxicity of Np 237.

Animals↗
PubMed1996

Intranuclear dense bodies after metal intoxication: a review of ultrastructural and microanalytical findings.

Abnormal intranuclear dense bodies are observed in several varieties of cells after intoxication by four varieties of metals: lead, bismuth, beryllium and neptumium. These inclusions have been studied by two microanalytical methods: Electron probe X-ray microanalysis (EPMA) and ion microscopy. A strong similarity has been observed in the ultrastructure of the dense bodies produced several weeks after beryllium and neptunium intoxication although there exists an important discrepancy between both elements concerning their physical, chemical and physico-chemical characteristics. Furthermore, these dense bodies are observed in the same varieties of cells (tubular proximal cells of kidneys, hepatocytes, pneumocytes). Intranuclear dense bodies produced by lead are also observed in the same types of cells, where they showed similar ultrastructure patterns as beryllium and neptunium inclusions but only after a long period, several years, after a chronic intoxication. The ultrastructure of the dense bodies produced by bismuth are clearly distinct from beryllium, neptunium or lead inclusions. Beryllium, neptunium and lead have been detected by EPMA or ion microscopy in the corresponding dense bodies although the real presence of bismuth remains to be confirmed in the nuclear dense bodies produced by this element.

Animals↗
PubMed1999

Chemical toxicity of some actinides and lanthanides towards alveolar macrophages: an in vitro study.

PURPOSE: To compare the toxicity of lanthanides (cerium, gadolinium) with actinides (thorium, neptunium, uranium) added in soluble form to rat alveolar macrophage cultures. MATERIALS AND METHODS: The metals were added 1 day after seeding alveolar macrophages extracted by pulmonary lavage, and the metal toxicity was scored 3 days later. Cell death was measured after vital staining to distinguish between apoptosis and necrosis; relative cell density was also quantified. The physico-chemical form of the metals in the culture medium was characterized using filtration and radioactive measurements. RESULTS: Except for thorium, induction of cell death was observed for all the elements studied and the death mechanism involved was apoptosis. Graduated toxicity was observed from uranium to neptunium, cerium and gadolinium, in the range of concentration from 10(-3)-10(-6) M. From pilot experiments, it was hypothesized that soluble compounds were mainly involved in lanthanide toxicity, whereas insoluble forms were mainly involved in actinide toxicity. CONCLUSION: This study demonstrates that the toxicity of neptunium and uranium was concomitant with the presence of insoluble forms in the culture medium. Further studies are needed to characterize the cell death mechanisms involved and the potential synergistic effects of chemical toxicity and irradiation.

Actinoid Series Elements↗
PubMed2004

Comparative study on Tp53 gene mutations in lung tumors from rats exposed to 239Pu, 237Np and 222Rn.

The tumor suppressor gene Tp53 was analyzed by polymerase chain reaction-amplification of genomic DNA extracted from paraffin-embedded tissue sections of rat lung tumors to compare mutations that occurred after inhalation exposures to plutonium dioxide, neptunium dioxide, or radon and radon progenies. Exons 5 to 8 of the gene were amplified in 16 plutonium-, 23 neptunium- and 15 radon-induced lung tumors, and their polymerase chain reaction products were examined for mutations by single strand conformational polymorphism analysis and direct sequencing method. Two point mutations were detected in the plutonium-induced tumors, i.e., a guanine to adenine transition at codon 219 of exon 6 and a cytosine to thymine transition at codon 266 of exon 8. Although only one point mutation was found at codon 175 of exon 5 (cytosine to thymine transition) from neptunium-induced tumors, no mutations were detectable from radon-induced tumors. These results indicate that the abnormalities of the Tp53 gene might not be so critical for the pulmonary carcinogenesis after the inhalation of different alpha emitters, even though the presence and frequencies of the Tp53 gene mutations were different.

Administration, Inhalation↗
PubMed1998

237Np: oxidation state in vivo and chelation by multidentate catecholate and hydroxypyridinonate ligands.

Chemically, 237Np(V) is as toxic as U(VI), and radiologically, about as toxic as 239Pu. Depending on redox conditions in vivo, 237Np exists as weakly complexing Np(V) (NpO2+) or as Np(IV), which forms complexes as stable as those of Pu(IV). Ten multidentate catecholate (CAM) and hydroxypyridinonate (HOPO) ligands with great affinity for Pu(IV) were compared with CaNa3-DTPA for in vivo chelation of 237Np. Mice were injected intravenously with 237NpO2Cl: those in a kinetic study were killed 1 to 2880 min; in ligand studies, fed mice were injected intraperitoneally with a ligand 5, 60, or 1440 min after 237Np(V) (molar ratio 5.6 to 73), mice fasted for 16 h were gastrically intubated with a ligand 3 min after 237Np(V) (molar ratio 5.6 to 274), and all were killed 24 h after ligand administration; tissues and excreta were radioanalyzed. Rapid plasma clearance and urinary excretion of 237Np(V) resemble U(VI); deposition and early retention in skeleton and liver resemble Pu(IV). The x-ray absorption near edge structure spectroscopy (XANES) spectra of femora of 237Np(V)-injected mice, compared with spectra of Np(V) and Np(IV) from reference solids, showed predominantly Np(IV). Significant in vivo 237Np chelation was obtained with all of the HOPO and CAM ligands injected at molar ratio 22; the HOPO ligands reduced 237Np in skeleton, liver, and other soft tissue, on average, to 72, 25, and 25% of control, respectively, while CaNa3-DTPA was ineffective. Two HOPO ligands injected 60 min after 237Np (molar ratio 5.6) significantly reduced body and liver 237Np, and three HOPO ligands given orally (molar ratio > or = 73) significantly reduced body and liver 237Np, compared with controls. Combined with earlier work, these results indicate that: the dominant neptunium species circulating and excreted in urine is Np(V), while that in bone and liver deposits is Np(IV); Np(V) must be reduced to Np(IV) before it can be stably chelated; efficient decorporation of neptunium requires multidentate ligands that form exceptionally stable actinide(IV) chelates and facilitate Np(V) reduction.

Administration, Oral↗