Biogeochemical changes induced in uranium mining waste pile samples by uranyl nitrate treatments under anaerobic conditions.

Response of the subsurface soil bacterial community of a uranium mining waste pile to treatments with uranyl nitrate over different periods of time was studied under anaerobic conditions. The fate of the added U(VI) without supplementation with electron donors was investigated as well. By using 16S rRNA gene retrieval, we demonstrated that incubation with uranyl nitrate for 4 weeks resulted in a strong reduction in and even disappearance of some of the most predominant bacterial groups of the original sample. Instead, a strong proliferation of denitrifying and uranium-resistant populations of Rahnella spp. from Gammaproteobacteria and of Firmicutes occurred. After longer incubations for 14 weeks with uranyl nitrate, bacterial diversity increased and populations intrinsic to the untreated samples such as Bacteroidetes and Deltaproteobacteria propagated and replaced the above-mentioned uranium-resistant groups. This indicated that U(VI) was immobilized. Mössbauer spectroscopic analysis revealed an increased Fe(III) reduction by increasing the incubation time from four to 14 weeks. This result signified that Fe(III) was used as an electron acceptor by the bacterial community established at the later stages of the treatment. X-ray absorption spectroscopic analysis demonstrated that no detectable amounts of U(VI) were reduced to U(IV) in the time frames of the performed experiments. The reason for this observation is possibly due to the low level of electron donors in the studied oligotrophic environment. Time-resolved laser-induced fluorescence spectroscopic analysis demonstrated that most of the added U(VI) was bound by organic or inorganic phosphate phases both of biotic origin.

Long-term accumulation of uranium in bones of Wistar rats as a function of intake dosages.

Groups of Wistar rats were fed with ration doped with uranyl nitrate at concentration A ranging from 0.5 to 100 ppm, starting after the weaning period and lasting until the postpuberty period when the animals were sacrificed. Uranium in the ashes of bones was determined by neutron activation analysis. It was found that the uranium concentration in the bones, as a function of A, exhibits a change in its slope at approximately 20 ppm-a probable consequence of the malfunctioning of kidneys. The uranium transfer coefficient was obtained and an analytical expression was fitted into the data, thus allowing extrapolation down to low doses. Internal and localized doses were calculated. Absorbed doses exceeded the critical dose, even for the lowest uranium dosage.

Absorption and biokinetics of U in rats following an oral administration of uranyl nitrate solution.

The absorption of U within the male Wistar rat was determined following oral gavage with uranyl nitrate solutions at seven different dosages. Gavage levels ranged from 0.003 to 45 mg U per kilogram body weight. Uranium tissue burdens were determined at 0.25, 0.5, 1, 2, 4, 8, 24, 48, 96 and 240 h following gavage. Blood, kidney, liver and bone were analyzed for U content using neutron activation followed by delayed neutron counting. Uranium rapidly localized in the kidneys and bone following ingestion. Bone was found to be the primary tissue of deposition. Skeletal and kidney burdens closely paralleled each other from 15 min to 10 d after oral gavage. Uranium burdens in the blood reached a maximum within 30 min but declined rapidly thereafter. Burdens of all tissues were well correlated with each other and with dosage at all dose levels. Equations relating body burdens with blood levels were developed and found to be useful for predicting body burdens for the initial 8 h following gavage. Gastrointestinal absorption (f1) was 0.6-2.8% over the range of U administered. Movement of U through the GI tract was assessed at two dosages. The transit time of U through the GI tract was approximately 48 h. Uranium loss from the stomach was described as a power function of time. The maximum value in the small intestine was attained within 2 h, and thereafter its rapid loss was linear up to 8 h. A minor residual loss component from the small intestine was evident beyond 8 h post-gavage.

Deposition and early disposition of inhaled 233UO2(NO3)2 and 232UO2(NO3)2 in the rat.

Little information exists on the metabolism and potential health effects of 233U and 232U, high-specific-activity U isotopes associated with Th breeder systems. This paper describes the distribution and retention of the two isotopes following inhalation of uranyl nitrate, a simulated process solution. The lungs of rats exposed to 233UO2(NO3)2 and 232UO2(NO3)2 aerosols contained from 7 to 23% of the total amount of U retained in the rat after a 30-min inhalation exposure. Uranium was translocated rapidly from the lung and was retained mainly in skeleton, kidney and liver. Amounts equivalent to from one-quarter to one-half the initial lung burden (ILB) of U were excreted in urine the first day after inhalation. Radiation dose estimates based on 233U and 232U retention kinetics indicate that lung and skeleton would be the target organs for delayed radiation effects.

A comparison of the distributions of the actinides uranium and thorium with the lanthanide gadolinium in the tissues and eggs of Japanese quail: concentrations of uranium in feeds and foods.

Japanese quail were given UCl3 , UO2 (NO3)2, Th(NO3)4, or GdCl3 ( 153Gd -labeled) intravenously in aqueous solution. Distribution of Th among the tissues was as for Gd; distributions of U(III) and U(VI) were markedly different. For example, 18 hr after a 1.5 mumol/100 g dose, accumulations in females were: growing oocytes, U(III) 2.0%, U(VI) 2.4%, Th 27.7%, Gd 44.7%; leg bones, U(III) 12.5%, U(VI) 14.1%, Th 1.2%, Gd 1.4%; liver, U(III) 1.1%, U(VI) 1.1%, Th 44.0%, Gd 40.2%. Whole body losses by 18 hr were: females, U 24%, Th 14%, Gd 4%; males, U 72%, Th 23%, Gd 1%. Cumulative depositions in yolks of eggs laid over 8 days were: U(III) 1.9%, U(VI) 1.7%, Th 57.3%, Gd 46.8%. The distribution of U in quail may be atypical of actinides . Concentrations of U in various feeds, foods, and mineral supplements ranged from 169 micrograms/g in a phosphate fertilizer for farm use to below the lower detectable limit of .01 microgram/g in many foods intended for human use. Two batches of the game bird laying ration supplied to the quail colony contained 3.05 and 4.42 micrograms U/g. Body burdens of 3.5 micrograms U/bird for noninjected quail were attributed to the U content of this feed.

The behaviour of uranium-233 oxide and uranyl-233 nitrate in rats.

233UO2 and 233UO2(NO3)2 in aqueous suspension have been administered to rats by pulmonary intubation. The 233U associated with the fraction of the 233UO2 less than 4 nm in diameter translocates from lungs to blood at the same rapid rate as 233U from 233UO2(NO3)2. Identical reactions with blood plasma and lung fluid were observed whether the 233U was administered as less than 4 nm 233UO2 particles or 233UO2(NO3)2. It is suggested that oxidation of UO2 to UO3 occurs followed by the formation of uranyl ion. In blood plasma, approximately 50 per cent of the 233U is bound to transferrin, 25 per cent to citrate and 25 per cent on bicarbonate.

Influence of uranyl nitrate upon tubular reabsorption and glomerular filtration in blood perfused isolated dog kidneys.

The early changes in tubular reabsorption, glomerular filtration, blood flow and sodium excretion brought about by uranyl nitrate were investigated in isolated, blood-perfused dog kidneys during water diuresis. No significant changes in urine volume were observed; the decrease in fluid reabsorption was counterbalanced quantitatively by a reduction in glomerular filtration rate; only a small diminution of renal blood flow was found. The balance between reabsorption and filtration was observed as well when angiotensin action or prostaglandin synthesis were inhibited. The intrarenal venous pressure rose, suggesting that an increase in proximal intratubular hydrostatic pressure caused the decrease in filtration. Tubular back-leak of fluid, or back-diffusion, induced by the toxin, were excluded. The presence of natriuretic compounds in the urine was confirmed.

[The reaction of the insect excretory tissue to a heavy metal: uranyl nitrate (author's transl)]. / Réaction du tissu excréteur d'un insecte à un métal lourd: le nitrate d'uranyle.

The present paper describes the modifications induced in Malpighian tubules of Locusta migratoria by uranyl nitrate. These modifications are observed only if doses injected are approximately a hundred times higher than those which affect the renal epithelium of Vertebrates. The elimination of the uranyl salts seem to occur by apical excretion of dense metallo-proteic granules. When strong doses are used, metallic particles are seen on the basal membrane and in the extracellular spaces. Such intracytoplasmic particles are rarely observed.