小剂量8102对大鼠急性铀中毒的促排效果

研究８１０２不同剂量和连续给药对大鼠急性铀中毒的促排效果。大鼠中毒硝酸铀酰（５００μｇ／鼠）后给予不同剂量８１０２（０～１００ｍｇ／ｋｇ），测定尿铀排出量及肾铀蓄积量。结果：大鼠肌肉注射８１０２及灌胃给予８１０２促排轴的最小有效剂量分别为５ｍｇ／ｋｇ和２０ｍｇ／ｋｇ；８１０２连续给药与一次性给药相比未见尿铀排出量的显著增高和肾铀蓄积量的显著降低。８１０２是一个很有希望的铀促排螯合剂，值得进一步深入研究。     

Toxicity of uranium, molybdenum, nickel, and arsenic to Hyalella azteca and Chironomus dilutus in water-only and spiked-sediment toxicity tests

A series of laboratory spiked-sediment toxicity tests with the amphipod Hyalella azteca and the midge Chironomus dilutus were undertaken to determine acute and chronic toxicity thresholds for uranium (U), molybdenum (Mo), nickel (Ni), and arsenic (As) based on both whole-sediment (total) and pore water exposure concentrations. Water-only toxicity data were also generated from separate experiments to determine the toxicities of these metals/metalloids under our test conditions and to help evaluate the hypothesis that pore water metal concentrations are better correlated with sediment toxicity to benthic organisms than whole-sediment metal concentrations. The relative toxicity of the four elements tested differed depending on which test species was used and whether whole-sediment or pore water metal concentrations were correlated with effects. Based on measured whole-sediment concentrations, Ni and As were the two most acutely toxic elements to H. azteca with 10-d LC50s of 521 and 532 mg/kg d.w., respectively. Measured pore water concentrations indicated that U and Ni were the two most acutely toxic elements, with 10-d LC50s to H. azteca of 2.15 and 2.05 mg/L, respectively. Based on pore water metal concentrations, the no-observed-effect concentrations (NOECs) for growth were (H. azteca and C. dilutus, respectively) 0.67 and 0.21 mg/L for U, <0.37 and 0.60 mg/L for Ni, and 16.43 and <0.42 mg/L for As. Pore-water lowest-observed-effect concentrations (LOECs) for growth were (H. azteca and C. dilutus, respectively) 2.99 and 0.48 mg/L for U, 0.37 and 2.33 mg/L for Ni, and 58.99 and 0.42 mg/L for As. For U and Ni, results from 96-h water-only acute toxicity tests correlated well with pore water metal concentrations in acutely toxic metal-spiked sediment. This was not true for As where metalloid concentrations in overlying water (diffusion from sediment) may have contributed to toxicity. The lowest whole-sediment LOEC reported here for As was 6.6- and 4-fold higher than the Canadian Council of Ministers of the Environment interim sediment quality guideline and the Canadian Nuclear Safety Commission (CNSC) lowest effect level (LEL), respectively. The lowest whole-sediment LOECs reported here for Ni, U and Mo were 4-, 17.5-, and >260-fold higher, respectively, than the CNSC LELs for these metals/metalloids. Data on pore water metal concentrations in toxic sediment would be a useful addition to future Guidelines documents.     

Neurological effects of acute uranium exposure with and without stress

Circulating uranium rapidly enters the brain and may cause adverse effects on the nervous system that are potentially modulated by stress. In this study, the neurological effects of a single intramuscular injection of 0, 0.1, 0.3, or 1 mg uranium/kg (as uranyl acetate, UA) in rats were examined in the presence and absence of stress. Treatment with UA produced time and dose-dependent increases in serum and regional brain uranium levels. While serum levels returned to control levels by day 30, brain levels remained elevated. Application of stress did not affect the distribution or retention of uranium. Exposure to 1 mg U/kg significantly decreased ambulatory activity, weight gain, forelimb grip strength and transiently impaired working memory. Effects on grip strength and memory were prevented by application of stress prior to uranium exposure. Striatal dopamine content was reduced by 30% 3 days after treatment with 1mg/kg (59+/-6 nmol/mg tissue versus 41+/-5 nmol/mg tissue), but levels returned to control 7 days after uranium exposure. The effect on dopamine was ameliorated by prior application of stress. Exposure to UA did not alter 3,4 dihydroxyphenylacetic acid (DOPAC) levels or numbers of D2 receptors in the striatum. No effect of uranium or stress was observed on levels of GABA, serotonin, norepinephrine, or glutathione (GSH) in the striatum, hippocampus, cerebellum, or cortex. These results indicate that single intramuscular exposures to uranium produce sustained elevation of brain uranium levels and at doses above 0.3 mg/kg can have adverse neurological effects. Application of stress prior to uranium administration modulates neurological effects, but the mechanism is not due to effects on uranium distribution. Uranium exposure also produced renal toxicity which must be considered to accurately assess the effects of uranium on neurological function.     

Uranium induces oxidative stress in lung epithelial cells

Uranium compounds are widely used in the nuclear fuel cycle, antitank weapons, tank armor, and also as a pigment to color ceramics and glass. Effective management of waste uranium compounds is necessary to prevent exposure to avoid adverse health effects on the population. Health risks associated with uranium exposure includes kidney disease and respiratory disorders. In addition, several published results have shown uranium or depleted uranium causes DNA damage, mutagenicity, cancer and neurological defects. In the current study, uranium toxicity was evaluated in rat lung epithelial cells. The study shows uranium induces significant oxidative stress in rat lung epithelial cells followed by concomitant decrease in the antioxidant potential of the cells. Treatment with uranium to rat lung epithelial cells also decreased cell proliferation after 72 h in culture. The decrease in cell proliferation was attributed to loss of total glutathione and superoxide dismutase in the presence of uranium. Thus the results indicate the ineffectiveness of antioxidant system’s response to the oxidative stress induced by uranium in the cells.     

螯合剂BPCBG对急性铀中毒大鼠的促排效果及肾损伤的保护作用

目的 探讨螯合剂BPCBG对急性铀中毒大鼠促排作用的量-效和时,效关系以及对铀致肾损伤的保护作用.方法 Sprague-Dawley( SD)雄性大鼠按随机数字表法分为正常对照组、铀中毒组、不同剂量BPCBG组和DTPA-CaNa3组.给药组大鼠于腹腔注射醋酸铀酰(100μg/只)后,立即分别肌肉注射60、120和600μmol/kg BPCBG及120和600μmol/kg DTPA-CaNa3,或于注射醋酸铀酰前0.5和2h、铀中毒后0、0.5、1及2h肌肉注射120 μmol/kg BPCBG,铀中毒组于注射醋酸铀酰后立即注射等体积生理盐水,正常对照组仅注射生理盐水.采用ICP-MS方法检测24 h尿铀排出量和肾、骨中铀蓄积量.大鼠注射醋酸铀酰(500 μg/只)后立即注射600 μmol/kg BPCBG和1200 μmol/kg DTPA-CaNa3,48 h后检测血清肌酐(SCR)与尿素氮(BUN)含量,取一侧肾脏做肾组织病理切片观察.结果 铀中毒后立即注射不同剂量BPCBG(60、120和600 μmoL/kg)使24h尿铀排出量比铀中毒组增加(t =2.22、4.43、5,80,P＜0.05),肾和骨铀蓄积量下降(t.3.33、5.59、4.53,P＜0.01和t=2.15、8.70、9.10,P＜0.05),随给药剂量增加促排效果明显提高.提前0.5h或延迟0.5和1h给予BPCBG,仍有较好的排铀效果(与铀中毒组比较,尿铀排出量:提前0.5 h t=4.34,延迟0.5 ht=3.35,P＜0.05;肾铀蓄积量:t=5.75、7.74、5.87,P＜005:骨铀蓄积量:t=6.43、5.22、2.60,P＜0.05),但随铀中毒和给药间隔时间的延长而下降.BPCBG立即给药能明显减轻铀中毒致肾脏的病理损伤,使SCR及BUN含量降低至正常对照组水平,对铀致肾功能损伤具有保护作用.DTPA-CaNa3虽然能明显降低大鼠肾铀蓄积量(与铀中毒组相比,120和600-μmol/kg,t =2.28、3.35,P＜0.05),但未能显著增加尿铀排出量,骨铀蓄积量还有增加趋势,并且对铀致大鼠肾损伤无保护作用.结论 BPCBG对急性铀中毒大鼠有良好的促排效果与肾脏保护作用,有可能成为一种新型铀促排螯合剂.     

Effets de la contamination chronique à l’uranium sur la mortalité : bilan d’une étude-pilote chez les travailleurs de l’industrie nucléaire en France

BackgroundThis article presents the mortality data compiled among a cohort of workers at risk of internal uranium exposure and discusses the extent to which this exposure might differentiate them from other nuclear workers.MethodsThe cohort consisted of 2897 Areva-NC-Pierrelatte plant workers, followed from 1st January 1968 through 31st December 2006 (79,892 person-years). Mortality was compared with that of the French population, by calculating Standardized Mortality Ratios (SMR) and 95 % confidence intervals (CI_95 %). External radiation exposure was reconstructed using external dosimetry archives. Internal uranium exposure was assessed using a plant-specific job-exposure-matrix, considering six types of uranium compounds according to their nature (natural and reprocessed uranium [RPU] and solubility [fast-F, moderate-M, and slow-S]). Exposure-effect analyses were performed for causes of death known to be related to external radiation exposure (all cancers and circulatory system diseases) and cancer of uranium target-organs (lung and hematopoietic and lymphatic tissues, HLT).ResultsA significant deficit of mortality from all causes (SMR = 0.58; CI_95 % [0.53–0.63]), all cancers (SMR = 0.72; CI_95 % [0.63–0.82]) and smoking related cancers was observed. Non-significant 30 %-higher increase of mortality was observed for cancer of pleura (SMR = 2.32; CI_95 % [0.75–5.41]), rectum and HLT, notably non-Hodgkin's lymphoma (SMR = 1.38; CI_95 % [0.63–2.61]) and chronic lymphoid leukemia (SMR = 2.36; CI_95 % [0.64–6.03]). No exposure-effect relationship was found with external radiation cumulative dose. A significant exposure-effect relationship was observed for slowly soluble uranium, particularly RPU, which was associated with an increase in mortality risk reaching 8 to 16 % per unit of cumulative exposure score and 10 to 15 % per year of exposure duration.ConclusionThe Areva-NC-Pierrelatte workers cohort presents a non-significant over-mortality from HLT cancers, notably of lymphoid origin, unrelated to external radiation exposure. The pilot study suggests an association between mortality from the HLT and lung cancers and exposure to slowly soluble RPU compounds. The results of this study should be investigated further in more powerful studies, with a dose-response analysis based on individual assessment of uranium absorbed dose to uranium-target organs.     

Determination of uranium in aqueous attenuating samples using gamma-ray spectrometry

In the present work, a method for determination of uranium concentration in aqueous solution in standard geometry from attenuating samples has been developed based on modification of the empirical approach of Venkataraman and Croft [2003. Determination of plutonium mass using gamma-ray spectrometry. Nucl. Instrum. Methods Phys. Res. A 505, 527–530]. The method makes use of the multiple gamma (γ)-rays emitted by ²³⁵U and depends on the empirical relation between apparent mass of the sample and γ-ray energy. It was possible to determine uranium concentration in the range of 12–400 mg/ml rapidly by this method without applying transmission corrections.     

铀促排药物研究Ⅵ．2，3－二羟基－5－甲氧羰基苄基胺羧酸酯的合成

铀促排药物研究Ⅵ．２，３－二羟基－５－甲氧羰基苄基胺羧酸酯的合成陈文致，谢毓元（中国科学院上海药物研究所，上海２０００３１）铀化合物侵入人体可导致肾脏损伤［１］，含铀粉尘在肺部沉积可引发肺癌［２］．对铀的防护和解毒药物的研究，已引起药学工作者的关注，...     

Studies on separation and purification of fission 99Mo from neutron activated uranium aluminum alloy

A new method has been developed for separation and purification of fission ⁹⁹Mo from neutron activated uranium–aluminum alloy. Alkali dissolution of the irradiated target (100 mg) results in aluminum along with ⁹⁹Mo and a few fission products passing into solution, while most of the fission products, activation products and uranium remain undissolved. Subsequent purification steps involve precipitation of aluminum as Al(OH)₃, iodine as AgI/AgIO₃ and molybdenum as Mo-α-benzoin oxime. Ruthenium is separated by volatilization as RuO₄ and final purification of ⁹⁹Mo was carried out using anion exchange method. The radiochemical yield of fission ⁹⁹Mo was found to be >80% and the purity of the product was in conformity with the international pharmacopoeia standards.     

International responses to the threat of nuclear smuggling from Russia*

In both Russia and the United States there is increasing awareness of the security problem left after the Cold War by former Soviet military nuclear establishments, compounded by the severe difficulties of the Russian economy. Attempts are underway to provide American and other assistance for improving security and transparency; halting the production of highly‐enriched uranium and plutonium; and disposing of the large surplus stocks of these weapon materials.