Changes in sleep-wake cycle after chronic exposure to uranium in rats

Uranium is a heavy metal known to induce toxicity in kidneys. It is also known to enter the central nervous system, thus inducing neurophysiological effects, after exposure to relatively high concentrations. The effect of chronic uranium exposure (40 mg l^− 1 in drinking water, for 90 days) on electroencephalographic architecture has been studied on freely moving rats using a telemetry technique. The main effects of uranium on the sleep–wake cycle were an increase in rapid eye movement sleep (REM-sleep) and theta band power during the light period, as early as Day 30 after exposure commenced. The most probable explanation for these effects is that uranium directly affects the brain. This increase in REM-sleep was previously described in human depression or models of chronically stressed rats and it may be assimilated with some protective or compensatory mechanisms.     

The Role of Chelation in the Treatment of Other Metal Poisonings

These proceedings will review the role of chelation in five metals—aluminum, cadmium, chromium, cobalt, and uranium—in order to illustrate various chelation concepts. The process of “chelation” can often be oversimplified, leading to incorrect assumptions and risking patient harm. For chelation to be effective, two critical assumptions must be fulfilled: the presumed “metal toxicity” must correlate with a given body or a particular compartment burden, and reducing this compartmental or the body burden (through chelation) attenuates toxicity. Fulfilling these assumptions requires an established dose–response relationship, a validated, reproducible means of toxicity assessment (clinical, biochemical, or radiographical), and an appropriate assessment mechanisms of body or compartment burden. While a metal might “technically” be capable of chelation (and readily demonstrable in urine or feces), this is an insufficient endpoint. Clinical relevance must be affirmed. Deferoxamine is an accepted chelator for appropriately documented aluminum toxicity. There is a very minimal treatment window in order to address chelation in cadmium toxicity. In acute toxicity, while no definitive chelation benefit is described, succimer (DMSA), diethylenetriaminepentaacetate (DTPA), and potentially ethylenediaminetetraacetic acid (EDTA) have been considered. In chronic toxicity, chelation is unsupported. There is little evidence to suggest that currently available chromium chelators are efficacious. Similarly, scant human evidence exists with which to provide recommendation for cobalt chelation. DTPA has been recommended for cobalt radionuclide chelation, although DMSA, EDTA, and N-acetylcysteine have also been suggested. DTPA is unsupported for uranium chelation. Sodium bicarbonate is currently recommended, although animal evidence is conflicting.     

饮用水水源地水中总铀浓度监测结果分析

目的 调查各种类型饮用水水源地水样中的总铀含量，分析饮用水水源地水体中总铀浓度、摄入量及其所致年待积有效剂量，为辐射环境安全监管提供科学依据。方法 通过现场采样，采用激光荧光法分析水中铀浓度，统计2010—2018年饮用水水源地水样总铀含量，计算年摄入量和年待积有效剂量。结果 监测分析结果显示，2010—2018年饮用水水源地水中总铀浓度为0.09～4.50 μg/L，所致公众总铀年摄入量儿童和成人的最大值分别为62.58 Bq、125.16 Bq，对应的年待积有效剂量分别为4.63 μSv、6.13 μSv，符合公众年待积有效剂量限值要求。结论 近岸海水的总铀浓度相对较高，湖库水和地下水的总铀含量较低且保持稳定，近海口的地表水总铀浓度有时偏高，可能是受潮汐影响。考虑公众影响，应制定铀元素的浓度限值标准。     

贫铀在土壤中迁移的实验室模型改进

目的 完善贫铀(DU)迁移的实验室模型,验证所建模型的可靠性。方法 对已建立的实验室模拟贫铀在土壤中的迁移的模型进行改进,采用分层取样,利用ICP-MS同时测量各层土样中铀含量及²³⁵U/²³⁸U值,根据测量值确定DU迁移深度。结果 对照组DU迁移到9~11cm,pH=4.0和pH=3.0的模拟酸雨使DU分别迁移到29cm及35cm以外;我国铀模拟实验舱周围、法国贫铀试验场、科索沃战场DU迁移深度分别为大于25cm、30cm、10cm~20cm。结论 酸雨可以促进贫铀的迁移;用改进的实验室模型模拟DU在土壤中的迁移,所得的迁移深度基本上与现实情况一致,说明模型的设计基本是成功的。     

Challenge assay: A functional biomarker for exposure-induced DNA repair deficiency and for risk of cancer

A variety of biomarkers have been used to monitor exposed populations to determine potential health hazards from their exposure to environmental toxic agents. However, the majority of these biomarkers have been focused onto the identification of biological damage from the exposure. Therefore, there is a need to develop functional biomarkers that can identify exposure-induced functional deficiencies. More importantly, these deficiencies should be positioned along pathways that are responsible for the development of specific diseases. One of such pathways belongs to the extensive and complex DNA-repair machinery. The machinery thus becomes a large target for damage from environmental toxic agents. The hypothesis is that damage to any component of a repair pathway will interfere with the pathway-specific repair activities. Therefore, when cells from exposed populations are challenged with a DNA-damaging agent in vitro, the in vivo exposure-induced repair deficiency will be dramatically amplified and the deficiency will be detectable in a challenge assay as increased chromosome aberrations, micronuclei or un-repaired DNA strand breaks. The challenge assay has been used in different laboratories to show that a variety of exposed populations (with exposure to air pollutants, arsenic, benzene, butadiene, cigarette smoke, incense smoke, lead, mercury, pesticides, uranium or xylene but not to low concentrations of air pollutants or butadiene) expressed abnormal challenge response. The predicted health consequences of some of these studies have also been validated. Therefore, the challenge assay is a useful functional biomarker for population studies. Details of the challenge assay and its application will be presented in this review.     

核电站周边地表水中铀的同位素丰度分析

目的 掌握核电站周边地区地表水中铀同位素丰度比值基线数据.方法 采集江苏、山东、浙江省境内3个核电站周边地区供饮用的地表水,利用磷酸三丁酯(TBP)萃淋树脂分离富集铀,电感耦合等离子体质谱(ICP-MS)法分析样品中的234 U/238U与235 U/238U的丰度比.结果 地表水中234 U/238U丰度比范围为4.575×10-5 ～7.752×10-5,235 U/238U丰度比范围为7.273 ×10-3～7.639×10-3.结论 地表水中234U被不同程度地富集.     

Major histopathological patterns of lung cancer related to arsenic exposure in German uranium miners

Objective  The mechanisms of action of arsenic in the development of lung cancer are still not yet elucidated. Considering the relationship between arsenic and squamous cell carcinomas of the skin, we hypothesized that arsenic exposure may be more closely associated with squamous cell carcinoma of the lung. Methods  A comprehensive histopathological database and a detailed job-exposure matrix developed for former German uranium miners with exposure to arsenic, radon, and quartz were analyzed to quantitatively assess the effect of arsenic regarding cell type of lung cancer. The distributions of major lung cancer cell types in 1,786 German uranium miners were associated with levels of arsenic exposure under control for the other lung carcinogens. To evaluate the arsenic effects in association with a frequent occupational lung disease in miners stratification by silicosis was performed. Results  There was an arsenic-related increase of the proportion of squamous cell carcinoma of the lung but restricted to miners without silicosis. The increase was found at all levels of co-exposure to radon and quartz dust. In miners with silicosis, the proportion of adenocarcinoma increased with rising arsenic exposure. Arsenic exposure was associated with non-small cell lung cancer. Silicosis turned out as major determinant of the cell type related with arsenic. Conclusion  These results indicate a cell type characteristic effect of arsenic in the development of lung cancer.     

螯合剂与金属硫蛋白对铀的竞争结合作用

目的 通过探讨螯合剂与金属硫蛋白（MT）竞争结合铀（U）（VI）的作用,建立铀促排螯合剂体外筛选的新方法。方法 采用竞争ELISA法,96孔酶标板经MT抗原包被、U（VI）或Zn²⁺预处理、螯合剂（CBMIDA-CaNa₂、BPCBG和DTPA-CaNa₃）处理、MT抗体免疫结合、HRP偶联二抗结合及OPD显色反应后,在波长490 nm处检测吸光度值以评价螯合剂与MT竞争结合U（VI）、Zn²⁺的能力。结果 本反应体系的吸光度值随MT质量浓度和MT抗体浓度增加而增加,其中最佳MT抗原包被浓度和MT抗体浓度均为2 μg/mL。与Zn²⁺的作用相似,U（VI）亦可使反应体系的吸光度值随其浓度增加而降低,其中最佳U（VI）和Zn²⁺浓度均为300 μg/mL。加入CBMIDA-CaNa₂和BPCBG则能明显提高U（VI）处理体系的吸光度值,CBMIDA-CaNa₂的作用强于BPCBG,而DTPA-CaNa₃则无明显作用;各螯合剂与MT竞争结合U（VI）能力的强弱顺序与以往细胞和动物U（VI）促排实验的结果相吻合。这3种螯合剂对Zn²⁺处理体系的吸光度值均无明显影响。结论 CBMIDA-CaNa₂和BPCBG能有效竞争结合于MT上的U（VI）,DTPA-CaNa₃无明显作用,竞争ELISA法可作为体外筛选U（VI）促排螯合剂的方法,具有简便、快速和高通量的优势。     

Uranium induces apoptosis in lung epithelial cells

Uranium is a naturally occurring radioactive material present everywhere in the environment. It is toxic because of its chemical or radioactive properties. Uranium enters environment mainly from mines and industry and cause threat to human health by accumulating in lungs as a result of inhalation. In our previous study, we have shown the effectiveness of antioxidant system response to the oxidative stress induced by uranyl acetate (UA) in rat lung epithelial (LE) cells. As part of our continuing studies; here, we investigated the mechanism underlying when LE cells are exposed to different concentration of UA. Oxidative stress may lead to apoptotic signaling pathways. LE cells treated with 0.25, 0.5 and 1 mM of UA results in dose and time-dependent increase in activity of both caspases-3 and -8. Increase in the concentration of cytochrome-c oxidase in cytosol was seen in LE cells treated with 1 mM UA as a result of mitochondria membrane permeability. The cytochrome-c leakage may trigger the apoptotic pathway. TUNEL assay performed in LE cells treated with 1 mM of UA showed significant incorporation of dNTPs in the nucleus after 24 h. In the presence of the caspase inhibitors, we observed the significant decrease in the activity of caspases-8 and -3 in 0.5 and 1 mM UA-treated LE cells.     

Intake of Po,U and U radionuclides with wine in Italy

²³⁸U, ²³⁴U and ²¹⁰Po activity concentration was determined in 70 samples of red and white wine coming from 16 Italian regions. The radionuclides were determined by alpha spectrometry after separation. The results show that the mean concentrations of ²³⁸U, ²³⁴U and ²¹⁰Po were 3.63 × 10⁻³ ± 2.19 × 10⁻³, 4.41 × 10⁻³ ± 3.10 × 10⁻³ and 6.85 × 10⁻² ± 3.79 × 10⁻² Bq L⁻¹ for red wine and 5.08 × 10⁻³ ± 4.20 × 10⁻³, 5.59 × 10⁻³ ± 8.49 × 10⁻³ and 3.92 × 10⁻² ± 2.63 × 10⁻² Bq L⁻¹ for white wine, respectively. The effective radiation dose due to the uranium and polonium ingestions by wine (0.5 l per day) ranges from 2.68 × 10⁻⁴ to 4.91 × 10⁻² mSv year⁻¹.