低剂量辐射对铀矿工健康潜在的影响

目的 探讨低剂量辐射对铀矿工人健康的损害作用。 方法 把某铀矿的工作人员按工种是否接触辐射有害因素,同时考虑年龄、性别的构成分为暴露组81人和对照组81人,对两组人员的血象学、肝肾功能、脂质学及甲状腺功能、微核检出率等指标进行检测并分析其差异。 结果 暴露组与对照组白细胞(white blood cell,WBC)、红细胞(red blood cell,RBC)、血红蛋白(hemoglobin,Hb)、血小板(platelet,PLT)、中性粒细胞百分比、淋巴细胞百分比、谷丙转氨酶(alanine aminotransferase,ALT)、谷草转氨酶(aspartate aminotransferase,AST)、总蛋白(total protein,TP)、尿酸(uric acid,UA)、胆固醇(cholesterol,CH)、甘油三脂(triglyceride,TG)、高密度脂蛋白(high-density lipoprotein cholesterol,HDL-C)、低密度脂蛋白(low-density lipoprotein cholesterol,LDL-C)等的异常率之间差异无统计学意义(P＞0.05),总胆红素(total bilirubin,TBIL)(38.27% vs.22.22%)、间接胆红素(indirect bilirubin,IBIL)(38.27% vs.22.22%)差异有统计学意义(χ²=4.945,P=0.040),血清游离三碘原氨酸(serum free triiodothyronine,FT3)(51.85% vs.34.57%)差异有统计学意义(χ²=4.930,P=0.039),血清游离甲状腺素(serum free thyroxine, FT4)、血清促甲状腺激素(serum thyroid stimulating hormone,TSH)差异无统计学意义(P＞0.05);暴露组微核检出率为96.29%。 结论 低剂量辐射对铀矿工可产生肝功能、甲状腺功能损害和DNA损伤。     

螯合剂BPCBG对铀的促排效果和防护铀致人肾小管上皮细胞损伤的作用

从动物和细胞水平观察螯合剂N,N'-1,2-亚乙基双[N-(2,3-二羟基苯甲基)]甘氨酸(BPCBG)对铀的促排效果,以及对铀致人肾近曲小管上皮细胞(HK-2)损伤的保护作用。大鼠腹腔注射(ip)醋酸铀酰后立即肌内注射(im)不同剂量的BPCBG,采用ICP-MS方法测定24 h的尿铀排出量和肾、骨中铀蓄积量。人肾近曲小管上皮HK-2细胞染铀24 h后给予不同剂量的BPCBG作用24 h,采用ICP-MS方法检测细胞内铀含量。不同剂量醋酸铀酰染毒HK-2细胞后立即或延迟24 h给予BPCBG作用24或48 h,采用CCK-8试剂盒检测细胞存活率,采用CB微核法观察BPCBG对铀致染色体损伤的影响,采用DCFH-DA荧光探针法检测BPCBG对铀诱导细胞内氧自由基生成的影响。以上实验均以DTPA-CaNa3作对照。结果表明,BPCBG(60、120和600μmol.kg-1)使24 h尿铀排出量较铀中毒对照组明显增加约37%～61%,肾、骨中铀蓄积量降低至中毒对照组的41%～31%和86%～42%,促排效果随给药剂量增加而明显增强。HK-2细胞铀染毒后延迟24 h给予10～250μmol.L-1 BPCBG作用...     

丰富环境对脑梗死大鼠缺血侧海马区血管内皮生长因子受体的影响

目的 研究丰富环境对大鼠局灶性脑梗死后缺血侧海马区血管内皮生长因子(VEGF)受体的影响.方法 采用开颅电凝法制作SD大鼠右侧大脑中动脉缺血(MCAO)模型.术后24h随机分为丰富环境(EE)组和标准环境(SE)组.以免疫组织化学法检测缺血侧海马区VEGF受体Flt-1及Flk-1的表达.结果 大鼠大脑中动脉闭塞后,Flt-1和Flk-1在缺血侧海马区表达明显增加,经丰富环境干预后,Flt-1和Flk-1表达大量增加,与SE组相比有显著性意义.结论 丰富环境可促使海马区VEGF受体表达上调.进而促进该区微血管新生,有利于脑损伤修复.

Abstract：

Objective To evaluate the effect of enriched environment on vascular endothelial growth factor receptor (VEGFR)expression in hippocampus of rats after unilateral local cerebral infarction.Methods The,4sat middle cerebral artery occlusion (MCAO)wag performed with electric coagulation in SD rata,then the animals were randomly divided into a enriched environment stimulation group(EE group)and a control group(standard environment stimulation group,SE group).The expression of VEGFR-1(Flt-1)and VEGFR-2(Flk-1)in hippocampus gone of brain infarction were measured at 1,3,7,14,28d after operation.Results After MCAO operation,the expression of Flt-1 and Flk-1 in hippocampus of rats in EE group was significantly hisher than that in SE group at all time points.Conclusions Enriched environment stimulation can increase the expression of VEGFR in hippocampus of rats.It can promote the blood vessel proliferation and reeovery in hippocampus of rats after unilateral local cerebral infarction.     

Renal dysfunction induced by long-term exposure to depleted uranium in rats

Depleted uranium (DU) is a kind of radioactive heavy metal which can enter into the body via inhalation (aerosols), ingestion (drinking and eating) and wounds (embedded), and causes chemical and/or radiation-induced toxicities. In this study, male Sprague Dawley rats were surgically implanted in gastrocnemius muscle with DU fragments at three dose levels (low-dose, medium-dose and high-dose), with biologically inert tantalum (Ta) fragments served as controls. At 1 day, 7 days, and 3, 6, and 12 months after implantation, the rats were euthanized and tissue samples were collected, and uranium levels were measured in a variety of tissues by inductively coupled plasma-mass spectrometry (ICP-MS) to analyze the dynamic changes and distribution of uranium in rats. Thereafter, at 3, 6 and 12 months after implantation, the rats were euthanized after the collection of 24 h urine, blood and kidney samples were collected for analysis of DU-induced renal histopathologic changes and renal dysfunction. It was observed that DU concentrations in all the DU implanted groups were higher than that in Ta control group, and DU concentrations in the kidney increased with the implanted times, peaked at the 90 days after implantation, with a high correlation to the implanted DU doses, and then began to decrease gradually and slowly, and the DU concentrations in kidney still maintained at a relatively high level even at the 360 days after implantation. Otherwise, chronic DU contamination could induce the pathological changes of renal glomeruli, tubules and mesenchyme, such as interstitial fibrosis, enlarged interstice of renal tubular epithelial cells, tumefactions and necrosis of epithelial cells, shrinkage and disappearance of cavity of Bowman’s capsule. By TEM, it was shown that the basement membrane of glomerulus was incrassated, mitochondrial of kidney proximal tubule had visible tumefaction and became bigger, and the mitochondrial cristae became shorter and disorderly in alignment. Compared to the control group, it was found that there was significant increase in the DU implantation group in terms of their blood urea nitrogen (BUN) and serum creatinine, urinary β2-microglobulin (β2-MG) and albumin, with a high correlation to the implanted DU dosage and periods. It was concluded that DU could accumulate in kidneys for a long period, and causes kidney injury by the toxic chemical/radioactive action such as renal dysfunction and structural damage.     

丰富环境可改善慢性脑低灌注的认知功能

目的慢性脑低灌注(chronic cerebral hypoperfusion,CCH)可导致认知功能的损害。丰富环境(enrich edenvironment,EE)可通过改善突触可塑性而提高学习和记忆能力。到目前为止EE对CCH所导致的认知功能损害的影响还不明确。为了进一步研究EE对CCH认知功能损害的影响,本科进行了EE对CCH所导致的认知功能损害和突触可塑性影响的研究。方法健康成年雄性Wistar大鼠被随机分为3组:假手术组(sham组),CCH组和CCH+EE干预组。检测各组大鼠的空间学习记忆能力,海马CA1区的长时程增强(long-term potentiation,LTP)、输入-输出关系曲线和双脉冲异化(paired-pulse facilitation,PPF)以及突触相关蛋白的表达水平变化。结果①EE干预可改善CCH所导致的大鼠空间学习记忆功能的损害。②与假手术组比较(195.5%±11.2%),CCH组大鼠的LTP发生显著的下降(128.6%±6.8%,P<0.01)。给予EE干预的CCH大鼠(176.4%±9.4%)LTP出现明显的增加(P<0.01)。③假手术组与CCH组的输入-输出关系曲线和PPF无明显差别(P>0.05)。当给予EE干预后也无显著性差异(P>0.05)。④CCH组大鼠的磷酸化环磷酸腺苷反应元件结合蛋白(phosphorylated cAMP responsive element binding protein,pCREB)的表达与假手术组比较下降了47%(P<0.01),而CCH+EE组的pCREB的表达是CCH组的177%(P<0.01)。对于CCH大鼠的突触素和微管相关蛋白-2(microtubule-associated protein2,MAP-2)的表达与假手术组比较分别减少了23%和29%(分别为P<0.05和P<0.01)。经过EE干预后CCH+EE组的突触素和MAP-2的表达与CCH组比较分别增加了31%和60%(分别为P<0.05和P<0.01)。结论 EE可改善CCH所导致的空间学习记忆功能和突触可塑性的损害,但不影响其基础传递效率和突触前的递质释放的概率。EE对CCH认知功能的改善可能源于其对突触后蛋白的调节起作用。     

Effects of Nitrogen Dioxide on Elastin and Collagen Contents of Lung

Male Syrian hamsters were exposed to 30 5 ppm nitrogen dioxide for 22 hr daily for 3 wk. Nitrogen dioxide-exposed hamsters sacrificed at various times during the 3 wk exposure showed a general loss of body weight and an increased dry lung weight when compared with the controls, which were housed in a similar, but nitrogen dioxide-free environment. Analysis of total lung collagen and total lung elastin revealed a net decrease in the moieties within 4 and 10 days, respectively, following commencement of nitrogen dioxide exposure. Total lung collagen returned toward pre-exposure levels by the 14th day of nitrogen dioxide exposure. Total lung elastin did not return toward normal until termination of nitrogen dioxide exposure. Recovery in room air for 3 wk following 21 days of nitrogen dioxide exposure restored the total pulmonary collagen and elastin to values similar to the control groups. These data suggest that the dynamics of elastin and collagen degradation and synthesis differ during and after nitrogen dioxide exposure. Lung collagen loss was observed earlier and was restored to normal values during the continuation of nitrogen dioxide exposure. Lung elastin loss occurred later and persisted during the entire period of exposure but returned to normal after exposure was terminated.     

不同取片方式对植入贫铀片大鼠组织铀浓度的影响

目的取出嵌入的贫铀弹片后,其周围组织中仍有高浓度的贫铀污染,研究何种取片方法能最低限度减轻这种污染,对减轻机体损伤有重要意义.方法动物麻醉状态下手术植入贫铀片,10 d后以各种不同的方法取出,分为常规手术组、术前4%碳酸氢钠去污组、创口去污组、更换手术器械组、剪去周围组织组和综合法组,在取片后第7、14、21天收集组织样本,测定铀含量.结果以常规手术组组织铀含量最高,术前去污组、切口去污组和更换器械组次之,剪去周围组织铀含量下降较大,综合组最低.结论综合应用各种方法实行手术,即术前4%碳酸氢钠去污 切口去污 更换器械 剪去周围组织效果最好,可大大减少铀吸收.     

浓缩铀诱发人白血病细胞凋亡及相关基因调控研究

目的　研究浓缩铀诱发人白血病HL 6 0细胞凋亡的损伤特征及对凋亡相关基因bcl 2和bax的调控作用。方法　研究受浓缩铀内照射不同时间诱发HL 6 0细胞凋亡的DNA凝胶电泳。运用免疫组织化学技术探讨浓缩铀对HL 6 0细胞bcl 2 bax的蛋白表达 ,以及RNA分子杂交技术探讨浓缩铀对HL 6 0细胞bcl 2mRNA的转录水平表达。结果　在浓缩铀作用下 ,HL 6 0细胞的DNA呈现出在核小体间断裂的阶梯状条带形成的凋亡特征 ;并且观察到对照HL 6 0细胞中bcl 2蛋白呈高度表达 ,为 (88± 7) % ,而受浓缩铀辐照后 ,可下调至 (6 1± 5 ) %。bax在对照细胞中的表达很低 ,在浓缩铀作用下 ,未见明显改变。而且受浓缩铀辐照后 ,可使HL 6 0细胞中bcl 2mRNA表达呈明显下调。结论　浓缩铀可诱发HL 6 0细胞凋亡发生 ,其诱发凋亡的程度随浓缩铀作用时间的延长而增加。并且发现浓缩铀诱发人白血病HL 6 0细胞的凋亡作用 ,与其下调凋亡相关基因bcl 2的表达相关联。     

Cholinergic system, rearing environment and trajectory learning during aging in mice

Three, 12- and 20-month-old C57BL6/J mice, reared in standard conditions or in enriched environments, were administered subcutaneously either scopolamine hydrobromide, 0.6 or 1.2 mg kg(-1), or physiological saline (control mice) 15 min before testing their abilities to find an invisible platform in a modified version of the Morris water maze, the starting point being kept unchanged throughout the experiment to allow the aged animals to solve the task. The results demonstrated that: 1) All control mice, whatever their age, were able to learn the platform location, but the number of trials needed to reach the learning criterion (3 consecutive trials in less than 8 s) increased with age; 2) All the scopolamine-treated mice, whatever their age, were also able to learn the platform location. However, compared to age-matched controls, the number of trials needed to reach the learning criterion was greater; 3) Rearing the animals in an enriched environment antagonized the effect of scopolamine, but only in the youngest (3 month-old) mice. All control and scopolamine-treated mice, whatever their age and their rearing environment, remembered, 7 days later, the platform location.     

Biological effects of alpha particle radiation exposure on human monocytic cells

Radon ((222)Rn) gas produces decay progeny that emits high energy alpha (α)-particles. Epidemiological studies have shown that exposure to (222)Rn is linked with elevated risk of developing lung cancer, however clear mechanisms leading to such effects have not been delineated. Cytokines play a critical role in inflammation and their dysregulated production often contributes to disease pathogenesis. In this study, Bio-plex multiplex technology was employed to investigate modulations of 27 pro-inflammatory cytokines following exposure of human monocytic cells to 1.5 Gy of α-particle radiation. Concurrently, DNA damage was assessed by examining the formation of phosphorylated H2A histone family X (γ-H2AX) sites. Of the 27 cytokines assessed, 4 cytokines were shown to be statistically downregulated by ～2 fold relative to the untreated controls and included the interleukin (IL) family of proteins (IL-2, IL-15 and IL-17) and macrophage inflammatory protein 1 beta (MIP-1b). Interferon-inducible protein-12 (IP-12), vascular endothelial growth factor and regulated on activation normal T cell expressed and secreted (RANTES) were shown to be high expressors and upregulated. Cells irradiated with α-particles ranging from 0.27 to 2.14 Gy showed statistically significant, dose-dependant increases in γ-H2AX formation. These data suggest that α-particle radiation causes dysregulation in the production of a number of pro-inflammatory cytokines and results in significant DNA damage.