Thimerosal in childhood vaccines contributes to accumulating mercury toxicity in the kidney

Mercury (Hg) is a hazardous chemical that accumulates in many cells and tissues, thereby producing toxicity. The kidney is a key target organ for Hg accumulation and toxicity. The contributing factors to Hg accumulation in humans include: (1) elemental and inorganic Hg exposure, often occurring by inhalation of Hg vapors; (2) exposure to methyl Hg (meHg), for example, through contaminated seafood; and (3) exposure to ethyl mercury (etHg) via thimerosal-containing vaccines. Systematic investigations on the toxic effects of etHg/thimerosal on the nervous system were carried out, and etHg/thimerosal emerged as a possible risk factor for autism and other neurodevelopmental disorders. There is, however, little known about the mechanisms and molecular interactions underlying toxicity of etHg/thimerosal in the kidney, which is the focus of the current review. Susceptible populations such as infants, pregnant women, and the elderly are exposed to etHg through thimerosal-containing vaccines, and in-depth study of the potential adverse effects on the kidney is needed. In general, toxicity occurring in association with different forms of Hg is related to: intracellular thiol metabolism and oxidative stress reactions; mitochondrial function; intracellular distribution and build-up of calcium; apoptosis; expression of stress proteins; and also interaction with the cytoskeleton. Available evidence for the etHg-induced toxicity in the kidney was examined, and the main mechanisms and molecular interactions of cytotoxicity of etHg/thimerosal exposure in kidney described. Such accumulating knowledge may help to indicate molecular pathways that, if modulated, may better handle Hg-mediated toxicity.     

Left-sided gastroschisis and bilateral multicystic dysplastic kidneys: a rare combination of anomalies

Left-sided gastroschisis is very rare. We report a case of left-sided gastroschisis associated with bilateral multicystic dysplastic kidneys. This combination of anomalies is unknown. The pathogenesis of gastroschisis is not well understood. It is now viewed as a malformation rather than disruption. The findings in this case support this view. The combination of dysplastic kidneys with ventral body wall defect suggests an early developmental defect. Copyright © 2007 John Wiley & Sons, Ltd.     

3种增塑剂单独和联合暴露对MCF-7细胞增殖的影响

为了探究结构差异较大、应用较为广泛的几类增塑剂雌激素活性的联合效应,选择邻苯二甲酸二丁酯(DBP)、双酚A(BPA)和壬基酚(NP)作为邻苯二甲酸酯、双酚A类和烷基酚类增塑剂的代表物进行试验.用DBP、BPA和NP单独及两两混合处理MCF-7细胞.采用MTT法检测培养24h、48 h、72 h和96h时的细胞增殖情况.采用流式细胞术检测药物培养48h后的细胞生长周期分布,并计算细胞增殖指数(PI).运用效应叠加模型(ES)判定联合效应类型.结果表明,在单独暴露试验中,DBP、BPA和NP组PI均大于1,且均能提高S期(DNA合成期)细胞比例.因此,DBP、BPA和NP均能显著促进MCF-7细胞增殖.混合暴露试验中,1)DBP和BPA在MTT试验中24h、48h、72 h和96h时的效应叠加指数(ESI)分别为1.013 9、1.023 8、0.9999、1.010 8,在流式细胞仪试验中ESI为1.014 1.因此,DBP和BPA的雌激素活性联合效应为加和作用.2)DBP和NP在MTT试验中24 h、48 h、72 h和96 h时的ESI分别为1.004 0、1.008 6、1.011 5、1.010 3,流式细胞仪试验中ESI为0.997 0.因此,DBP和NP的雌激素活性联合效应为加和作用.3)BAP和NP在MTT试验中24h、48 h、72 h和96h时的ESI分别为0.980 6、0.981 8、0.977 7、0.973 3,流式细胞仪试验的ESI为0.912 8.由此可知,BPA和NP的雌激素活性联合效应为拮抗作用.因此,可以采用MCF-7细胞增殖试验研究环境污染物雌激素活性联合效应.     

鄱阳湖悬浮颗粒物絮凝沉降典型藻类的动力学研究

为了探讨鄱阳湖水动力条件改变引起的悬浮颗粒物浓度变化可能导致的鄱阳湖浮游植物群落结构的变化,本文研究了鄱阳湖悬浮颗粒物絮凝沉降3种典型藻类的动力学过程.以铜绿微囊藻(蓝藻)、四尾栅藻(绿藻)和菱形藻(硅藻)为研究对象、鄱阳湖采集沉积物为悬浮颗粒物,使用混凝试验搅拌仪模拟动力学条件,在颗粒物投加量为20 mg·L-1时分别研究了静置沉降时间、扰动强度和扰动时间对颗粒物絮凝沉降藻细胞的影响.结果表明,絮凝沉降效率:蓝藻绿藻硅藻.在扰动强度为20 s-1、扰动时间为30 min时,0.5~4 h静置沉降时间均促进3种藻类的絮凝沉降.绿藻和硅藻的絮凝沉降效率随着静置沉降时间的延长而降低,前0.5 h的絮凝沉降效率最大;而蓝藻的絮凝沉降效率变化无明显规律.扰动时间和静置沉降时间均为30 min时,随着扰动强度在2~40 s-1增加时,3种藻的絮凝沉降效率逐渐增大.扰动强度为20 s-1、静置沉降时间为30 min时,5~60 min扰动时间均促进藻细胞的絮凝沉降,并且随着扰动时间的增加,絮凝沉降效率呈先增大后降低的趋势.30 min为蓝藻絮凝沉降的最佳扰动时间,絮凝沉降效率为12.56%;45 min为绿藻和硅藻絮凝沉降的最佳扰动时间,絮凝沉降效率分别为11.93%和7.54%.因此,水动力条件的改变可以引起悬浮颗粒物与藻类的絮凝沉降效率发生变化,从而对藻类的群落结构以及水华发生规律产生影响.     

检测细胞DNA断裂损伤效应的彗星实验法的改良

为了解决彗星实验过程中常出现的脱胶、细胞核分离操作繁琐、重复性低等问题,对彗星实验方法进行了改良,初步建立了彗星实验的快速操作流程。结果显示,通过对载玻片进行预处理,可确保凝胶悬挂均匀;采用改良机械法分离的细胞核浓度适中;以0.5%(w/v)涂层琼脂糖作为基层、以1.5%(w/v)低熔点包埋琼脂糖作为叠加层的"双层凝胶法",辅以"推片法"铺胶,操作便捷且不发生脱胶现象;细胞核膜经裂解处理后再进行电泳和荧光观察,彗星图像清晰,杂质少。应用改良后的彗星实验方法,操作简便,耗时更短,实验效果良好,可快速检测出细胞DNA损伤效应。     

Se-Ca联合膳食干预缓解Cd诱导小鼠肝肾毒性

为探究Se-Ca联合膳食干预对生物Cd中毒的缓解效果,选取88只BALB/c小鼠,随机划分为19组,在相同饲料Cd暴露浓度下(2mg/kg)分别设置低、中、高浓度的Se和Ca单独和联合膳食干预处理,并观察30d后小鼠的生长发育、肝肾功能、氧化应激状态和组织病理变化.结果显示,Se-Ca联合干预可有效缓解Cd蓄积所致小鼠生长发育迟缓现象,且进一步促进小鼠生长;肝肾功能及氧化应激指标测定结果表明,Se-Ca联合干预对Cd暴露下小鼠肝脏AST、GSH、SOD、GSH-Px和肾脏BUN、MDA、SOD的保护效果优于单一元素干预;联合干预仅需较小剂量即可达到单独Se或Ca干预对肝肾病理损伤的最佳缓解效果.Se-Ca联合膳食干预可有效缓解Cd摄入导致的生长发育缓慢和肝肾毒性,且较之单一元素的干预效果更佳.     

代森锰及其代谢物的神经毒性影响与机制研究

以SH-SY5Y和PC12细胞为实验模型,深入探讨了代森锰(Maneb)及其代谢产物对多巴胺能神经细胞的毒性影响与机制.结果表明,Maneb的有机部分和金属离子成分单独暴露不具有明显的毒性作用,联合暴露具有协同效应,且对细胞活性的抑制程度与同一浓度水平的Maneb相当,其原因与诱导活性氧自由基生成、细胞凋亡相关.此外,蛋白免疫印迹法发现,Maneb下调Bcl-2的表达、上调Bax、细胞色素C的水平,同时激活Caspase-3,提示线粒体凋亡途径在Maneb诱导多巴胺能神经细胞凋亡过程中的重要作用.