高铅血症对儿童神经行为功能影响的研究进展

铅是神经毒性为主的重金属元素,对中枢和周围神经系统均有明显而肯定的损害作用.儿童的神经系统正处于快速生长和成熟时期,比成人对铅的毒性更为敏感,铅的神经毒性作用往往在明显的临床表现出现之前的亚临床阶段即能危及儿童的认知和神经行为功能[1].     

铅的神经发育毒性研究进展

铅是具有神经毒性的重金属元素，能影响神经系统的多种功能，发育中的神经系统对铅尤为敏感。铅可对血脑屏障、神经元及神经胶质细胞发育过程产生神经毒性作用，干扰各种细胞发育，扰乱神经信号传导等关键因素产生神经毒性作用。     

沈阳市苏家屯区儿童血铅含量检测分析

人体中血铅含量过高,会引起许多器官系统功能紊乱,更为严重的是铅对中枢神经系统的毒性作用不可逆转,即使在极低的铅暴露水平下,不产生神经毒性作用,也可能产生免疫毒性.     

研究金属毒物神经毒性应注意的问题

多种金属具有神经毒作用,最具代表性而且研究最多的是铅、锰、汞和铝.锰是体内必需微量元素,而铅和铝是体内不需要的.这些金属元素或者在自然界大量存在,通过生活途径进入体内,如铝;或者是工业生产和污染物中的主要成分,如铅、汞和锰.这些金属毒物不仅危害职业人群,而且作为环境毒物危害所有人群,尤其是通过母体胎盘和乳汁对胎儿、婴儿产生危害,对儿童的神经系统发育造成难以恢复的损害.同时锰和铝还被认为与某些神经退行性疾病,例如巴金森氏病和阿尔茨海默病有关.人们对铅毒性认识较早,对铅神经毒性的研究已超过一个世纪,对汞和锰神经毒性的研究也有半个世纪;人们原先认为铝是一种安全无毒的金属元素,但近二三十年来其毒性作用越来越引起人们的关注.关于金属毒物神经毒性的研究很多,     

铅的神经发育毒性机制

铅是具有神经毒性的重金属元素 ,能影响神经系统的多种功能 ,发育中的神经系统对铅尤为敏感。铅不仅对血脑屏障、神经元及神经胶质细胞发育过程产生神经毒性作用 ,同时还可通过阻断钙通道、干扰蛋白激酶和一氧化氮合酶活性、抑制神经递质受体来影响突触形成和信息传递     

沿锌对脑发育影响研究进展

铅是对人体有害的重金属元素,随着工业和交通业的日益发展,铅对环境的污染越来越重.铅具有很强的神经发育毒性.锌是维持人体生命必需的微量元素之一,对脑发育有重要影响.本文综述了脑发育中铅的危害与锌的作用.     

052铅的神经发育毒性机制

铅是具有神经毒性的重金属元素，能影响神经系统的多种功能，发育中的神经系统对铅尤为敏感。铅不仅对血脑屏障、神经元及神经胶质细胞发育过程产生神经毒性作用，同时还可通过阻断钙通道、干扰蛋白激酶和一氧化氮合酶活性、抑制神经递质受体来影响突触形成和信息传递。     

铅中毒与镉中毒

随着经济的快速发展以及工业化、城镇化和经济全球化的不断推进,职业病危害问题,尤其是重金属中毒日渐突出.铅中霉铅的健康影响有哪些？铅对人体无任何生理功能,反而会产生多种不良影响.铅对全身各系统和器官均有毒性作用.铅及其无机化合物可通过呼吸道与胃肠道吸收,一般不经皮肤吸收,有机铅如醋酸铅可由少量经皮肤吸收,四乙基铅易经皮肤吸收.主要累积造血、神经、消化、肾脏系统;除此之外对生殖系统及儿童的生长发育有一定的毒性作用.     

铅对神经行为的毒作用

铅对神经行为的毒作用上海医科大学劳动卫生教研室（２０００３２）时圣利（综述）陈自强（审校）神经系统对铅的毒作用极为敏感。铅对神经系统可产生早期的持续影响。关于铅的神经行为毒性，国内外已有大量报道，但其毒作用机制仍不十分清楚。本文就近几年来国内外有关铅...     

铅对胎儿的神经毒性

铅对神经发育有很强的毒性,即使是低水平铅接触,胚胎和发育期的中枢神经系统仍是其主要靶器官.胎儿期较低水平铅暴露可以对胎儿及出生后神经系统发育产生不良影响.本文就铅的胎盘转运,铅对胎儿毒性的可能机理进行综述.     

Lead neurotoxicity in children: decomposing the variability in dose-effect relationships

BACKGROUND: Enormous progress has been made in recent decades in our understanding of lead neurotoxicology in children, but an important obstacle to additional progress is the striking variability that is evident in any plot of a lead biomarker versus a health endpoint. METHODS: In this article, three potential sources of variability are identified: (1) errors or imprecision in characterizing dose (and/or outcome); (2) incomplete characterization of endpoint variance attributable to factors other than lead; and (3) inter-individual differences in susceptibility to lead neurotoxicity. RESULTS: Strategies are suggested for reducing the variability contributed by these sources, including the development of validated PBPK models and biomarkers of early biological effects; the development of more comprehensive models of outcome variance and, specifically, the application of multi-level models that incorporate supra-individual and supra-family risk factors; and the use of study designs that permit assessments of the effect modifying influence of contextual factors on the form and severity of neurotoxicity. CONCLUSION: Decomposing the variability in the distribution of observed scores around the best-fit lines that describe the dose-effect relationships for lead neurotoxicity in children is a major research need.     

锰致神经毒性作用中神经递质的改变及其重要意义

锰作为一种神经毒物，长期接触可导致神经递质紊乱从而产生神经毒性作用。结合锰的生物学特性及锰中毒的临束表现，对锰影响单胺类神经递质多巴胺、氨基酸类神经递质γ-氨基丁酸和谷氨酸的有关研究进展，本文予以综述报道.     

Effects of N-Acetylcysteine on Lead-Exposed PC-12 Cells

The neurotoxicity of lead has been well established through numerous studies. However, the cellular processes of lead neurotoxicity, as well as techniques to prevent or reverse cellular damage after lead exposure, remain unknown. If oxidative stress plays a primary role in lead-induced neurotoxicity, antioxidants should assist in reviving lead-exposed cells. The present study explores N-acetylcysteine (NAC) as an antioxidant agent in PC-12 cells after lead exposure. Selective oxidative stress parameters, including glutathione (GSH), glutathione disulfide (GSSG), and malondialdehyde (MDA), were measured in PC-12 cells exposed to various concentrations of lead acetate. Administering NAC after lead exposure improved cell survival as measured by Trypan Blue exclusion. NAC treatment also increased the GSH/GSSG ratio compared to the lead-only group, and reduced MDA to near control levels. These results imply that NAC protects cells from lead-induced oxidative damage by boosting the PC-12 cells’ antioxidant defense mechanisms.     

δ-氨基-γ-酮戊酸脱水酶基因与铅中毒关系研究进展

此文通过综合分析国内外近年来对不同水平接铅及其血铅、骨铅变化和由此引起的肾毒性、神经毒性、性激素反应与ALAD基因型个体的分布特性研究,阐述了ALAD基因与铅中毒的关系。     

铅的中枢神经毒性机制研究进展

铅在人体蓄积产生毒性,大脑为其最主要的靶器官之一,铅对发育中的大脑可产生不可逆的神经毒性。本文就近年来铅的神经毒性及其机制的相关研究进行综述,旨在为后续研究提供参考。     

Neurotoxicity of organophosphorus and dithiocarbamate compounds

The neurotoxicity of organophosphorus compounds (OPs) including leptophos, TOCP and triphenyl phosphite and dithiocarbamate compounds were reviewed in this study. The major neurotoxicities of OPs were acute toxicity produced by the acetylcholine esterase (AChE) inhibiting action of OPs and delayed neurotoxicity produced by such OPs as leptophos and TOCP. The direct action of OP on the muscarinic and/or nicotinic acethylcholine receptors in the synaptic membranes have lately attracted attention in relation to acute toxicity. Delayed neurotoxicity is a delayed onset of prolonged locomotor ataxia resulting from a single or repeated exposure to an OP. Although neurotoxic esterase (NTE) inhibition might be related to the onset of organophosphate-induced delayed neurotoxicity (OPIDN), the precise mode of action is not yet clear. The effect of dithiocarbamates on the nervous system is also mentioned, because the compounds are currently suspected not only for neurotoxicity, but also as endocrine-disrupting chemicals. Although dithiocarbamates showed weak neurotoxicity in adult animals, we need to pay more attention to developmental neurotoxicity.     

Alteration of glucose metabolism in the spinal cord of experimental lead poisoning rats: microdetermination of glucose utilization rate and distribution volume

To examine the effects of lead on glucose metabolism in the spinal cord, glucose utilization rate (GUR) and distribution volume of glucose (DV) in the anterior horn and white matter were determined in 9 rats exposed to lead for 4 weeks and 10 control rats. The GUR and DV were determined by the quantitative microdetermination method using non-tracer amount of 2-deoxyglucose based on the three-compartments model of Sokoloff. The GUR and DV in the anterior horn in the lead-exposed rats were significantly lower than those in the controls. It is thus suggested that glucose metabolism, as measured by the GUR and DV, in the anterior horn is inhibited by lead; the anterior horn cells seem sensitive to lead neurotoxicity.     

铅中毒儿童的智力改变与脑诱发电位研究

目的:研究儿童铅中毒的智力改变与脑诱发电位的关系,探索儿童铅中毒的神经毒性和心理行为改变的电生理依据。方法:通过测定血铅及社会家庭情况问卷调查,在排除了影响智力的几个重要因素后,把6～12岁的45例符合条件的儿童分为高铅组(血铅值≥10μg/dl)和正常组(血铅值<10μg/dl),进行韦氏智力量表(WISC)的测定及体感诱发电位(SEP)和事件相关电位(ERP)P300的检测。全面评价铅中毒对儿童智力、感觉系统、高级神经功能的损害程度。结果:铅中毒儿童的总智商和言语智商较正常儿童显著降低,有统计学差异。操作智商虽也有降低,但与正常对照组相比无统计学差异。铅中毒儿童SEP的早期皮层电位P15、N20、P25与正常对照组相比无明显改变,但晚期皮层电位有明显异常,主要表现在N35、P45、和N60的潜伏期延长。铅中毒儿童的P300各波中,N100、P200与正常对照组相比无明显差别,但P300及N200的波幅较正常儿童明显降低,潜伏期也明显延长。结论:上述研究为儿童铅中毒的神经毒性和认知心理行为的异常提供了具有客观性的电生理依据,为儿童铅中毒的神经毒性的预防、诊断和治疗的观察提供了电生理依据。     

职业性铅接触对行为功能的影响

对35名铅作业工人进行成套的行为功能测验,接触组与对照组比较,16项行为功能测验中有14项得分有统计学意义(P<0.01或P<0.05)。半数项目行为功能测验得分有随着铅作业工龄增长而呈该增或该减的趋势。作者认为铅对作业工人行为功能的影响是肯定的,用行为功能测验的方法来研究铅的神经毒性是可取的简便的方法。     

Reductions in blood lead overestimate reductions in brain lead following repeated succimer regimens in a rodent model of childhood lead exposure

Although many studies have demonstrated the efficacy of succimer chelation in reducing blood and brain lead levels, the relative efficacy of the drug in the two tissues is less well understood. This issue is important because blood lead levels after chelation are used clinically to estimate reductions in the brain, the most critical organ in considering lead-induced neurotoxicity. The present study was designed to further investigate this issue, using multiple chelation regimens. Long-Evans rats were exposed to one of three lead exposure regimens from birth until postnatal day 40, followed by treatment with succimer (one or two 3-week regimens) or vehicle. The results indicated that one succimer regimen was significantly superior to vehicle treatment in lowering lead levels in both blood and brain across the entire 8-week follow-up period. Similarly, a second succimer regimen offered significant additional benefit relative to one regimen for both blood and brain across the 4-week follow-up period. However, several findings revealed that succimer-induced reductions in brain lead lagged behind reductions in blood lead and were generally smaller in magnitude. Furthermore, a rebound was detected in blood, but not brain, lead levels after both succimer regimens. Given the results of this study, we urge caution in using blood lead as a surrogate for brain lead levels, particularly during and immediately after chelation treatment when reductions in blood lead levels overestimate reductions in brain lead levels. The present results suggest that, in clinical use, succimer treatment may need to extend beyond the point at which blood lead levels have dropped to an "acceptable" target value in order to effectively reduce brain lead levels and minimize neurotoxicity.