汞及其化合物的慢性神经毒性

本文介绍了在慢性汞中毒中，各种形式的汞在机体内的吸收、分布、代谢和排泄。神经方面的临床表现。综合介绍了当前汞神经毒作用的可能机制。     

汞神经毒性机制研究进展

汞是一种应用很广的重金属.由于工业生产过程中将含汞工业废水直接排放到水域中,导致无机汞和有机汞存在于水体中,进入环境中的无机汞可经微生物作用转化为有机汞,并通过生物链富集在鱼等水生生物中,人一旦食用被污染的鲜鱼和贝类等产品就会影响健康[1].     

环境中汞神经毒性的自由基机制研究进展

汞是一种难以降解的全球性污染物 ,在工农业、医药卫生和日常生活等诸方面广泛应用 ,并造成局部的污染。 1970～ 1979年 ,全世界排入大气的汞达 10万吨 ;排入水体的汞约1.6万吨 ;排入土壤的汞约 10万吨[1] 。铅、铜、锌矿的熔融向大气中排放汞 ,据估计全球每年为 10 0吨[2 ] 。 1995年我国仅燃煤就排放汞 30 2 .9吨[3 ] 。甲基汞 (MeHg)在脑组织中以原型蓄积 ,使脑细胞出现退行性变。损害最为严重的部位是小脑和大脑两半球。临床上表现为小脑性共济失调、视野缩小、语言、感觉、听力障碍等。此外肢体感觉神经损害症状也很常见。胎儿比成人…     

汞对人体神经的毒性及其危害

汞是室温下唯一的液体金属,有流动性。汞在工业上用途广泛,在生活中也有很多的接触机会。汞及其化合物有相似的毒性,进入人体过量即可中毒。因此认识和防治汞污染是非常必要的。     

氯氰菊酯的神经毒性及其机制的研究进展

氯氰菊酯是一种拟除虫菊酯类杀虫剂,在农业及卫生害虫防治中被广泛应用,其对人类产生的潜在毒性也日益受到人们的关注。氯氰菊酯的主要的靶器官是神经系统,其可通过对神经递质、离子通道、脂质过氧化作用等产生影响而发挥其神经毒性作用。本文对氯氰菊酯对哺乳动物的神经毒性及其机制的研究进展进行综述,以期为氯氰菊酯的安全生产和使用提供参考。     

锰的神经毒性及其机制研究进展

锰是人体的一种必需微量元素,具有非常重要的生理功能,但过量摄入则会对人体造成损害,主要表现为神经精神系统的慢性毒性作用,以类帕金森综合症的椎体外系神经损害为特征。锰中毒的主要机理涉及神经细胞凋亡、神经递质代谢紊乱、突触传导功能障碍,亦与基因易感性和遗传多态性有关。     

乙醇的神经行为毒性及其作用机制

乙醇的神经行为毒性及其作用机制上海医科大学劳动卫生教研室（２０００３２）汪根盛综述陈自强审校酒是人们日常消费品之一，但过量饮用对人体和社会造成的危害很大。据交通部门统计，１９９６年我国平均每天交通事故７８８起，直接经济损失达４７１万元。而酒后驾车的交...     

汞的毒性效应及作用机制研究进展

汞是人体非必需元素,它可以多种物理和化学形态广泛存在于自然界中。通过不同途径进入人体的汞及其化合物能够引起以神经系统和肾脏为主的多系统损害。目前,随着汞在生产和生活中的广泛应用,人们对其引起的健康危害日益关注。为了更好的了解汞及今后更加深入的进行研究,本文对汞的毒性效应及作用机制做一概述。     

汞作业工人神经行为功能的研究

对某金矿工人１９９人（对照组１０８人）进行的神经行为功能研究表明：接触组情绪状况得分（除有力－好动一项）和其余各项行为学指标得分均低于对照组。且随接触汞浓度增加，大多数行为功能得分呈递减趋势。在较低汞浓度接触组（平均为０．０１１４ｍｇ／ｍ＾３）神经行为功能得分明显低于对照组。尿汞含量〈４９．８５ｎｍｏｌ／Ｌ的汞作业工人神经行为异常人数明显高于对照组。提示：长期职业接触汞蒸气在未引起明显的临床损害之     

钒神经毒性机制及抗钒神经毒性物质研究进展

钒是一种过渡金属,是人体生长发育过程中必需的微量元素.但长期过量接触会对人体多个器官或系统造成功能性和器质性损害.本文从钒神经毒性的线粒体损伤与氧化应激、炎症反应、神经递质途径等机制及利用抗氧化类、多巴胺类及其他化合物降低钒神经毒性作用来进行综述,为钒神经系统损害的防治提供参考.     

Peripheral neurotoxicity in workers exposed to inorganic mercury compounds

Nerve conduction velocity (NCV) of the median motor, median sensory, and sural nerves was assessed in 16 workers chronically exposed to various inorganic mercury compounds. Exposed workers were compared with an unexposed control group using t test analyses. Slowing of the median motor nerve NCV was found, which was correlated with both increased levels of mercury in blood and urine, and with increased number of neurologic symptoms. Sensitive evaluation of neural function was found to be practical and informative for investigating mercury toxicity. Such evaluation can help determine safe mercury levels at the workplace.     

Elemental mercury exposure: peripheral neurotoxicity

Nerve conduction tests were performed on the right ulnar nerve of factory workers exposed to elemental mercury vapour. Time integrated urine mercury indices were used to measure the degree of exposure. Workers with prolonged distal latencies had significantly higher urine mercury concentrations when compared with those with normal latencies. Significant correlations between increasing urine mercury concentrations and prolonged motor and sensory distal latencies were established. Elemental mercury can affect both motor and sensory peripheral nerve conduction and the degree of involvement may be related to time-integrated urine mercury concentrations.     

Elemental mercury exposure: peripheral neurotoxicity.

Nerve conduction tests were performed on the right ulnar nerve of factory workers exposed to elemental mercury vapour. Time integrated urine mercury indices were used to measure the degree of exposure. Workers with prolonged distal latencies had significantly higher urine mercury concentrations when compared with those with normal latencies. Significant correlations between increasing urine mercury concentrations and prolonged motor and sensory distal latencies were established. Elemental mercury can affect both motor and sensory peripheral nerve conduction and the degree of involvement may be related to time-integrated urine mercury concentrations.     

Organophosphorus ester-induced chronic neurotoxicity

Organophosphorus compounds are potent neurotoxic chemicals that are widely used in medicine, industry, and agriculture. The neurotoxicity of these chemicals has been documented in accidental human poisoning, epidemiological studies, and animal models. Organophosphorus compounds have 3 distinct neurotoxic actions. The primary action is the irreversible inhibition of acetylcholinesterase, resulting in the accumulation of acetylcholine and subsequent overstimulation of the nicotinic and muscarinic acetylcholine receptors, resulting in cholinergic effects. Another action of some of these compounds, arising from single or repeated exposure, is a delayed onset of ataxia, accompanied by a Wallerian-type degeneration of the axon and myelin in the most distal portion of the longest tracts in both the central and peripheral nervous systems, and is known as organophosphorus ester-induced delayed neurotoxicity (OPIDN). In addition, since the introduction and extensive use of synthetic organophosphorus compounds in agriculture and industry half a century ago, many studies have reported long-term, persistent, chronic neurotoxicity symptoms in individuals as a result of acute exposure to high doses that cause acute cholinergic toxicity, or from long-term, low-level, subclinical doses of these chemicals. The author attempts to define the neuronal disorder that results from organophosphorus ester-induced chronic neurotoxicity (OPICN), which leads to long-term neurological and neurobehavioral deficits. Although the mechanisms of this neurodegenerative disorder have yet to be established, the sparse available data suggest that large toxic doses of organophosphorus compounds cause acute necrotic neuronal cell death in the brain, whereas sublethal or subclinical doses produce apoptotic neuronal cell death and involve oxidative stress.     

职业性汞中毒诊断及驱汞治疗进展

正在贵重金属制造、水银温度计、血压计生产行业中,金属汞是最主要的职业病危害因素。近年来,职业人群接汞剂量逐步减小,并且随着《职业病防治法》的两次修订,国家对职业人群健康的重视程度日益提高,明确低浓度长期接汞量效关系,对职业接触汞危害的人群进行预防、诊断与治疗,具有参考价值。1职业性汞中毒诊断研究进展1.1确定职业性汞暴露的量效关系明确汞毒性效应的量效关系是汞中毒诊断的前提。尽管