微量元素与精神疾患

<正> 微量元素对精神活动的影响主要是通过干扰大脑中枢神经系统的生理功能,经证实,与精神疾患有关的微量元素有:铁、锌、铜、锰、钴、锡、氟、碘、铅、镉、汞、砷、铝、锂等兹分述如下:     

中枢神经系统与内分泌

神经与内分泌共同调控全身各脏器的生理功能和代谢过程,中枢神经系统对内分泌系统起主导作用,同时内分泌系统也给中枢神经系统非常大的影响,因此两个关系非常密切。一、中枢神经系统对内分泌系统的调控(一)大脑——下丘脑——垂体——靶腺系统:大脑(特别是额颞叶)有特异性的下行纤维     

人发中微量砷共振光散射法测定

砷是环境毒性元素之一,无机砷为致癌物[1],并对生殖发育[2]和中枢神经系统[3]等有毒性作用.当前痕量砷的测定报道较多的是原子荧光分析法[4,5],利用砷和钼酸铵反应生成砷钼杂多酸并与染料缔合来测定砷的分光光度法也有报道[6-8],但利用共振光散射技术来测定报道则较少.     

染砷小鼠脑突触结构变化及相关基因差异表达

目的 观察染砷小鼠大脑神经突触结构变化及相关基因表达.方法 30只昆明种小鼠,按体重分为3组,即对照组、1和4 mg/L染砷组,染毒60 d.应用电镜和基因芯片技术观察砷对小鼠大脑神经突触结构及相关基因表达的影响.结果 对照组小鼠大脑突触结构清晰,突触前膜、间隙和后膜特化带清晰,前突触中可见较多的突触小泡.染砷组小鼠大脑突触前膜、间隙及后膜轮廓清晰,突触前膜的突触小泡数量明显减少.基因芯片结果 显示,染砷组小鼠大脑突触相关基因差异表达共有10条.上调基因为依赖于钙-钙调蛋白的蛋白激酶Ⅳ(Camk4)、速激肽1(Tac1)、多巴胺受体D1A(Drd1a)和多巴胺受体D2(Drd2);表达下调的基因共有6条,分别为complexin蛋白2(Cplχ2)、钙通道α1A亚单位(Cacna1a)、谷氨酸受体互变异构NMDA2B(Grin2b)、亲代谢性谷氨酸受体7(Grm7)、肌萎缩性(脊髓)侧素硬化2(Als2)和亲代谢性谷氨酸受体2(Grm2).结论 亚慢性砷暴露对小鼠大脑突触结构及相关基因表达造成损伤性影响,提示大脑神经元突触可能是砷神经毒性作用靶部位.     

砷对学习记忆影响的机制

学习记忆能力对人的生命活动至关重要,中枢神经系统的功能活动强弱可以通过人的学习记忆活动最直接的表现出来,其功能活动也受到多方面的影响,神经系统对毒物的毒性作用较其他组织系统更为敏感。砷在自然界分布很广,多以重金属的砷化合物和硫砷化合物形式存在,天然水中也含微量砷。因此,关于砷对学习记忆影响机制的研究,对阐明砷在脑发育过程中所起的作用有着重要的意义。     

亚急性砷中毒对脑海马和皮质AChE、NOS活性影响

砷及其化合物广泛存在于自然界,应用于工业、农业和医药等领域。砷中毒引起皮肤过度角化及多系统、多器官损害,导致皮肤或器官癌变。近年来有关砷对中枢神经系统作用越来越引起人们重视,砷能通过血、脑屏障进入脑组织,影响脑中化学物质稳定性,从而引起人的思维、学习和行为变化〔1-3〕。本研究通过建立亚急性砷中毒动物模型,观察大鼠     

大脑胶质瘤病综述

大脑胶质瘤病（cerebral glioma CG）。是一种罕见的中枢神经系统原发性肿瘤。临床表现无特异性，神经影像学也缺乏特征件，确诊主要依靠病理学诊断。1938年Nevin首次报道此病并命名为大脑胶质瘤病。按世界卫生组织最新中枢神经系统肿瘤组织分类，大脑胶质瘤病是来源不明的神经上皮肿瘤，属于胶质瘤的一种特殊类型，肿瘤病理分级相当于星形细胞瘤Ⅰ-Ⅱ级。     

高频与微波作业人员脑电图随访观察

本文对高频、微波作业人员进行脑电图(EEG)随访观察,认为高频与微波辐射可以引起大脑负荷能力降低,有造成脑功能低下的趋势,但对脑电图的对称性变化影响不大,尚不至于引起中枢神经系统大脑的调节紊乱。     

蛋白质糖基化修饰在儿童中枢神经系统疾病中的作用

蛋白质糖基化修饰是一种重要的翻译后修饰,对蛋白质的功能和结构形成具有重要作用,参与调控生物体的多项生命活动,如细胞粘附、转移、细胞间通讯、受体激活、信号转导等。近年来发现多种糖基化途径参与大脑发育的过程,异常的糖基化蛋白表达对大脑发育产生负面影响,并参与神经系统疾病的发生、发展。本文就蛋白质的糖基化修饰对神经功能的影响及糖基化异常导致的儿童中枢神经系统疾病进行论述,为儿童中枢神经系统疾病寻找新的糖基化蛋白诊断标志物和治疗靶点提供视角。     

婴幼儿奶粉砷国家标准限值的探讨

<正>1砷的来源、分布及危害砷在公元1250年被Albertus Magnus发现以来,在农业(农药、杀虫剂)、畜牧业、工业、电子、冶金等行业广泛使用,现在国际癌症研究所(IARC)已确认砷及其化合物为致癌物。大量的流行病学研究表明,砷可以诱发许多疾病,如急性砷中毒造成的中枢神经系统障碍,导致全身麻痹,呼吸道和消化道病变,甚至快速死亡。慢性中毒引起神经系统紊乱,全身乏力,食欲减退、恶心,皮肤     

砷对健康危害的研究进展

地球化学因素造成的局部地区饮水高砷和人为因素造成的砷污染对健康产生的危害是值得关注的问题。本文对国内外近些年来有关砷在机体中的代谢 ,砷对皮肤、循环系统、神经系统、泌尿生殖系统、消化系统、呼吸系统和免疫系统的损害及其机制的研究进行了综述。     

砷的毒性及排砷研究进展

砷是有毒的类金属元素,通过环境污染和职业性接触进入体内,对人体的皮肤、神经系统、心血管、肝脏及肾脏等有明显的损伤。在砷中毒治疗中,常用临床药物虽然排砷效果好,但具有一定的局限性,寻求一种高效、价廉、无不良反应且能广泛用于患者的排砷药物是当务之急。笔者就近年来国内外学者有关砷对机体的损害及排砷治疗的研究进展进行综述。     

砷的生物学指标研究进展

砷是有毒的类金属元素,对人体的皮肤、神经系统、心血管、肝脏及肾脏等有明显的损伤,其毒作用机制尤其是分子机制尚不清楚,在生物监测中,用尿砷总量来评估砷暴露量有一定的局限性,没有考虑到砷形态的变化。本文就对砷暴露量的检测以及对反映砷毒性的生物效应指标的检测等方面,对有关砷的生物学指标的研究进展进行综述。     

孕期和哺乳期母鼠饮水砷暴露对子代大鼠脑组织神经递质代谢酶的影响

目的了解砷对神经递质代谢酶的影响,探讨砷对学习、记忆能力影响的机制。方法选取清洁级Wistar大鼠,按雌∶雄为2∶1合笼。将64只孕鼠随机分为3个暴露组（分别为10、50、100mg/L剂量组）和1个对照组（蒸馏水）。暴露组于妊娠第6天（胎鼠器官分化开始）开始用NaAsO2溶液进行饮水染毒。仔鼠出生后,母鼠继续染毒。仔鼠出生后28d断乳,染毒至出生后第42天。在仔鼠出生后第0、28、42天,测量其大脑皮质和海马中谷氨酰胺合酶（GS）、乙酰胆碱酯酶（AChE）活力。结果出生后第0、28、42天,各暴露组子鼠脑皮质和海马中GS活力与对照组比较,经方差分析,差异均无统计学意义（P〉0.05）。出生后第0天,各组仔鼠的脑组织中AChE活力比较,经方差分析,差异无统计学意义（P〉0.05）。出生后第28、42天,100mg/L组子鼠脑海马中AChE活力高于对照组,差异均有统计学意义（P〈0.05）;且AChE活力均随染毒剂量的增加而增强,相关系数分别为0.408和0.374,呈统计学正相关（P〈0.05）,有明显的剂量-效应关系;其他各组仔鼠脑皮质AChE活力比较,经方差分析,差异均无统计学意义（P〉0.05）。结论砷暴露能够引起发育中的仔鼠脑组织AChE活力改变,可能会导致相应的中枢神经系统的一些改变。     

环境砷污染对人体健康影响的研究进展

环境砷污染的危害日益受到人们的重视。该文综述了环境砷污染对人体皮肤、消化系统、泌尿系统、免疫功能、神经系统、心血管系统、呼吸系统和生殖发育毒性的损害,为全面深入地认识环境砷污染对人体健康的危害及其作用机制提供了理论依据,并为今后进一步的研究提出了建议。     

Interactions between arsenic-induced toxicity and nutrition in early life

Exposure to arsenic through drinking water is a major public health problem affecting most countries, although the situation is particularly severe in low-income nations. The health consequences of chronic arsenic exposure include increased risk for various forms of cancer and numerous noncancer effects, including diabetes, skin diseases, chronic cough, and toxic effects on liver, kidney, cardiovascular system, and peripheral and central nervous systems. In recent years increasing reports of effects on fetal and child development have appeared. There seems to be a wide variation in susceptibility to arsenic toxicity, which is likely to be related to factors such as variation in arsenic metabolism, nutrition, host-related defense mechanisms, and genetic predisposition. The main mechanisms of arsenic-nutrition interactions include arsenic-induced oxidative stress, which requires nutrient-dependent defense systems, and arsenic metabolism (methylation) via 1-carbon metabolism, which requires methyl groups, folic acid, vitamin B-12, and betaine for the remethylation of homocysteine to methionine. An efficient first methylation step in combination with a slow second methylation step seems to be most critical from a toxicological point of view. A third mode of arsenic-nutrition interaction involves epigenetic effects and fetal programming via DNA methylation.     

饮水高含砷地区新生儿畸形的调查分析

目的 探讨饮水高含砷地区新生儿畸形发生率水平及特点.方法 采用横断面调查方法,对饮水高含砷地区1998-2004年7年间的新生儿出生情况进行调查,畸形诊断分类以国际疾病分类为基础(ICD-10),参考我国常规监测的先天畸形分类诊断,确定了6类24种先天畸形分类软件.结果 本次共调查新生儿2467例,发现新生儿畸形49例,检出率为198.62/万;饮水高含砷地区新生儿畸形率明显高于一般人群;检出类型中按照系统划分依次为中枢神经系统畸形、肢体畸形、先天性心脏病.结论 饮水高含砷地区新生儿的畸形发生率高于一般人群.     

Arsenic in drinking water and peripheral nerve conduction velocity among residents of a chronically arsenic-affected area in Inner Mongolia

BACKGROUND: It remains unclear whether chronic ingestion of arsenic in drinking water affects the peripheral nervous system. We examined the effects of arsenic exposure on nerve conduction velocity using electromyography. METHODS: A cross-sectional study was conducted of a population living in an arsenic-affected village in Hetao Plain, Inner Mongolia, China. A total of 134 (93.7%) of 143 inhabitants took part in the study, and 36 (76.6%) of 47 inhabitants in a low-arsenic exposed village were recruited as a control group. Of the participants, 109 inhabitants in the arsenic-affected village and 32 in the low-arsenic exposed village aged > or =18 years were used for the analyses. An expert physician performed skin examinations, and median nerve conduction velocity was examined by electromyography. Arsenic levels in tube-well water and urine were measured. A mean level of arsenic in tube-well water in the arsenic-affected village was 158.3 microg/L, while that in the low-arsenic exposed village was 5.3 microg/L. RESULTS: No significant differences in the means of the motor nerve conduction velocity (MCV) and sensory nerve conduction velocity (SCV) were observed in relation to arsenic levels in tube wells, urine, and the duration of tube-well use. Further, no differences in mean MCV or SCV were found between the subjects with and without arsenic dermatosis, with mean SCV of 52.8 m/s (SD 6.3) in those without and 54.6 m/s (5.2) in subjects with arsenic dermatosis (p=0.206). CONCLUSION: These findings suggest that chronic arsenic poisoning from drinking water is unlikely to affect nerve conduction velocity, at least within the range of arsenic in drinking water examined in the present study.     

Respiratory cancer in a cohort of copper smelter workers: results from more than 50 years of follow-up

Several studies have linked inhalation of airborne arsenic with increased risk of respiratory cancer, but few have analyzed the shape of the exposure-response curve. In addition, since inhaled airborne arsenic affects systemic levels of inhaled arsenic, there is concern that inhaled arsenic may be associated with cancers of the skin, bladder, kidney, and liver, which have been linked to ingested arsenic. The authors followed 8,014 white male workers who were employed for 12 months or more prior to 1957 at a Montana copper smelter from January 1, 1938 through December 31, 1989. A total of 4,930 (62%) were deceased, including 446 from respiratory cancer. Significantly increased standardized mortality ratios (SMRs) were found for all causes (SMR = 1.14), all cancers (SMR = 1.13), respiratory cancer (SMR = 1.55), diseases of the nervous system and sense organs (SMR = 1.31), nonmalignant respiratory diseases (SMR = 1.56), emphysema (SMR = 1.73), ill-defined conditions (SMR = 2.26), and external causes (SMR = 1.35). Internal analyses revealed a significant, linear increase in the excess relative risk of respiratory cancer with increasing exposure to inhaled airborne arsenic. The estimate of the excess relative risk per mg/m3-year was 0.21/(mg/m3-year) (95% confidence interval: 0.10, 0.46). No other cause of death was related to inhaled arsenic exposure.     

Long-Term Prospective Study of 6104 Survivors of Arsenic Poisoning During Infancy Due to Contaminated Milk Powder in 1955

Background

In 1955, an outbreak of arsenic poisoning caused by ingestion of arsenic-contaminated dry milk occurred in western Japan. We assessed the excess mortality among Japanese who were poisoned during this episode as infants.

Methods

We identified and enrolled 6104 survivors (mean age at enrollment, 27.4 years) who had ingested contaminated milk when they were age 2 years or younger; they were followed until 2006 (mean duration of follow-up, 24.3 years). Death certificates of subjects who died between 1982 and 2006 were examined to calculate cause-specific standardized mortality ratios (SMRs) using the mortality rate among Osaka residents as the standard.

Results

There was no significant excess overall mortality (SMR: 1.1, 95% confidence interval: 1.0–1.2). However, significant excess mortality in both sexes was observed from diseases of the nervous system (3.7, 1.9–6.2). Excess mortality from all causes of death decreased to unity beyond 10 years after study enrollment. The 408 men who were unemployed at the time of enrollment in the study had a significantly elevated risk of death from diseases of the nervous system (25.3, 10.8–58.8), respiratory diseases (8.6, 3.1–16.8), circulatory diseases (3.2, 1.6–5.2), and external causes (2.6, 1.4–4.1).

Conclusions

As compared with the general population, survivors of arsenic poisoning during infancy had a significantly higher mortality risk from diseases of the nervous system.Key words: arsenic poisoning, mortality, prospective study, food poisoning, standardized mortality ratio