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【medical-news】锰诱发神经系统疾病的机制
For decades, scientists have known that chronic exposure to high concentrations of the metal manganese can cause movement abnormalities resembling symptoms of Parkinson’s disease, but apparently without the same neuron damage characteristic of Parkinson’s patients. Now, researchers from the Johns Hopkins Bloomberg School of Public Health and Thomas Jefferson University have discovered a potential explanation to why these neurological symptoms may occur with manganese exposure. The study found that dopamine neurons in the brain of animals exposed to manganese do not release dopamine when stimulated, suggestive of a dysfunctional dopamine system even though the neurons do not show the damage present with Parkinson’s disease. Dopamine is a key neurotransmitter necessary for normal motor function. In addition, the researchers found that effects of manganese exposure occurred at blood concentrations in the upper range of levels documented in children and adults with environmental or occupational exposure. The study is published in the online version of the journal Experimental Neurology.
Manganese is a metal used in welding, battery making and in other industrial settings. In Canada, it replaced lead as a gasoline additive. Manganese, in the form of MMT, is approved in the United States as a gasoline additive but is not in use. The symptoms of “manganism” include behavioral and memory disturbances as well as Parkinson’s-like symptoms. Tremors occur with movement as opposed to the resting tremors typical of Parkinson’s disease.
“These findings may provide an explanation for some of the differences between manganism and idiopathic Parkinson’s disease, as well as why patients with manganese-induced neurological symptoms do not seem to respond to traditional Parkinson’s therapies,” said the study’s lead author, Tomás R. Guilarte, PhD, a professor in the Department of Environmental Health Sciences at the Bloomberg School of Public Health.
For the study, researchers observed a group of animals that were given incremental levels of manganese. The animals were monitored for behavioral changes and Positron Emission Tomography (PET) was used to assess various markers of dopamine neurons in the brain. According to the study, in addition to decreased in vivo dopamine release, manganese exposure produced subtle deficits in behavior and fine motor function.
“More work is needed to understand the relationship between the changes in behavior and the alterations in the dopamine system,” explained Jay S. Schneider, professor of pathology, anatomy and cell biology at Thomas Jefferson University and co-author of the study.
“There are other aspects of manganese neurotoxicity that this on-going study is examining that are likely to change the way that we view the risk of manganese exposure today,” said Guilarte.
“Nigrostriatal dopamine system dysfunction and subtle motor deficits in manganese-exposed non-human primates” was written by Tomás R. Guilarte, Ming-Kai Chen, Jennifer L. McGlothan, Tatyana Verina, Dean F. Wong, Yun Zhou, Mohab Alexander, Charles A. Rohde, Tore Syversen, Emmanuel Decamp, Amy Jo Koser, Stephanie Fritz, Heather Gonczi, David W. Anderson and Jay S. Schneider. 我来译此篇 文章倒数第二段感觉没译好，请战友们提供更好的译本让我学习。
一个新的镁导致神经功能紊乱的机制被发现。
几十年来，科学家们已经知道长期接触高浓度的金属镁会导致类似于帕金森病样的运动异常。但是明显没有与帕金森患者相同的特征性的神经损害。来自约翰.霍普金.布鲁博格公共卫生学院、托马斯.杰弗逊大学的研究者们已经发现一种潜在的解释。说明为什麽镁接触会出现神经症状。这一研究发现在接触镁动物的大脑中多巴胺神经在被刺激时不会释放多巴胺，说明尽管神经没有表现出帕金森病中出现的损害，但是多巴胺系统已经功能失调。多巴胺是正常运动功能的关键神经递质。而且，研究者还发现了镁接触开始产生损害的血中浓度上限，这已在环境或职业镁接触的儿童、成人中被证实。
镁这一种金属可被用于焊接、电池制造、其他一些工业制造业中。 在加拿大，它已替代铅作为汽油添加剂。镁以MMT的形式，已在美国被允许作为汽油添加剂，但还未投入使用。镁中毒症状包括行为、记忆障碍、以及帕金森样症状。其震颤与帕金森病典型的静止时发作相反，运动时发作。
“这些发现可能提供了一些解释，能说明镁中毒与特发性帕金森病间的差别，以及患者由于镁中毒造成的神经症状对传统的帕金森病治疗方法似乎没有疗效。” Tomás R. Guilarte,博士这一研究的发起人说道。他是布鲁博格公共卫生学院环境卫生学系教授。
在这个研究中，研究人员观察了一群动物，它们被给予的镁浓度递增。监测动物的行为改变，应用PET评估大脑中多巴胺神经元的不同标记物。根据这一研究发现，除了体内多巴胺释放降低，镁接触还能产生行为精细运动功能的缺陷。
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作者:admin@医学,生命科学 2011-02-16 17:14
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