Neurotoxicity and molecular effects of methylmercury
Neurotoxicity and molecular effects of methylmercury
复制标题
DOI：
10.1016/s0361-9230(01)00458-0
复制
发表时间：
2001-05-15
影响因子：
3.8
通讯作者：
Manzo, L
中科院分区：
文献类型：
--
作者：
Castoldi, AF;Coccini, T;Manzo, L
高浓度甲基汞的神经毒性和发育中的大脑的高敏感性在人类和实验动物中都得到了很好的证实。产前中毒的儿童表现出一系列的影响，从严重的脑瘫到轻微的发育迟缓。目前尚不清楚损害神经发育的最低剂量。人类接触的主要来源是鱼类。迄今为止，从食鱼人群的流行病学研究中获得的数据并不一致。美国环境保护署根据对伊拉克的研究确定了每天0.1微克/千克的参考剂量！子宫内接触甲基汞的儿童。然而，这些接触在有限的时间内发生在高水平，因此不是与鱼类消费相关的较低慢性接触水平的典型情况。估算甲基汞阈值剂量的主要障碍包括：产前接触甲基汞后，神经发育受到的影响延迟出现，以及对这些神经变化背后的细胞和分子过程了解有限。在这方面，旨在确定环境相关水平甲基汞敏感分子目标的战略可能对风险评估特别有用。这里介绍了低剂量/低浓度甲基汞分子效应的一些例子。(C)2001 Elsevier Science Inc.
The neurotoxicity of high levels of methylmercury (MeHg) and the high susceptibility of the developing brain are well established both in humans and experimental animals. Prenatally poisoned children display a range of effects varying from severe cerebral palsy to subtle developmental delays. Still unknown is the lowest dose that impairs neurodevelopment. The primary source of human exposure is the fish. The data obtained so far from epidemiological studies on fish-eating populations are not consistent. A reference dose of 0.1 mug MeHg/kg per day has been established by the U.S. Environmental Protection Agency based on a study on Iraq! children exposed to MeHg in utero. However, these exposures occurred at high level for a limited period of time, and consequently were not typical of lower chronic exposure levels associated with fish consumption. Major obstacles for estimation of a threshold dose for MeHg include the delayed appearance of the neurodevelopmental effects following prenatal exposure and limited knowledge of cellular and molecular processes underlying these neurological changes. In this respect, a strategy which aims at identifying sensitive molecular targets of MeHg at environmentally relevant levels may prove particularly useful to risk assessment. Here some examples of MeHg molecular effects occurring at low doses/concentrations are presented. (C) 2001 Elsevier Science Inc.