Struve Melanie F, McManus Brian E, Wong Brian A, Dorman David C
CIIT Centers for Health Research, The Hamner Institutes for Health Sciences, Research Triangle Park, North Carolina 27709, USA.
Am J Ind Med. 2007 Oct;50(10):772-8. doi: 10.1002/ajim.20489.
Manganese neurotoxicity in humans is recognized as a form of parkinsonism with lesions occurring predominantly within the globus pallidus, subthalamic nucleus, putamen, and caudate nucleus.
This study evaluated dopamine, 3,4-dihydroxyphenylacetic acid, homovanillic acid, serotonin, norepinephrine, 5-hydroxyindoleacetic acid, gamma-aminobutyric acid (GABA), and glutamate concentrations in the globus pallidus, caudate, and putamen of male rhesus monkeys exposed subchronically to either air or manganese sulfate (MnSO4) at 0.06, 0.3, or 1.5 mg Mn/m3.
An approximate 1.5-6-fold increase (vs. air-exposed controls) in mean brain manganese concentration was observed following subchronic MnSO4 exposure. A marginally significant (P < 0.1) decrease in pallidal GABA and 5-hydroxyindoleacetic acid concentration and caudate norepinephrine concentration occurred in monkeys exposed to MnSO4 at 1.5 mg Mn/m3.
Despite the presence of increased tissue manganese concentrations, high-dose exposure to MnSO4 was associated with relatively few changes in basal ganglial neurotransmitter concentrations.
人类锰神经毒性被认为是一种帕金森综合征形式，病变主要发生在苍白球、丘脑底核、壳核和尾状核。
本研究评估了雄性恒河猴在亚慢性暴露于空气或浓度为0.06、0.3或1.5mg锰/立方米的硫酸锰（MnSO4）后，苍白球、尾状核和壳核中的多巴胺、3,4-二羟基苯乙酸、高香草酸、5-羟色胺、去甲肾上腺素、5-羟吲哚乙酸、γ-氨基丁酸（GABA）和谷氨酸的浓度。
亚慢性暴露于硫酸锰后，平均脑锰浓度相较于暴露于空气的对照组增加了约1.5至6倍。暴露于1.5mg锰/立方米硫酸锰的猴子，其苍白球GABA和5-羟吲哚乙酸浓度以及尾状核去甲肾上腺素浓度有轻微显著降低（P < 0.1）。
尽管组织锰浓度升高，但高剂量暴露于硫酸锰与基底神经节神经递质浓度的相对较少变化有关。
