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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Astrocytes and manganese neurotoxicity.
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Astrocytes and manganese neurotoxicity.

机译：星形胶质细胞和锰的神经毒性。

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Increasing evidence suggests that astrocytes are the site of early dysfunction and damage in manganese neurotoxicity. Astrocytes accumulate manganese by a high affinity, high capacity, specific transport system. Chronic exposure to manganese leads to increased pallidal signal hyperintensities on T1-weighted magnetic resonance images and selective neuronal loss in basal ganglia structures together with characteristic astrocytic changes known as Alzheimer type II astrocytosis. Manganese is sequestered in mitochondria where it inhibits oxidative phosphorylation. Exposure of astrocytes to manganese results in important changes including (i) decreased uptake of glutamate; (ii) increased densities of binding sites for the "peripheral-type" benzodiazepine receptor (PTBR), a class of receptor localized to mitochondria of astrocytes and involved in oxidative metabolism, mitochondrial proliferation, and neurosteroid synthesis; (iii) increased gene expression and activity of the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), known to be associated with apoptosis; (iv) increased uptake of L-arginine, a precursor of nitric oxide, together with increased expression of the inducible form of nitric oxide synthase (iNOS). Potential consequences of these alterations in astrocytic gene expression include failure of energy metabolism, production of reactive oxygen species (ROS), increased extracellular glutamate concentration and excitotoxicity which could play a key role in manganese-induced neuronal cell death as a direct result of impaired astrocytic-neuronal interactions.
机译：越来越多的证据表明，星形胶质细胞是锰神经毒性的早期功能障碍和损害的部位。星形胶质细胞通过高亲和力，高容量，特定的转运系统积聚锰。长期暴露于锰会导致T1加权磁共振图像上的苍白细胞信号高强度增加以及基底神经节结构中的选择性神经元丢失，以及特征性的星形细胞变化，称为Alzheimer II型星形细胞增多症。锰被隔离在线粒体中，从而抑制氧化磷酸化。星形胶质细胞暴露于锰会导致重要的变化，其中包括：（i）降低谷氨酸的吸收; （ii）增加“外周型”苯二氮卓受体（PTBR）的结合位点的密度，这是一类定位于星形胶质细胞线粒体并参与氧化代谢，线粒体增殖和神经固醇合成的受体; （iii）已知与细胞凋亡有关的糖酵解-3-磷酸甘油醛脱氢酶（GAPDH）的基因表达和活性增加; （iv）增加一氧化氮的前体L-精氨酸的摄取，并增加可诱导形式的一氧化氮合酶（iNOS）的表达。这些改变的星形细胞基因表达的潜在后果包括能量代谢失败，活性氧（ROS）的产生，细胞外谷氨酸浓度的增加和兴奋性毒性，这可能是锰引起的神经元细胞死亡的直接原因，这是星形细胞受损的直接结果-神经元相互作用。

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