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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 >Expression and regulation of brain metallothionein.
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Expression and regulation of brain metallothionein.

机译：脑金属硫蛋白的表达和调控。

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Many, but not all, zinc-containing neurons in the brain are a subclass of the glutamatergic neurons, and they are found predominantly in the telencephalon. These neurons store zinc in their presynaptic terminals and release it by a calcium-dependent mechanism. These "vesicular" pools of zinc are viewed as endogenous modulators of ligand- and voltage-gated ion channels. Metallothioneins (MTs) are low molecular weight zinc-binding proteins consisting of 25-30% cysteine, with no aromatic amino acids or disulfide bonds. The areas of the brain containing high contents of zinc such as the retina, the pineal gland, and the hippocampus synthesize unique isoforms of MT on a continuous basis. The four MT isoforms are thought to provide the neurons and glial elements with mechanisms to distribute, donate, and sequester zinc at presynaptic terminals; or buffer the excess zinc at synaptic junctions. In this cause, glutathione disulfide may participate in releasing zinc from MT. A similar nucleotide and amino acid sequence has made it difficult to obtain cDNA probes and antibodies capable of distinguishing indisputably among MT isoforms. MT-I and MT-II isoforms are found in the brain and in the peripheral tissues; MT-III isoform, possessing an additional seven amino acids, is expressed mostly in the brain and to a very minute extent in the intestine and pancreas; whereas MT-IV isoform is found in tissues containing stratified squamous epithelial cells. Since MTs are expressed in neurons that sequester zinc in their synaptic vesicles, the regulation of the expression of MT isoforms is extremely important in terms of maintaining the steady-state level of zinc and controlling redox potentials. The concentration of zinc has been shown to be altered in an extensive number of disorders of the central nervous system, including alcoholism. Alzheimer-type dementia, amyotrophic lateral sclerosis, Down's syndrome, epilepsy, Friedreich's ataxia, Guillaine-Barre syndrome, hepatic encephalopathy, multiple sclerosis, Parkinson's disease, Pick's disease, retinitis pigmentosa, retinal dystrophy, schizophrenia, and Wernicke-Korsakoff syndrome. The status of MT isoforms and other low molecular weight zinc-binding proteins in these conditions, diseases, disorders, or syndromes is being delineated at this time. Since several of these disorders, such as amyotrophic lateral sclerosis, are associated with oxidative stress, and since MT is able to prevent the formation of free radicals, it is believed that cytokine-induced induction of MT provides a long-lasting protection to avert oxidative damage.
机译：大脑中的许多（但不是全部）含锌神经元是谷氨酸能神经元的一个亚类，并且主要在端脑中发现。这些神经元将锌储存在突触前末端，并通过钙依赖性机制释放锌。这些锌的“囊状”池被视为配体和电压门控离子通道的内源性调节剂。金属硫蛋白（MTs）是由25-30％的半胱氨酸组成的低分子量锌结合蛋白，没有芳香族氨基酸或二硫键。锌含量高的大脑区域（例如视网膜，松果体和海马体）连续合成MT的独特同工型。认为这四种MT同工型为神经元和神经胶质元件提供了在突触前末端分配，捐赠和隔离锌的机制。或在突触连接处缓冲多余的锌。因此，谷胱甘肽二硫化物可能参与从MT释放锌。相似的核苷酸和氨基酸序列使得难以获得能够在MT同工型之间毫无区别地区分的cDNA探针和抗体。在大脑和周围组织中发现了MT-I和MT-II异构体。 MT-III亚型具有另外7个氨基酸，主要在大脑中表达，在肠道和胰腺中表达的程度很小。而MT-IV亚型则存在于含有分层鳞状上皮细胞的组织中。由于MTs在螯合突触小泡中的锌的神经元中表达，因此在维持锌的稳态水平和控制氧化还原电位方面，调节MT亚型的表达极为重要。锌的浓度已显示在包括酒精中毒在内的多种中枢神经系统疾病中发生改变。阿尔茨海默氏型痴呆，肌萎缩性侧索硬化症，唐氏综合症，癫痫病，弗里德里希共济失调，格林巴利氏综合症，肝性脑病，多发性硬化症，帕金森氏病，皮克氏病，色素性视网膜炎，视网膜营养不良，精神分裂症和沃克尼克病。目前正在描述在这些状况，疾病，病症或综合症中MT同工型和其他低分子量锌结合蛋白的状态。由于这些疾病中的几种（例如肌萎缩性侧索硬化症）与氧化应激相关，并且由于MT能够阻止自由基的形成，因此人们认为，细胞因子诱导的MT诱导可提供长期保护，从而避免氧化损伤。

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