Neurotoxicity of zinc: the involvement of calcium homeostasis and carnosine (特集 臨床における亜鉛の有効性の探索) Neurotoxicity of Zinc : The Involvement of Calcium Homeostasis and Carnosine

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Zinc is an essential trace element that is abundantly present in the brain. In spite of its importance for normal brain functions, it is widely recognized that excess zinc is neurotoxic. Numerous studies have indicated that zinc is crucial for neuronal injury after transient global ischemia and is linked with the pathogenesis of vascular type of dementia. We have investigated the molecular mechanisms of zinc-induced neurotoxicity in vitro and have explored substances that protect zinc-induced neurotoxicity. Pharmacological evidence based on results of our own and numerous other studies has indicated the significance of Ca<sup>2+</sup> dyshomeostasis in the mechanism of zinc-induced neuronal injury. The introduction of zinc into neurons is reportedly mediated through several types of Ca<sup>2+</sup>-permeable channels. Ca<sup>2+</sup> channel blockers attenuate zinc-induced neurotoxicity. Furthermore, calcium overload attenuates zinc neurotoxicity, and vice versa. In this paper, we review the routes of zinc entry and mechanisms of zinc-induced neuronal death in relation with calcium homeostasis. The possible role of carnosine (β-alanyl histidine), a dipeptide that is present in the brain, as an endogenous protective substance for neuronal injury is also discussed.

収録刊行物

  • Biomedical research on trace elements  

    Biomedical research on trace elements 18(1), 26-34, 2007-03-31 

    Japan Society for Biomedical Research on Trace Elements

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各種コード

  • NII論文ID(NAID)
    10018910865
  • NII書誌ID(NCID)
    AN10423256
  • 本文言語コード
    ENG
  • 資料種別
    REV
  • ISSN
    0916717X
  • NDL 記事登録ID
    8769288
  • NDL 雑誌分類
    ZS8(科学技術--医学--解剖学・生理学・生化学)
  • NDL 請求記号
    Z19-3255
  • データ提供元
    CJP書誌  CJP引用  NDL  J-STAGE 
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