Ethanol reduces zincosome formation in cultured astrocytes.

Aims: Zinc is an ion that participates in basic cellular and tissular functions. Zinc deficiency is present in many physiological and health problems affecting most body organs, including the brain. Among the circumstances involved in zinc deficiency, ethanol consumption is probably one of the most...

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Publicado en:Alcohol & Alcoholism Vol. 46; no. 1; pp. 17 - 26
Autores principales: Ballestín, Raúl, Molowny, Asunción, Marín, María Pilar, Esteban-Pretel, Guillermo, Romero, Ana María, Lopez-Garcia, Carlos, Renau-Piqueras, Jaime, Ponsoda, Xavier
Formato: pictorial research Journal Article
Publicado: Oxford University Press / USA Jan/Feb2011
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Jan/Feb2011
      vid: 46
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      pub: Oxford University Press / USA
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        atl: Ethanol reduces zincosome formation in cultured astrocytes.
      aug:
        au:
          Ballestín, Raúl
          Molowny, Asunción
          Marín, María Pilar
          Esteban-Pretel, Guillermo
          Romero, Ana María
          Lopez-Garcia, Carlos
          Renau-Piqueras, Jaime
          Ponsoda, Xavier
        affil: Biologia Cellular, Universitat de València, Avda. Dr. Moliner 50, 46100 Burjassot, Spain
      sug:
        subj:
          Alcoholism Complications
          Ethanol Pharmacodynamics
          Macrophages Classification
          Zinc Deficiency
          Animal Studies
          Equipment and Supplies
          Funding Source
          Microscopy, Electron
          Rats
          T-Tests
          Zinc Physiology
      ab: Aims: Zinc is an ion that participates in basic cellular and tissular functions. Zinc deficiency is present in many physiological and health problems affecting most body organs, including the brain. Among the circumstances involved in zinc deficiency, ethanol consumption is probably one of the most frequent. A dietary zinc supplement has been proposed as possibly being an efficient method to palliate zinc deficiency. Astrocytes form part of the hematoencephalic barrier, and they are apparently implicated in the homeostasis of the neuronal medium. In this work, we analyze the effect of ethanol on extracellular zinc management by rat astrocytes in culture. Methods: Intracellular levels of ‘free zinc ions’, in controls and 30 mM ethanol-treated astrocytes, were visualized by using the zinc fluorochrome TSQ. Cytoplasmic fluorescence and zincosome formation were measured after adding extracellular 50 µM ZnSO4 to cell monolayers. Zincosomes were also observed at the electron microscopy level. Results: Exposure to ethanol for 7 days lowered the basal zinc levels of astrocytes by ∼30%. This difference was consistently maintained after the zinc pulse. Zinc ions were confined to bright fluorescent particles, the ‘zincosomes’, which appeared to be formed by the endocytic pathway. Zincosomes were less abundant in alcohol-treated cells, indicating a deficit in endocytoses as the origin of low zinc intake in astrocytes after ethanol treatment. Conclusions: Ethanol reduces both intracellular ionic zinc levels and extracellular zinc uptake, resulting in poorer zincosome formation. Given the endocytic nature of zincosomes, the effect of ethanol on membrane trafficking is apparently the origin of this deficit.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        Journal Article
      ougenre: Article
    language: English
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