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RESEARCH PRODUCT

Ethanol reduces zincosome formation in cultured astrocytes.

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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 ZnSO(4) 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.