Ethanol impairs extracellular zinc intake in cultured astrocytes

• Main Authors: Ponsoda i Martí, Xavier, Ballestín Hinojosa, Raúl, Molowny, Asunción, Marín Muela, María Pilar, Esteban Pretel, Guillermo, Romero, Ana María, Renau Piqueras, Jaime, López García, Carlos
• Format: Conference Object
• Language: English
• Published: 2009
• Subjects: ethanol; zinc; astrocytes; UNESCO::CIENCIAS DE LA VIDA; Olympus; Orca
• Online Access: https://hdl.handle.net/10550/82219

Zinc is an ion that participates in increasing described cellular and tissular functions. On the other hand, zinc deficiency is also present in many physiological and health problems affecting most organs along the body, including teratological problems. Among circumstances involved in zinc deficiency, ethanol consumption is probably one of the most frequent. In the central nervous system zinc is also present and it is especially important in neurons that include zinc in the transmission synaptic vesicles. This zinc is delivered as the neurotransmitter exerting a neuromodulator role in the synaptic transmission. Neighbour astrocytes have to maintain the extracellular zinc homeostasis in order to maintain neurons continuously able to perform synaptic transmission. It has been proposed that an efficient method to palliate zinc deficiency it could be a dietary supplement. In this work we analyze the ability of cultured astrocytes in the management of extracellular zinc. Cultured rat astrocytes were used in this work, incubated in presence or not of 30 mM Ethanol for 7 days. Intracellular zinc levels were visualized by using the TSQ zinc fluorochrome, after addition or not of 50 µM ZnSO4. Fluorescence was recorded with an Olympus microscope BX50WI, equipped with a Hamamatsu ORCA digital camera controlled with the Aquacosmos software. Basal zinc levels in cultured astrocytes was greatly and significantly lower in ethanol treated cells (about 30% of control cultures). These differences were consistently maintained after addition of extracellular zinc to cell monolayers, resulting in a lower ability to uptake or retain zinc. The zinc was uptaked by the endocitic pathway, as demonstrated with the endosome marker FM 1-43 and was mainly confined to bright organelles that were more abundant in control cells. In conclusion, ethanol impairs astrocyte zinc management resulting in a lower capacity for extracellular zinc intake in resting conditions and after extracellular addtion. Consequently the efficiency of a dietary zinc supplementation may not be enough for recovery of cellular normal function.