Acute ethanol exposure disrupts actin cytoskeleton and generates reactive oxygen species in c6 cells.
Central nervous system dysfunctions are among the most significant effects of exposure to ethanol and the glial cells that play an important role in maintaining neuronal function, are extremely involved with these effects. The actin cytoskeleton plays a crucial role in a wide variety of cellular functions, especially when there is some injury. Therefore the aim of the present study was to analyze the short-term effects of ethanol (50, 100 and 200 mM) on the cytoskeleton of C6 glioma cells. Here we report that acute ethanol exposure profoundly disrupts the actin cytoskeleton in C6 cells decreasing stress fiber formation and downregulating RhoA and vinculin immunocontent. In contrast, microtubule and GFAP networks were not altered. We further demonstrate that anti-oxidants prevent ethanol-induced actin alterations, suggesting that the actions of ethanol on the actin cytoskeleton are related with generation of reactive oxygen species (ROS) in these cells. Our results show that ethanol at concentrations described to be toxic to the central nervous system was able to target the cytoskeleton of C6 cells and this effect could be related with increased ROS generation. Therefore, we propose that the dynamic restructuring of the cytoskeleton of glial cells might contribute to the response to the injury provoked by binge-like ethanol exposure in brain.
Loureiro
Samanta Oliveira
SO
Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil.
Heimfarth
Luana
L
Reis
Karina
K
Wild
Luiza
L
Andrade
Cláudia
C
Guma
Fátima Theresinha Costa Rodrigues
FT
Gonçalves
Carlos Alberto
CA
Pessoa-Pureur
Regina
R
D000199:Actins / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D002491:Central Nervous System Agents / Q000037:antagonists & inhibitors / Q000633:toxicity*; D003599:Cytoskeleton / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D015536:Down-Regulation / Q000187:drug effects; D000431:Ethanol / Q000037:antagonists & inhibitors / Q000633:toxicity*; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D009457:Neuroglia / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D009994:Osmolar Concentration; D018384:Oxidative Stress / Q000187:drug effects; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism*; D022502:Stress Fibers / Q000187:drug effects / Q000378:metabolism; D013997:Time Factors; D016596:Vinculin / Q000378:metabolism; D020742:rhoA GTP-Binding Protein / Q000378:metabolism
D000199:Actins; D000975:Antioxidants; D002491:Central Nervous System Agents; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; C488956:Vcl protein, rat; D016596:Vinculin; D000431:Ethanol; D020742:rhoA GTP-Binding Protein