Protein Traffic Is an Intracellular Target in Alcohol Toxicity

Pharmaceuticals

Guillermo Esteban-Pretel²  Mar໚ Pilar Marín²  Ana M. Romero²  Xavier Ponsoda¹  Raul Ballestin¹  Juan J. Canales³ 

[1] Department of Biología Celular, Universidad de Valencia, Valencia, Spain; E-Mails:;Sección de Biología y Patología Celular, Centro de Investigación, IIS-La Fe, Valencia, Spain; E-Mails:;Behavioural Neuroscience, Department of Psychology, University of Canterbury, Private Bag 4800, Christchurch 8140, New Zealand; E-Mail:

关键词: ethanol;    neurons;    astrocytes;    intracellular traffic;    nucleocytoplasmic transport;   

DOI  :  10.3390/ph4050741

来源: mdpi

【 摘 要 】

Eukaryotic cells comprise a set of organelles, surrounded by membranes with a unique composition, which is maintained by a complex synthesis and transport system. Cells also synthesize the proteins destined for secretion. Together, these processes are known as the secretory pathway or exocytosis. In addition, many molecules can be internalized by cells through a process called endocytosis. Chronic and acute alcohol (ethanol) exposure alters the secretion of different essential products, such as hormones, neurotransmitters and others in a variety of cells, including central nervous system cells. This effect could be due to a range of mechanisms, including alcohol-induced alterations in the different steps involved in intracellular transport, such as glycosylation and vesicular transport along cytoskeleton elements. Moreover, alcohol consumption during pregnancy disrupts developmental processes in the central nervous system. No single mechanism has proved sufficient to account for these effects, and multiple factors are likely involved. One such mechanism indicates that ethanol also perturbs protein trafficking. The purpose of this review is to summarize our understanding of how ethanol exposure alters the trafficking of proteins in different cell systems, especially in central nervous system cells (neurons and astrocytes) in adult and developing brains.

【 授权许可】

CC BY   
© 2011 by the authors; licensee MDPI, Basel, Switzerland.