Alcohol & Alcoholism Vol. 39, No. 3, pp. 203-212, 2004
Alcohol & Alcoholism Vol. 39, No. 3 © Medical Council on Alcohol 2004; all rights reserved
PRENATAL ETHANOL EXPOSURE ALTERS THE CYTOSKELETON AND INDUCES GLYCOPROTEIN MICROHETEROGENEITY IN RAT NEWBORN HEPATOCYTES
1 Centre for Investigation, Hospital La Fe, Valencia, 2 Department of Cellular Biology and Anatomical Pathology, Faculty of Medicine, Institute for Biomedical Investigation August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona and 3 Department of Human Anatomy and Embryology, Faculty of Medicine, University of Granada, Granada, Spain
* Author to whom correspondence should be addressed at: Sect. Cell Biology and Pathology, Ctr Invest., Hospital ‘La Fe’, Av. Campanar 21, E-46009 Valencia, Spain. Tel.: +34 963 862700 (ext. 50411); Fax: +34 961 973018; E-mail: renau_jai{at}gva.es
(Received 27 October 2003; first review notified 9 December 2003; in revised form 3 January 2004; accepted 12 January 2004)
Aims: Prenatal ethanol exposure (PEA) increases both liver weight and total protein content in the Golgi complex and alters its morphological and functional properties. As PEA-induced protein retention could be the synergetic consequence of alterations in the cytoskeleton and in the glycan biosynthesis, and there are no data that in liver PEA perturbs the cytoskeleton, we examined in hepatocytes whether PEA affects the main cytoskeleton elements. We also analysed whether ethanol induces glycoprotein microheterogeneity by altering the sugar composition of glycoproteins. Methods: Livers from 0-day newborn control and PEA rats were used. The carbohydrate moiety of glycoproteins was determined by lectin blotting. The content and intracellular distribution of cytoskeleton proteins was analysed using immunoblotting, immunofluorescence and immunogold. Results: PEA delayed the post-Golgi transport of albumin but not of transferrin. PEA also increased the levels of cytokeratin and tubulin, but it decreased the amount of tubulin capable of assembling into functional microtubules. PEA perturbed the distribution of cytokeratin and tubulin and induced microheterogeneity in several glycoproteins. Conclusions: PEA-induced retention of proteins in fetal hepatocytes could be the result of an alteration of glycoprotein biosynthesis and cytoskeleton-mediated transport.
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