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Alcohol exposure during development has been demonstrated to produce a wide spectrum of alterations in offspring, including growth deficiency, behavioral abnormalities, microcephaly and CNS damage (fetal alcohol syndrome). Hepatic disfunction and histopathological alterations have also been described in childrens with this syndrome. In previous studies we have demonstrated that prenatal alcohol exposure affects the morphological, structural and functional features of the Goigi apparatus (GA), thus altering the glycosylation process in developing hepatocytes. In order to elucidate the cellular mechanisms 80 underlaying these alterations, we have analyzed the effect of alcohol exposure in 70 utero on the activity of liver galactosyltransferase (GT), the distribution and amount of sugar residues and the Golgi 60 ~-COP protein in hepatocytes. For this, livers from 21-day-old fetuses were obtained from 50 control and ethanol-fed rats. GT activity was determined in isolated GA cis and trans fractions. Colloidal gold labelled lectin 40 cytochemistry was used to analyze sugar residues and, finally, the distribution of 30 p-COP was analyzed by immunocytochemistry. Prenatal alcohol exposure induces a significant increase in both liver weight and total protein in the trans GA. The analysis of enzyme marker distribution and electron microscopy indicated a good separation of the different GA fractions and agrees with previous studies in adult liver. Our results showed that alcohol exposure significantly reduced the GT activity in both trans (GAF1) and cis (GAF2) GA fractions (fig. 1). Electron microscopy showed, as reported earlier, that prenatal exposure to ethanol induces, in about 30% of hepatocytes, a disorganization of the GA The appearance of this cell component in the remaining treated hepatocytes was similar to that of control cells. Immunolabeling of p-COP protein was seen over GA cisternae and vesicles in both control and alcohol exposed hepatocytes. However,this treatment induced a 75% reduction, from the control values, in the number of anti-J3-COP binding sites (fig. 2). On the other hand, the labelling pattern for each lectin over GA was similar to that reported for other cell types, indicating that lectins interact with different sugars that are added stepwise by a series of glycosyltransferases distinctively located among the GA cisternae. Our results indicated that alcohol increases a-L-Fuc residues (UEA I), while it decreases a-Man (Con AI, GlcNAc-(P 1,4,GlcNAc)" (WGA), GalNAc a 1,3GaINAc (HPA), GalNAc (MPA) and a-Gal (8S-I) residues. We show' for the first time that prenatal ethanol exposure induces, as in the adult liver, an increase in liver weight and enhancement of the total liver protein. These results are consistent with the enlargement of hepatocytes and with the liver glycoprotein accumulation observed in previous studies after this ethanol treatment. Impairment of glycosylation and secretion of glycoproteins as well as water retention, due to the corresponding osmotic effect of protein accumulation, have been suggested to participate in hepatocyte swelling after acute and chronic ethanol treatments. Therefore, it is possible that a similar mechanism might be involved in the enlargement of hepatocytes observed after prenatal alcohol exposure. We also confirm that prenatal alcohol exposure induces morphological changes in about 30% of GA. In addition, we demonstrate that this treatment causes a significant decrease in the labeling of p-COP protein. ~-COP is a protein associated with the non-clathrin-coated vesicles which appears to be involved in intra-GA-transport, transport from the endoplasmic reticulum to GA and protein transit between the intermediate compartment and Ul100 9 Body WT UIIOO 9 Body WT

the international journal of developmental biology

Alcohol consumption during pregnancy alters glycoconjugates, galactosyltransferase activity and beta-COP proteins in the Golgi apparatus of hepatocytes in developing liver.