PRENATAL ALCOHOL EXPOSURE AFFECTS GALACTOSYLTRANSFERASE ACTIVITY AND GLYCOCONJUGATES IN THE GOLGI-APPARATUS OF FETAL-RAT HEPATOCYTES

Prenatal exposure to alcohol affects the morphological, structural, an d functional features of the Golgi apparatus (GA), thus altering the g lycosylation process in fetal hepatocytes. To elucidate the cellular m echanisms underlying these alterations, we have studied the effect of alcohol exposure in utero on the activity of liver galactosyltransfera se, an enzyme involved in the glycosylation process, and on the hepati c glycoprotein sugar composition, For this, livers from 21-day-old fet uses obtained horn control and ethanol-fed rats were used, Galactosylt ransferase (GT) activity was determined in isolated GA cis and trans f ractions, Colloidal gold-labeled lectin cytochemistry was used to anal yze sugar residues in hepatocytes at the subcellular level, Finally, t he integrity of the GA after alcohol treatment was assessed by electro n microscopy and by evaluating the distribution of the Golgi beta-COP, a protein involved in vesicular trafficking. Prenatal alcohol exposur e induces a significant increase in both liver weight and total protei n content in the trans Golgi, Moreover, this treatment decreases the a ctivity of galactosyltransferase, increases alpha-L-Fuc residues, and reduces the number of alpha-Man, GlcNAc(beta 1,4,Gl-cNAc)(1,2) GalNAc alpha 1,3GalNAc, alpha-GalNAc, and alpha-Gal residues, Alcohol exposur e also causes the Golgi cisternae to disappear in about 30% of the hep atocytes, and reduces 75% the number of anti-Golgi beta-COP protein bi nding sites, Our results suggest that the decrease in galactosyltransf erase activity, the alterations in the oligosaccharide chain compositi on, and the reduction in the amount of Golgi beta-COP protein could be involved in the alterations in the glycosylation process, as well as in the accumulation of hepatic proteins observed after prenatal alcoho l exposure, These alterations could contribute, therefore, to the alco hol-induced injury in the developing liver.