Galectin-1 is a major receptor for ganglioside GM1, a product of the growth-controlling activity of a cell surface ganglioside sialidase, on human neuroblastoma cells in culture

Cell density-dependent inhibition of growth and neural differentiation in the human neuroblastoma cell line SK-N-MC are associated with a ganglioside sialidase-mediated increase of GM1 and lactosylceramide at the cell surface. Because these glycolipids expose galactose residues, we have initiated the study of the potential role of galectins in such cellular events. Using specific antibodies, galectin-1 but not galectin-3 was found to be present at the cell surface. Assessment of carbohydrate-dependent binding revealed a saturable amount of ligand sites approaching 2.6 x 10(6) galectin-1 molecules bound/cell. Presence during cell culture of the sialidase inhibitor 2-deoxy-2,3-dehydro-N-acetylneuraminic acid or of the GM1-binding cholera toxin B subunit effected a decrease of the presentation of galectin-1 ligands by 30-50%. The assumption that GM1 is a major ligand for galectin-1 was reinforced by the correlation between the number of carbohydrate-dependent 125I-iodinated GM1-neoganglioprotein binding sites and the amount of immunoreactive surface galectin-1, the marked sensitivity of probe binding to the presence of anti-galectin-1 antibody, and the inhibition of cell adhesion to surface-immobilized GM1 by the antibody. The results open the possibility that the carbohydrate-dependent interaction between ganglioside GM1 and galectin-1 may relay sialidase-dependent alterations in this cell system.     

Joint influence of alcohol, tobacco, and coffee on biological markers of heavy drinking in alcoholics

BACKGROUND: Recent reports suggest that gamma-glutamyl transferase (GGT) decreases with coffee intake. The aim of this study was to examine the joint influence of alcohol, tobacco, cotinine, coffee, and caffeine on biological markers of heavy drinking in an alcoholic population. METHODS: Subjects were 160 alcohol-dependent inpatients. Biological assessments, performed at admission, were plasma levels of GGT, apolipoprotein AI, aspartate aminotransferase, and mean corpuscular volume (MCV), and urine cotinine and caffeine indexes. Years of alcohol abuse and of smoking, alcohol and coffee intake, and smoking rate were estimated in a semistructured interview, and Fagerstr?m Tolerance Questionnaire was completed by inpatients. RESULTS: Coffee intake, but not caffeine, correlated negatively with biological markers of heavy drinking, after controlling for alcohol and tobacco intake. Years of smoking correlated positively to MCV, after controlling for alcohol and coffee intake. CONCLUSIONS: Concerning the effect of coffee, the most likely hypothesis is that noncaffeine coffee fractions have a protective effect on liver cells. Concerning the effect of smoking, one can propose that the increase of MCV with smoking could be a consequence of carbon monoxide inhalation, leading to hypoxemia, or of folate deficiency.