| Autor: |
Holownia A; Clinical Phar macology Unit, Ludwik Zamenhof Children's Hospital, Medical Academy of Bialystok, J. Waszyngtona 17, 15-274 Bialystok, PolandLaboratoire de Biochimie-Nutrition, Faculté de Médecine, 22 Avenue Camille Desmoulins, 29285 BrestLaboratoire de Neurobiologie Ontogenique, Centre de Neurochimie, CNRS, 5 Rue Blaise Pascal, 67084 Strasbourg, France., Meskar A; Clinical Phar macology Unit, Ludwik Zamenhof Children's Hospital, Medical Academy of Bialystok, J. Waszyngtona 17, 15-274 Bialystok, PolandLaboratoire de Biochimie-Nutrition, Faculté de Médecine, 22 Avenue Camille Desmoulins, 29285 BrestLaboratoire de Neurobiologie Ontogenique, Centre de Neurochimie, CNRS, 5 Rue Blaise Pascal, 67084 Strasbourg, France., Menez JF; Clinical Phar macology Unit, Ludwik Zamenhof Children's Hospital, Medical Academy of Bialystok, J. Waszyngtona 17, 15-274 Bialystok, PolandLaboratoire de Biochimie-Nutrition, Faculté de Médecine, 22 Avenue Camille Desmoulins, 29285 BrestLaboratoire de Neurobiologie Ontogenique, Centre de Neurochimie, CNRS, 5 Rue Blaise Pascal, 67084 Strasbourg, France., Ledig M; Clinical Phar macology Unit, Ludwik Zamenhof Children's Hospital, Medical Academy of Bialystok, J. Waszyngtona 17, 15-274 Bialystok, PolandLaboratoire de Biochimie-Nutrition, Faculté de Médecine, 22 Avenue Camille Desmoulins, 29285 BrestLaboratoire de Neurobiologie Ontogenique, Centre de Neurochimie, CNRS, 5 Rue Blaise Pascal, 67084 Strasbourg, France., Braszko JJ; Clinical Phar macology Unit, Ludwik Zamenhof Children's Hospital, Medical Academy of Bialystok, J. Waszyngtona 17, 15-274 Bialystok, PolandLaboratoire de Biochimie-Nutrition, Faculté de Médecine, 22 Avenue Camille Desmoulins, 29285 BrestLaboratoire de Neurobiologie Ontogenique, Centre de Neurochimie, CNRS, 5 Rue Blaise Pascal, 67084 Strasbourg, France. |
| Abstrakt: |
It has been shown that free radical damage may be involved in ethanol-induced cytotoxicity in cultured neural cells. Since changes in oxidative metabolism and the resulting lipid peroxidation readily modify biological membranes and alter cell functions we studied the effect of ethanol and its metabolite acetaldehyde on rat astroglial fatty acids profiles in the most common lipid classes of mitochondrial and microsomal membranes, i.e. phosphatidylcholine (PC) and phosphatidylethanolamine (PE). Rat astroglial cells were grown for 1 week in the presence of 50 m M or 100 m M ethanol. To examine acetaldehyde effects we used a 4-day co-culture model consisting of astroglial cells and alcohol dehydrogenase-transfected Chinese hamster ovary (CHO) cells. Acetaldehyde produced by these cells reached 172 mu M and 265 mu M, respectively, for ethanol concentrations of 10 and 20 m M. Mitochondrial and microsomal membranes were prepared by differential centrifugation, phosphatidylcholine and phosphatidylethanolamine were separated using thin layer chromatography and fatty acid quantitation was performed by GLC. Neither ethanol nor acetaldehyde changed the mitochondrial phosphatidylcholine or phosphatidylethanolamine profiles of total saturated, mono-unsaturated or polyunsaturated fatty acids. However, some significant alterations in particular fatty acids appeared especially after acetaldehyde but also after the highest ethanol dose. In microsomal phosphatidylcholine monounsaturated fatty acids were significantly increased after both, ethanol and acetaldehyde exposure. Among polyunsaturated fatty acids, arachidonic acid was found to be especially affected by both ethanol and acetaldehyde. Similar decreases were observed in adrenic, docosapentaenoic and docosahexaenoic acids in the groups treated with ethanol. In microsomal phosphatidylethanolamine, ethanol and acetaldehyde decreased monounsaturated and some polyunsaturated fatty acids. These data support the role of peroxidative processes in cultured rat astroglia exposed to ethanol and point to the role of acetaldehyde in this mechanism. |
