Ethanol Increases Cytochrome P4502E1 and Induces Oxidative Stress in Astrocytes
Article first published online: 23 NOV 2002
Journal of Neurochemistry
Volume 65, Issue 6, pages 2561–2570, December 1995
How to Cite
Montoliu, C., Sancho-Tello, M., Azorin, I., Burgal, M., Vallés, S., Renau-Piqueras, J. and Guerri, C. (1995), Ethanol Increases Cytochrome P4502E1 and Induces Oxidative Stress in Astrocytes. Journal of Neurochemistry, 65: 2561–2570. doi: 10.1046/j.1471-4159.1995.65062561.x
- Issue published online: 23 NOV 2002
- Article first published online: 23 NOV 2002
- Received March 28, 1995; revised manuscript received June 5, 1995; accepted June 5, 1995.
- Cytochrome P4502E1;
- Lipid peroxidation
Abstract: We demonstrate the presence of cytochrome P4502E1 (CYP2E1) in astrocytes in primary culture, its induction by ethanol, and the concomitant generation of free radical species. Double immunofluorescence using anti-CYP2E1 and anti-glial fibrillary acidic protein showed that CYP2E1 was distributed over the cytoplasm and processes, although labeling was more pronounced over the nuclear membrane. Immunogold labeling confirmed this pattern of distribution. Addition of 25 mM ethanol to the astrocyte culture medium for 14 days resulted in an increase in the CYP2E1 content, as determined by confocal microscopy and dot blot. In addition, ethanol induced a dose-dependent increase in the formation of reactive oxygen species that was partially prevented by incubating the astrocytes with anti-CYP2E1. Alcohol also induced a dose-dependent increase in malonaldehyde and hydroxynonenal formation and a depletion of the glutathione (GSH) content. These results suggest that ethanol induces oxidative damage in astrocytes, which could explain some of the toxic effects of ethanol on these cells, such as cytoskeletal alterations. This assumption is supported here by the fact that an increase in GSH content prevents the deleterious effects of alcohol on the cytoskeleton of astrocytes. These results suggest that importance of oxidative stress as a mechanism involved in alcohol-induced neural and brain damage.