Jan A. Graw and Clarissa von Haefen contributed equally to this work.
Chronic Alcohol Consumption Increases the Expression of Uncoupling Protein-2 and -4 in the Brain
Version of Record online: 25 JUN 2013
Copyright © 2013 by the Research Society on Alcoholism
Alcoholism: Clinical and Experimental Research
Volume 37, Issue 10, pages 1650–1656, October 2013
How to Cite
Graw, J. A., von Haefen, C., Poyraz, D., Möbius, N., Sifringer, M. and Spies, C. D. (2013), Chronic Alcohol Consumption Increases the Expression of Uncoupling Protein-2 and -4 in the Brain. Alcoholism: Clinical and Experimental Research, 37: 1650–1656. doi: 10.1111/acer.12144
- Issue online: 3 OCT 2013
- Version of Record online: 25 JUN 2013
- Manuscript Accepted: 7 MAR 2013
- Manuscript Received: 6 NOV 2012
- Chronic Alcohol Consumption;
- Uncoupling Proteins;
Chronic alcohol consumption leads to oxidative stress in a variety of cells, especially in brain cells because they have a reduced oxidative metabolism of alcohol. Uncoupling proteins (UCPs) are anion channels of the inner mitochondrial membrane, which can decouple internal respiration. “Mild uncoupling” of the mitochondrial respiratory chain leads to a reduced production of free radicals (reactive oxygen species) and a reduction in oxidative cell stress. The extent to which chronic alcohol consumption regulates UCP-2 and -4 in the brain is still unknown.
We examined the effects of a 12-week 5% alcohol diet in the brain of male Wistar rats (n = 34). Cerebral gene and protein expression of UCP-2, -4, as well as Bcl-2, and the release of cytochrome c out of the mitochondria were detected by real-time polymerase chain reaction and Western blot analysis. The percentage of degenerated cells was determined by Fluoro–Jade B staining of brain slices.
Brains of rats with a chronic alcohol diet showed an increased gene and protein expression of UCP-2 and -4. The expression of the antiapoptotic protein Bcl-2 in the brain of the alcohol-treated animals was decreased significantly, whereas cytochrome c release from mitochondria was increased. In addition increased neurodegeneration could be demonstrated in the alcohol-treated animals.
Chronic alcohol consumption leads to a cerebral induction of UCP-2 and -4 with a simultaneous decrease in the antiapoptotic protein Bcl-2, cytochrome c release from mitochondria and increased neurodegeneration. This study reveals a compensatory effect of UCP-2 and -4 in the brain during chronic alcohol consumption.