Details

Autor(en) / Beteiligte

• Graw, Jan A.
• von Haefen, Clarissa
• Poyraz, Deniz
• Möbius, Nadine
• Sifringer, Marco
• Spies, Claudia D.

Titel

Chronic Alcohol Consumption Increases the Expression of Uncoupling Protein-2 and -4 in the Brain

Ist Teil von

• Alcoholism, clinical and experimental research, 2013-10, Vol.37 (10), p.1650-1656

Ort / Verlag

England: Blackwell Publishing Ltd

Erscheinungsjahr

2013

Link zum Volltext

Quelle

Wiley Online Library - AutoHoldings Journals

Beschreibungen/Notizen

• Background 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. Methods 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. Results 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. Conclusions 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.