Effects of chronic ethanol consumption on brain synaptosomes and protective role of betaine

KANBAK G., Arslan O. C., Dokumacioglu A., Kartkaya K., Inal M. E.

NEUROCHEMICAL RESEARCH, cilt.33, sa.3, ss.539-544, 2008 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 33 Sayı: 3
  • Basım Tarihi: 2008
  • Doi Numarası: 10.1007/s11064-007-9472-0
  • Dergi Adı: NEUROCHEMICAL RESEARCH
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.539-544
  • Anahtar Kelimeler: ethanol, brain, synaptosome, neurotoxicity, betaine, methyl donor, neuroprotective effect, MDA, adenosine deaminase, protein carbonyl, ADENOSINE-DEAMINASE, PROTEIN OXIDATION, LIPID-PEROXIDATION, LIVER-INJURY, RAT-BRAIN, MEMBRANE, METABOLISM, SYSTEM, HIPPOCAMPUS, METHIONINE
  • Eskişehir Osmangazi Üniversitesi Adresli: Evet

Özet

To evaluate the cytotoxic effects of chronic ethanol consumption on brain cerebral synaptosomes and preventive role of betaine as a methyl donor andS-adenosylmethionine precursor, 24 male Wistar rats were divided into three groups: control, ethanol (8 g/kg/day) and ethanol plus betaine(0.5% w/v) group. Animals were fed 60 ml/diet per day for two months, then sacrificed. Malondialdehyde (MDA), protein carbonyl contents and adenosine deaminase (ADA) activities were determined in synaptosomal/mitochondrial enriched fraction isolated from rat cerebral cortexes. When compared to controls, ethanol containing diet significantly increased MDA levels (P < 0.05), also increased protein carbonyl levels and adenosine deaminase activities. But these were not statistically significant (P > 0.05). However, adding betaine to ethanol containing diet caused a significant decrease in MDA, protein carbonyl levels and adenosine deaminase activities (P < 0.05). These results indicate that betaine may appear as a protective nutritional agent against cytotoxic brain damage induced by chronic ethanol consumption.