Format

Send to

Choose Destination
Cell Physiol Biochem. 2008;22(5-6):769-76. doi: 10.1159/000185560. Epub 2008 Dec 9.

Alpha--lipoic acid decreases DNA damage and oxidative stress induced by alcohol in the developing hippocampus and cerebellum of rat.

Author information

1
Department of Physiology and Biochemistry, Faculty of Medicine, Urmia University of Medical Science, Urmia, Armenia.

Abstract

BACKGROUND/AIMS:

The present study was initiated in order to investigate the protective effects of alpha-lipoic acid upon ethanol-induced DNA damage, lipid peroxidation and protein oxidation in the developing rat hippocampus and cerebellum.

METHODS:

Pregnant Wistar rats received ethanol with, or without lipoic acid from gestation day (GD) 7 throughout lactation. The changes in DNA damage, protein carbonyl, lipid hydroperoxide, catalase and superoxide dismutase activities were measured in the hippocampus and cerebellum of male offspring at the end of the lactation period.

RESULTS:

The results indicated that DNA damage, lipid peroxidation and protein oxidation in the hippocampus and cerebellum were significantly elevated in animals that received alcohol. However, the catalase and superoxide dismutase activity results showed patterns that differed from those of DNA damage, lipid peroxidation and protein oxidation. Lipoic acid treatment significantly decreased DNA damage compared with the group that were administered alcohol alone, and restored the elevated protein carbonyl and lipid hydroperoxide levels to the levels of the control group.

CONCLUSIONS:

Our findings confirm that oxidative stress and DNA damage occur in the developing hippocampus and cerebellum as a result of alcohol administration, and also suggest that lipoic acid has protective effects as an antioxidant against alcohol-induced disorders in the developing hippocampus and cerebellum.

PMID:
19088458
DOI:
10.1159/000185560
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for S. Karger AG, Basel, Switzerland
Loading ...
Support Center