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Oxidative Medicine and Cellular Longevity - Volume 2015 2015, Article ID 741612, 8 pages -

Research Article

Australasian Research Institute, Sydney Adventist Hospital, Sydney, NSW 2076, Australia

Department of Pharmacology, School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney, NSW 2052, Australia

Neuropharmacology Group, MND and Neurodegenerative Diseases Research Centre, Macquarie University, Sydney, NSW 2109, Australia

Sydney Adventist Hospital Clinical School, University of Sydney, Sydney, NSW 2076, Australia

Received 15 February 2015; Revised 17 April 2015; Accepted 30 April 2015

Academic Editor: Angel Catalá

Copyright © 2015 Jade Guest et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Excessive alcohol consumption is associated with reduced brain volume and cognition. While the mechanisms by which ethanol induces these deleterious effects in vivo are varied most are associated with increased inflammatory and oxidative processes. In order to further characterise the effect of acute ethanol exposure on oxidative damage and NAD

levels in the brain, human U251 astroglioma cells were exposed to physiologically relevant doses of ethanol 11 mM, 22 mM, 65 mM, and 100 mM for ≤ 30 minutes. Ethanol exposure resulted in a dose dependent increase in both ROS and polyADP-ribose polymer production. Significant decreases in total NADH and sirtuin 1 activity were also observed at concentrations ≥ 22 mM. Similar to U251 cells, exposure to ethanol ≥22 mM decreased levels of NADH in primary human astrocytes. NADH depletion in primary astrocytes was prevented by pretreatment with 1 μM of lycopene for 3.5 hours. Unexpectedly, in U251 cells lycopene treatment at concentrations ≥ 5 μM resulted in significant reductions in NADH. This study suggests that exposure of the brain to alcohol at commonly observed blood concentrations may cause transitory oxidative damage which may be at least partly ameliorated by lycopene.

Autor: Jade Guest, Gilles J. Guillemin, Benjamin Heng, and Ross Grant



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