An artificial antioxidant appears to protect brain cells from the damage caused by alcohol, according to research on rats by an international team.

The study by scientists at Cornell University in New York and the University of Valencia in Spain, worked with groups of rats, keeping some of them drunk for six weeks. The results appear in this week's issue of the journal, Proceedings of the National Academy of Sciences.

The scientists, led by Dr Daniel Herrera of Cornell, were testing the theory that neurogenesis - the formation of new brain cells - is disrupted by oxidative damage from alcohol.

Neurogenesis occurs during childhood, but stops in adulthood with the exception of two areas of the brain - the olfactory bulb and the hippocampus, which both produce new neurons throughout life. Tests in the past have shown that if the generation of new neurons on the hippocampus is interrupted, memory problems ensue.

The researchers fed groups of rats either a regular liquid diet or one containing moderate doses of ethanol (pure alcohol). The alcohol diet is used because it replicates the effects of chronic alcoholism in humans, including a decrease in antioxidant enzymes in the body.

Selected rats in each group also received supplemental doses of ebselen, a synthetic antioxidant previously shown to counter other alcohol-related damage. If the death of brain cells is being caused by the oxidation of alcohol, then the rats being fed the antioxidant should have escaped this damage.

Ebselen is a compound containing selenium. It is a synthetic antioxidant, not one found naturally in foods or drinks that normally carry antioxidants, such as tea or red wine.

The research was done over a six week period. At the end of the experiment, the researchers looked at the part of the rat brain that is involved in learning and memory, called the dentate gyrus.

The rats on the alcohol-only diet not only had 66.3% fewer new neurons created, they also had three times as many brain cells killed off than the control rats. But the rats which had also been given ebselen had neither of these effects from the alcohol. The ebselen did not affect the amount of alcohol the rats consumed, or how it was metabolised.

"Our studies indicate that alcohol abuse, even for short duration, results in the death of newly formed neurons within the adult brain and that the underlying mechanism is related to oxidative or nitrosative stress," Herrera and colelagues write.

The work may help explain the cognitive impairments associated with alcoholism in humans, they said.

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