A new study from the University of Alabama at Birmingham has suggested that an antioxidant may prevent damage to the liver caused by excessive alcohol.
The findings may have implications for new treatments to reverse steatosis, or fatty deposits in the liver that can lead to cirrhosis and cancer.
The research team, led by Victor Darley-Usmar, professor of pathology at UAB, introduced an antioxidant called mitochondria-targeted ubiquinone, or MitoQ, to the mitochondria of rats that were given alcohol every day for five to six weeks in an amount sufficient to mirror excessive intake in a human.
When alcohol is metabolized in the liver, it creates free radicals that damage mitochondria in the liver cells and prevent them from using sufficient amounts of oxygen to produce energy.
Moreover, the low-oxygen condition called hypoxia worsens mitochondrial damage and promotes the formation of the fatty deposits that can progress to cirrhosis.
Darley-Usmar and his collaborators said that the antioxidant MitoQ is able to intercept and neutralize free radicals before they can damage the mitochondria, preventing the cascade of effects that ultimately leads to steatosis.
"There has not been a promising pharmaceutical approach to preventing or reversing the long-term damage associated with fatty deposits in the liver that result from excessive consumption of alcohol," said Darley-Usmar.
"Our findings suggest that MitoQ might be a useful agent for treating the liver damage caused by prolonged, habitual alcohol use," he said.
Darley-Usmar said the findings also might have significance for the treatment of metabolic syndrome.
The study was published online April 21, 2011, in the journal Hepatology.