An antioxidant may prevent damage to the liver caused by excessive alcohol, according to new research from the University of Alabama at Birmingham (UAB) and collaborating institutions. The findings, published in the May 2011 issue of the journal Hepatology, may point the way to treatments to reverse steatosis, or fatty deposits in the liver that can lead to cirrhosis and cancer. The research team, led by Dr. 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. Chronic alcoholics, those who drink to excess every day, experience a buildup of fat in the liver cells. 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. Dr. Darley-Usmar and his collaborators say 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 Dr. Darley-Usmar. "Our findings suggest that MitoQ might be a useful agent for treating the liver damage caused by prolonged, habitual alcohol use." "Previous studies have shown that MitoQ can be safely administered long-term to humans," said Dr.
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