Antioxidant may prevent alcohol-induced liver disease

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Washington: An antioxidant that may help prevent damage to the liver caused by excessive drinking has been identified, which scientists say could pave the way for new treatments to reverse steatosis or fatty deposits in the liver that can lead to cirrhosis and cancer.

Researchers at the University of Alabama in Birmingham (UAB) found that the antioxidant, called mitochondria-targeted ubiquinone, or MitoQ, has been effective in intercepting and neutralising free radicals in alcoholics` livers before they can damage the organ.

For their study, published in the journal Hepatology, the researches introduced MitoQ to the mitochondria – an organelle which converts energy into forms that are usable by the cell — of rats who 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 metabolised 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.

But, the UAB researchers found that MitoQ has been able to intercept and neutralise 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 lead researcher Dr Victor Darley-Usmar.

"Our findings suggest that MitoQ might be a useful agent for treating the liver damage caused by prolonged, habitual alcohol use."

As past studies have shown that MitoQ can be safely administered long-term to humans, the researchers believe it may also have potential to ameliorate the initial stages of fatty liver disease in patients liver disease.

Dr Darley-Usmar said his team is in discussions with the National Institutes of Health to develop a whole family of drugs based around interactions with mitochondria.

He suggested that such drugs might be effective in treating cardiovascular disease, kidney disease and neurodegenerative disorders.

"We know that free radicals play a role in human disease, and we have developed antioxidants that can eliminate free radicals in the laboratory," he said.

Dr Darley-Usmar also said that the findings may have significance for the treatment of metabolic syndrome — a rapidly growing condition that affects some 50 million Americans alone.

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