Antioxidant may prevent alcohol-induced liver disease

Antioxidant may prevent alcohol-induced liver disease

Alcohol-induced liver disease (ALD) is a major cause of illness and death in the United States. Women are more likely to be affected by alcohol-induced liver disease because women can be affected by smaller amounts of alcohol than men. Research had revealed that the brains of heavy drinkers can be affected at an early stage of their affliction -- and that organic changes such as widening of the brain's ventricles, or cavities, may take place. So far, however, the significance of these changes is not fully understood. The changes in the nervous system are largely caused by vitamin B deficiency, and can to some extent be reversed by taking vitamin pills or by injections.

Liver damage is mostly due to the poisonous action of the alcohol itself. There are three such types of liver disease:
1. Alcoholic fatty liver -- this occurs in most problem drinkers and is reversible if the patient stops drinking and follows a planned diet

2. Alcoholic hepatitis (inflammation of the liver) -- this may be reversible, or it may worsen and lead to cirrhosis. In the United States, cirrhosis is the seventh leading cause of death among young and middle-age adults. Approximately 10,000 to 24,000 deaths from cirrhosis may be attributable to alcohol consumption each year

3. Alcoholic cirrhosis (replacement of liver cells by fatty tissue) -- this is irreversible, although with abstinence it may not progress

After many years of heavy drinking, most people develop serious complications of alcohol-induced liver disease which can be serious and life-threatening. These complications are

    * Accumulation of fluid in the abdomen
    * Bleeding from veins in the esophagus
    * High blood pressure in the liver
    * Enlarged spleen
    * Kidney failure
    * Liver Cancer
    * Changes in mental function, and coma

It is important to control one's drinking habit. Remember that serious Alcohol-induced liver disease (ALD) includes alcoholic hepatitis, characterized by persistent inflammation of the liver, and cirrhosis, characterized by progressive scarring of liver tissue. Approximately 10 to 35 percent of heavy drinkers develop alcoholic hepatitis, and 10 to 20 percent develop cirrhosis.

Alcohol-related liver damage can cause a variety of life-threatening health problems if the patient cannot stop drinking. For these patients, their health and life expectancy can only improve if they stop drinking. Abstinence is the cornerstone of ALD therapy. In order to stop drinking, patients or drinkers can look for various drug detox and prescription drug treatment. Women or patients with alcohol-induced liver disease and those with cirrhosis from any cause should stop using alcohol completely -- Even small amounts of alcohol can be dangerous when taken with medications containing acetaminophen, found in many over-the-counter pain relievers. The combination of alcohol and acetaminophen can be very harmful to the liver for anyone who drinks. Never take acetaminophen with alcohol, or immediately after a period of heavy drinking. ChillPharm.com is an online drug resources providing a varieties of useful drug information such as articles on oxycontin withdrawal and also heroin rehab and many more.

An antioxidant may prevent damage to the liver caused by excessive alcohol, according to new research from the University of Alabama at Birmingham. The findings, published online April 21, 2011, in 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 Victor Darley-Usmar, Ph.D., 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.
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 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 Balu Chacko, Ph.D., a research associate and co-author of the study. "As it has been shown to decrease liver damage in hepatitis C patients, it may have potential to ameliorate the initial stages of fatty liver disease in patients with alcoholic and non-alcoholic liver disease."

The Annals of Hepatology estimate that alcohol abuse costs $185 billion annually in the United States, and that 2 million people have some form of alcoholic liver disease. It links as much as 90 percent of cirrhosis of the liver is related to alcohol abuse and up to 30 percent of liver cancer.


Darley-Usmar, who is also the director of the Center for Free Radical Biology at UAB, says his team is in discussions with the National Institutes of Health to develop a whole family of drugs based around interactions with mitochondria. He suggests 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. "Unfortunately, previous trials using antioxidants in humans have not been as successful as anticipated. The difference with our current findings is that we targeted a specific part of the cell, the mitochondria. This is a unique approach, and this is one of the few pre-clinical trials that shows effectiveness."

Darley-Usmar says the findings also may have significance for the treatment of metabolic syndrome, a rapidly growing condition that affects some 50 million Americans, according to the American Heart Association.

"Metabolic syndrome describes a complex interaction of factors caused by obesity which includes damage to the liver due to an increase in free radicals, hypoxia and deposition of fat," said Darley-Usmar. "It's quite similar to alcohol-dependent hepatotoxicity. It would be interesting to see if an antioxidant such as MitoQ had any therapeutic effect in preventing liver damage in those with metabolic syndrome."