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Archive - May 3, 2011

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Antioxidant May Prevent Alcohol-Induced Liver Disease

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.

Scientists Track Evolution and Spread of Deadly Fungus

New research has shed light on the origins of a fungal infection which is one of the major causes of death from AIDS-related illnesses. The study, published on April 28, 2011, in the journal PLoS Pathogens, shows how the more virulent forms of Cryptococcus neoformans evolved and spread out of Africa and into Asia. Cryptococcus neoformans is a species of often highly aggressive fungi. One particular strain of the fungus – known as Cryptococcus neoformas varietygrubii (Cng) – causes meningitis amongst patients with compromised immune systems following HIV infection. There are believed to be up to a million cases of cryptococcal meningitis each year, resulting in over 600,000 deaths. Infection with the fungus, which invades the central nervous system, is treated with a life-long therapy of antifungal drugs, which can have highly unpleasant side effects. Sitali Simwami and Dr. Matthew Fisher from Imperial College London, together with colleagues from St Georges, University of London, Naresuan University, Thailand, and the CBS Fungal Biodiversity Centre, The Netherlands, used genetic sequencing techniques to compare the genetic diversity of Cng in 183 samples taken from the clinic and the environment in Thailand against the 77 samples from a global database. Thailand has an emerging HIV epidemic and nearly one in five HIV-infected patients is affected by cryptococcal infection. "Cryptococcal meningitis kills hundreds of thousands of people each year, almost as many as malaria, yet gets little attention," explains Dr. Fisher. "We know very little about where it originated from and how it evolved. If we can track its evolution and diversity, then we can begin to understand where the pathogen originates from, how it infects people, and how it adapts to become more – or less – virulent.