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Rutgers, Massachusetts General investigators find novel way to prevent drug-induced liver injury
Date:1/15/2012

ged cells, amplifying inflammation and injury. The current study examined inhibiting the action of liver-specific gap junctions to limit drug-induced liver injury.

The researchers first used a strain of genetically mutated mice that lack a particular liver-specific gap junction. The mice were administered various liver-toxic drugs such as acetaminophen, a commonly used medication best known under the Tylenol brand name. Acetaminophen overdoses are the most frequent cause of drug-induced liver injury.

Compared to normal mice, those lacking liver gap junctions were fully protected against liver damage, inflammation and death caused by administration of liver-toxic drugs. The team then identified a small-molecule inhibitor of liver gap junctions that, when given with or even after the toxic drugs, protected the livers of normal mice against injury and prevented their death.

"This finding is very exciting and potentially very powerful from a number of basic science and clinical application standpoints, which we are continuing to explore," said Martin Yarmush, senior author of the report and the Paul and Mary Monroe Professor of Biomedical Engineering at Rutgers. "However, before we can think about applying this approach to patients, we need to know more about any off-target effects of gap junction inhibitors and better understand the long-term ramifications of temporarily blocking liver-specific gap junction channels."

Additionally, cell culture experiments indicated that blocking gap junctions limited the spread through liver cells of damaging free radicals and oxidative stress, suggesting a possible mechanism for the observed protection.


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Contact: Carl Blesch
cblesch@ur.rutgers.edu
732-932-7084 x616
Rutgers University
Source:Eurekalert  

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