Source:
Duke University
Summary: Researchers
were testing more than 20 non-steroidal anti-inflammatory drugs (NSAID) in an
attempt to make the zebrafish a new model for studying chemical injury in the
gut. What they found was unexpected: the gut was systematically sloughing off
epithelial cells as a defense mechanism against a molecule that inhibited the
MDR efflux pumps that protect cells.
A team of Duke researchers has discovered that cells lining the gut of zebrafish -- and probably humans too -- have a remarkable defense mechanism when faced with certain kinds of toxins: they hit the eject button.
"The gut has the challenging job of handling all the
chemicals that we consume or produce, and some of those chemicals can be
damaging. So the gut has evolved many interesting ways to defend against
damage," said Ted Espenschied, a Duke graduate student who led the effort
as part of his dissertation research.
The Duke team was testing more than 20 non-steroidal
anti-inflammatory drugs (NSAID) in an attempt to make the zebrafish a new model
for studying chemical injury in the gut. The fish are cheap to maintain, easy
to breed, and most importantly, translucent for the early part of their lives,
Rawls said. It's also easy to administer chemical exposures and measure their
environmental conditions via the tank water.
The researchers found something unexpected. "It's often the
case that drugs have multiple off-target effects," said John Rawls, an
associate professor of molecular genetics and microbiology and director of the
Duke Microbiome Center.
But only one of the drugs they tested seemed to create any measurable
differences in the fish, an old NSAID called Glafenine. It had been an
over-the-counter oral painkiller used in Europe and the Middle East for three
decades, but was taken off the market after being linked to kidney and liver
damage.
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