Fish with Insensative Dioxin Receptor Survive in PCB Polluted Hudson River

http://www.sciencenews.org/view/gene...way_the_poison

Packing Away The Poison
Genetic mutation allows Hudson River fish to adapt to PCBs, Dioxins
2/17/2011

Some fish in New York’s Hudson River have become "resistant" to
several of the waterway’s more toxic pollutants. Instead of getting
sick from dioxins and related compounds including some polychlorinated
biphenyls, Atlantic tomcod harmlessly store these poisons in fat, a
new study finds.

But what’s good for this bottom-dwelling species could be bad for
those feeding on it, says Isaac Wirgin of the New York University
School of Medicine’s Institute of Environmental Medicine in Tuxedo.
Each bite of tomcod that a predator takes, he explains, will move a
potent dose of toxic chemicals up the food chain — eventually into
species that could end up on home dinner tables.

From 1947 to 1976, two General Electric manufacturing plants along the
Hudson River produced PCBs for a range of uses, including as
insulating fluids in electrical transformers. Over the years, PCB and
dioxin levels in the livers of the Hudson’s tomcod rose to become
“among the highest known in nature,” Wirgin and his colleagues note
online February 17 in Science. Because these fish don’t detoxify PCBs,
Wirgin explains, it was a surprise that they could accumulate such
hefty contamination without becoming poisoned. His team now reports
that the tomcod’s protection traces to a single mutation in one gene.
The gene is responsible for producing a receptor protein needed to
unleash the pollutants’ toxicity.

All vertebrates contain molecules in their cells that will bind to
dioxins and related compounds. Indeed, these proteins — aryl
hydrocarbon receptors, or AHRs — are often referred to as dioxin
receptors. Once these poisons diffuse into an exposed cell, each
molecule can mate with a receptor and together they eventually pick up
a third molecule. This trio can then dock with select segments of DNA
in the cell’s nucleus to inappropriately turn on genes that can poison
the host animal.

The tomcod actually has two types of AHRs, with AHR-2 offering the
most effective binding to dioxin-like pollutants. But one naturally
occurring AHR-2 variant, the result of a gene mutation, proves a very
poor mate, Wirgin’s team has found. It takes five times more of the
pollutants to get substantial binding than is needed with the
conventional AHR-2.

In local rivers relatively free of dioxins and PCBs, 95 percent of
tomcod possess AHR-2 only in the conventional form. But in the PCB-
rich Hudson, Wirgin’s group finds, the only kind of AHR-2 protein in
99 percent of tomcod is the poorly binding variant.

The mutant receptor appears to have evolved long ago and to be widely
dispersed. But in the Hudson, fish with the gene to make the mutant
receptor have thrived, while those without it have died out ...

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For more on POPs & Insulin Resistance, see
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854721/