Photo: Mark Mattson Some fish in the Hudson River in upstate New York have developed resistance to several toxic pollutants into the rivers. Instead of getting sick of having ingested dioxin-like compounds and polychlorinated biphenyls some, Atlantic tomcod defends itself by accumulating these poisons in the fat, according to a new study.
But if it helps this species of fish shoals to survive, it could endanger the species that feed on them, according to Isaac Wirgin Institute of Environmental Medicine New York University School of Medicine in Tuxedo. Each mouthful of tomcod ingested by a predator contains a powerful dose of toxic chemicals that migrate into the food chain, possibly in species that could result in our plates.
From 1947 to 1976, two plants of General elecric on the banks of the Hudson River PCBs were generated that had several purposes, including insulating fluids in electrical transformers. For years, the levels of PCBs and dioxins in the livers of tomcod have increased to such an extent that they were the highest in nature. M. Wirgin and collèques wrote online 17 February 2011 in the journal Science. Because these fish do not detoxify their PCBs, according Wirgin, it was a surprise that this contamination accumulated fish without poisoning. His team now reports that tomcod protects itself with a mutation of a single gene. This gene enables the production of a protein that appears to address the toxicity of pollutants. 
All vertebrates contain molecules that attach to their cells Dioxins and similar compounds. Indeed, these proteins called aryl hydrocarbon receptor (AHR) are also called the dioxin receptor. Once these poisons are in a cell, each molecule with a receptor can unite and together they cling to a third. This trio can then dock with certain segments of DNA in the cell nouyeau to turn on genes that are stocking the animal receptor. The tomcod 
In relatively less polluted local rivers to dioxins and PCBs, 95% carry the tomcod AHR-2 in its conventional form only. But in charge of the Hudson River PCBs, Wirgin team found that 99% had tomcod AHR protein-2 in its variant that binds with difficulty. mutated receptors appear to have evolved long ago and have spread widely in the population. But in the Hudson River, fish with the gene that causes the mutant receptor are many, while others have not died, says Wirgin.
The adaptations to resist poisons often exist in molecular biology by John Stegeman toxicologist at the Woods Hole Oceanographic Institution in Massachusetts. This process explains why some pesticides have a greater impact on target species and that is why some microbes become resistant to antibiotics.
Mr. Stegeman has written extensively on resistance to toxic PCBs and polycyclic aromatic hydrocarbons in another coastal species, the kill: "But the defense mechanism of killifish is not yet known, despite our hard work to find out. "he said.
Knowing the genetic mechanisms at the source of the chemical resistance can help predict the emergence of resistance in the making, he says, and can help discover ways to take advantage of the mechanism of resistance, even understand how a chemical is toxic. " Mechanisms of genetic resistance to chemicals in wildlife are known in some invertebrates, such as certain insects. Stegeman according to his knowledge, this discovery in a tomcod is a first for a vertebrate.
Photo: Rob Yasinsac
"Packing away the poison
Genetic mutation allows Hudson River fish to adapt to PCBs, dioxins
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 (2011)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 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, Wirgin notes.
Adaptation to resist poisons occurs throughout biology, observes molecular toxicologist John Stegeman of the Woods Hole Oceanographic Institution in Massachusetts. This process explains why some pesticides no longer kill their targets and why some microbes become immune to antibiotics.
Stegeman has been chronicling resistance to toxic PCBs and polycyclic aromatic hydrocarbons in another coastal species, a killifish. “But the mechanism in the killifish has not been uncovered, despite a long effort to determine it,” he says.
Knowing the genetic underpinnings for chemical resistance can help predict the likelihood of that resistance developing, he explains, and can point to “how one might exploit resistance — even understand why chemicals are toxic.” Genetic mechanisms for chemical resistance in wild species are invertebrates Known For Some, Such as bugs. Stegeman says, to His Knowledge, this tomcod Finding Is the first in a vertebrate. "
Excerpts from Article Written by Janet Raloff published in ScienceNews here:
http://www.sciencenews.org/view/generic/id/69976 / title / Packing_away_the_poison
Photo: dec.ny.gov
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