Double Trouble for Trout / Wisconsin Sea Grant

Double Trouble for Trout
Researchers explore dioxin’s effects on cellular processes

As embryos and sac fry, lake trout are among the most vulnerable of all fish to PCBs, dioxins, and similar pollutants. When laboratory trout are exposed to these compounds at levels found in the environment, their heads develop abnormally, their yolk sacs swell with fluid, their cardiovascular systems collapse, and they die.

A normal rainbow trout yolk sac (left) seven days after hatching. Blood flow makes blood vessels readily apparent. Yolk sac of a trout exposed to dioxin (right) is swollen with fluid and blood flow has completely stopped.

With support from UW Sea Grant, Warren Heideman and Richard Peterson, toxicologists at UW-Madison, are working to reveal the precise cellular processes that underlie dioxin’s pernicious effects on young trout.

The team is also studying what dioxin does to cellular mechanisms in zebrafish, a well-studied species that is easier to work with than trout. “They’re the fruit fly of the vertebrate world,” Heideman said.

The work will help scientists better understand the risks that dioxin poses to lake trout. It will also provide a framework for assessing those risks to other freshwater fish without having to test tens of thousands of species individually, he said.

“If we understood what’s going on biochemically [in trout], we might be able to come up with markers for other fish that would say, ‘Oh this other fish is really sensitive, so if we have this fish population that’s downstream of some source of pollution, it would really be at risk. But another species might not,’” Heideman said.

Heideman says his work with Peterson will also help scientists understand how contaminants can worsen the adverse effects of other environmental stresses, such as low oxygen concentrations in water. Such combinations of stresses may be fatal to fish that might withstand either stress alone.

Heideman suggests that dioxin may commandeer cellular communications systems and direct certain genes to sabotage cells’ normal operations.

A central part of this communications system is a protein called an aryl hydrocarbon (Ah) receptor. This receptor acts as an “on” switch for certain genes, telling them to manufacture molecules required for specific cellular functions. These functions are required only at certain times, and under normal conditions the Ah receptor sends the “on” signal only when it is needed.

When dioxin enters the cell, however, it effectively jams the Ah receptor switch in the “on” position-even if it should be off. That directs the target genes to crank out their special-purpose molecules continually, wreaking havoc in the cell.

Dioxin may cause double trouble in trout, as Peterson and Heideman recently found in another project supported by UW Sea Grant. They discovered that rainbow trout, unlike mammals, actually have two forms of Ah receptors. These two forms may allow dioxin to misdirect more genes in trout than it does in mammals, Heideman says.

“That may explain why certain fish species respond so sensitively to PCBs and dioxin compared to mammals,” Heideman said.

Heideman and Peterson hope to identify the genes that are regulated by the two different Ah receptors in trout. If they succeed, they and other scientists will be better equipped to describe the risk posed by combinations of dioxin, PCBs, and environmental stresses to wild populations of lake trout and other fish species in the Great Lakes.

- John Karl