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Paralytic shellfish toxins cause mutation that allows clams to accumulate 100 times more toxin

Exposure to toxins that cause paralytic shellfish poisoning can result in a mutation that makes clams much more resistant to the toxin than other clams, making them more dangerous to humans, according to a study published this week in the journal Nature. Paralytic shellfish toxins (PSTs) are produced by algae that appear in certain coastal areas in the United States in an event known as an algal bloom, commonly called a "red tide." People who eat clams exposed to the PSTs can suffer the paralytic effects of the toxins, and there is no cure for the poisoning.

Researchers found that softshell clams in areas frequently affected by harmful algal blooms are more resistant to PSTs than clams from other areas. They knew from earlier work that the toxins block the function of the sodium ion channel, a molecular switch that generates the nerve impulse and therefore is vital to neural and muscular activity. What they did not know was why some clams were more resistant than others.

The collaborative team of scientists from Washington, Maine, and Nova Scotia determined that the toxins cause a small mutation that prevents them from binding to the sodium ion channels in the clam's nerve tissue. Instead of binding to the ion channels and causing paralysis and later death, the toxins build up in the clam, accumulating about 100 times more toxin than in clams without the mutation. The resistance allows them to continue feeding during the harmful algal bloom and accumulate levels of toxins that increase risk of paralytic shellfish poisoning in humans.

Scientists and public health officials knew that clams carrying the toxins could survive after an algal bloom, which is why clams are tested well after a "red tide" event to reduce the risk of poisoning in humans. But no one knew until now why the clams were accumulating the toxins.

"It is quite surprising that the toxins could serve as selective agents for a mutation in the sodium ion channel, and that the mutation
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Contact: Justin Reedy
jreedy@u.washington.edu
206-685-0382
University of Washington
6-Apr-2005


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