Red tides can prove fatal to sharks


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Red tides can alter the brain chemistry of sharks, causing hyper-excitability and death, according to research published in the most recent issue of the journal Aquatic Toxicology.

The study by Dong-Ha Nam and colleagues concluded that poisonous substances (known as brevetoxins) from red tides (harmful algal blooms comprising predominantly of dinoflagellates) have the ability to modify the neurochemistry of shark brains, making them over-excited and even killing them. 

Although the authors focused on the Lemon shark (Negaprion brevirostris), they believe that their results applied to all sharks.

The authors collected 30 Lemon sharks off the coast of central Florida over a period of three years. 

The sharks were collected both during red tide events, as well as during non-bloom (normal) periods. 

One of the sharks collected was a dead individual that had presumably died as a result of exposure to the toxic algal bloom. 

The authors assayed for the levels of brevetoxins in the tissues, neurochemical enzyme activity, as well as neurochemical receptor binding. They found high levels of brevetoxins in the liver, gills and brains of sharks that had been exposed to red tides. They also found significant changes in neurochemical enzymes and receptors that were strongly correlated to elevated levels of brevetoxins in the brains.

According to the authors, the brevetoxin is capable of easily crossing the blood-brain barrier (that protects the brain) and binding very strongly to a protein that controls sodium flow in the brain.  This disruption of the sodium flow causes the nerve cells to overfire, leading to hyperexcitability and ultimately, death. 

The study raises concerns about the physiological and ecological effects of red tides on the marine biota.

For more information, see the paper: Nam, D-H, DH Adams, LJ Flewelling and N Basu (2010) Neurochemical alterations in lemon shark (Negaprion brevirostris) brains in association with brevetoxin exposure. Aquatic Toxicology 99, pp. 351–359.