Brevetoxins or neurotoxic shellfish poisons

Certain microalgae produce a large lipophilic polyether toxin, called brevetoxin. A long history of toxic microalgal blooms exists in the Gulf of Mexico, blooms that have caused massive fish kills and respiratory irritation in humans. It was later realised that the toxin in these blooms could also be passed to humans via shellfish to cause a syndrome named neurotoxic shellfish poisoning (NSP). Reports of NSP was limited for a long time to the Americas until cases were reported in the early 1990’s in New Zealand and Australia.

The NSP syndrome

Victims of NSP can be mistaken as suffering the fish-poisoning syndrome, ciguatera. Typical symptoms are tingling in the face, throat and digits, dizziness, fever, chills, muscle pains, abdominal cramping, nausea, diarrhoea, vomiting, headache, reduced heart rate and pupil dilation. There have been no reported fatalities from NSP although the toxin kills test mammals when administered by various routes, including orally.

The NSP causing toxins, the brevetoxins

The origin of these NSP inducing toxins is a dinoflagellate called Ptychodiscus (formerly Gymnodiunium) brevis from which the toxin name is derived. The brevetoxins are lipophilic 10- and 11-ring polyether chemicals. There two classes of brevetoxins with the first containing 11 6-membered rings except for two heptameric and an 8-membered ring (Figure 1). The second class of brevetoxins have only 10 rings with great variation in the size of the rings with the smallest having only five bonds and the largest having nine (Figure 2). Solutions with a pH beyond 2 or 10 degrade the toxins.

Figure 1 Brevetoxin-A, a type I brevetoxin

Figure 2 Brevetoxin-B, a type II brevetoxin

How the toxins work

Brevetoxins bind to the ion channel of nerve and muscle tissue that selectively allows sodium to pass into the cell. These sodium channels open during an action potential in response to the change in the electrical potential across the cell membrane. Brevetoxins change the voltage at which this opening occurs nearer to the voltage threshold that triggers this process essentially making the sodium channel and consequently the affected nervous and muscular cells hyperexcitable.

Further reading

Atchison WD, Luke VS, Narahashi T, Vogel SM (1986) Nerve membrane sodium channels as the target site of brevetoxins at neuromuscular junctions. Br J Pharmacol 189, 731-738.

Baden DG & Mende TJ (1982) Toxicity of two toxins from the Florida red tide marine dinoflagellate, Ptychodiscus brevis. Toxicon 20, 457-461.

Baden DG (1989) Brevetoxins: unique polyether dinoflagellate toxins. FASEB J 3, 1807-1817.

Lin Y, Risk M, Ray SM, van Engen D, Clardy J, Golik J, James JC & Nakanishi K (1981) Isolation and structure of brevetoxin B from "red tide" dinoflagellate Ptychodiscus brevis (Gymnodinium breve). J Am Chem Soc 103, 6773 -6776.

Lombet A, Bidard JN & Lazdunski M (1987) Ciguatoxin and brevetoxins share a common receptor site on the neuronal voltage-dependent Na+ channel. FEBS Lett 219, 355-359.

K Nakanishi (1985) The chemistry of brevetoxins: a review. Toxicon 23, 473-479.

Ray SM & Aldrich DV (1965) Gymnodinium breve: induction of shellfish poisoning in chicks. Science 148, 1748 -1750.

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Page last updated - December 18, 2008

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