Key result
An unknown toxin from Dinophysis sp.-contaminated mussels decreased stimulated peak tension, shortened action potential duration, inhibited L-type Ca current, and increased outward current in frog heart.
Why the study?
Does an unknown toxin from Dinophysis sp.-contaminated mussels alter the electrical and mechanical activity of frog heart muscle?
Does an unknown toxin from Dinophysis sp.-contaminated mussels alter the electrical and mechanical activity of frog heart muscle?
An unknown toxin from Dinophysis sp.-contaminated mussels alters cardiac electrical and mechanical activity by inhibiting L-type calcium currents and increasing outward potassium currents, distinct from okadaic acid.
Answers are grounded in this paper and cite their sources.
Suggests possible cardiotoxicity from Dinophysis toxins; leaves open translation to mammalian or human hearts.
The effects of an unknown toxin, isolated along with okadaic acid from the hepatopancreas of French mussels contaminated by Dinophysis sp., producing ataxia, neurologic symptoms, bradycardia, arrhythmias, electrocardiographic changes, and cardiac arrest, have been studied in terms of the electrical and mechanical activity of frog atrial heart muscle. The toxin, in a dose-dependent manner, decreased the amplitude of the stimulated peak tension of isolated fibers. The toxin (1-36 micrograms/ml) did not modify the membrane resting potential but decreased the amplitude of the plateau and shortened the duration of the action potential. The toxin inhibited the Cd-sensitive L-type Ca current and increased a 4-aminopyridine-sensitive outward current in voltage-clamped cardiac myocytes. The data show that the cardiac effect of the toxin is markedly different from that of okadaic acid.
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Sauviat et al. (1996) studied this question. Unknown toxin isolated from Dinophysis sp.-contaminated French mussels was evaluated on Electrical and mechanical activity of frog atrial heart muscle. An unknown toxin from Dinophysis sp.-contaminated mussels decreased stimulated peak tension, shortened action potential duration, inhibited L-type Ca current, and increased outward current in frog heart.
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