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Equinatoxins: A Review

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Marine and Freshwater Toxins

Part of the book series: Toxinology ((TOXI))

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Abstract

Equinatoxins are basic pore forming proteins isolated from the sea anemone Actinia equina. Pore formation is the underlying mechanism of their hemolytic and cytolytic effect. Equinatoxin concentrations required for pore formation are higher than those causing significant effects in heart and skeletal muscle. This means that other mechanisms must also be involved in the toxic and lethal effects of equinatoxins. Effects of equinatoxins have been studied on lipid bilayers, several cells and cell lines, on isolated organs and in vivo. Different cells have distinct susceptibilities to the toxin, ranging from <1 pM up to >100 nM. The cells are swollen after a prolonged treatment with low concentrations of equinatoxin II, or rapidly when 100 nM or higher concentrations of the toxin are used. Equinatoxins increase cation-specific membrane conductance and leakage current, affect the function of potassium and sodium channels in nerve, muscle and erythrocytes, increase intracellular Ca2+ activity, and cause a significant increase of cell volume. In smooth muscle cells and in neuroblastoma NG108-15 cells, an increase in intracellular Ca2+ activity is observed after exposure to 100 nM equinatoxin II. The large difference in toxin concentrations needed for the pore formation and other effects suggest that equinatoxins exert their effects through at least two different mechanisms. It is well known that lipid environment is important for the proper functioning of membrane channels and other membrane proteins. It is possible that toxin monomers disturb local conditions around ionic channels and/or receptors by binding in the vicinity of those structures, thus altering their function.

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Correspondence to Dušan Šuput .

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Šuput, D. (2016). Equinatoxins: A Review. In: Gopalakrishnakone, P., Haddad Jr., V., Tubaro, A., Kim, E., Kem, W. (eds) Marine and Freshwater Toxins. Toxinology. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-6419-4_1

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