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The mechanism of action of the actino­porins, substances from the sea anemone Actinia equina, is by cation selective pore formation in the cellular membranes that consequently cause cell lysis. The aim of the present study was to inves­tigate the mechanism of the toxicity of actinoporin equinatoxin I. In in vivo experiments the measurements of ECG (lead I), respiratory activ­ity and arterial blood pressure were taken, the hematological and biochemical analysis of the blood samples were performed. The tissue sam­ples were taken for pathomorphologic examina­tion. After application of equinatoxin I there was a fall in the arterial pressure. A prominent brady­cardia was followed by the phase of the relative tahycardia. During the bradycardia the amplitude of P waves was diminished and the P-Q interval was prolonged. Eventually ventricular extrasistoly developed and P waves disappeared. The tahypnoe was followed by the breathing cessation. In a while the animal started to breath and termi­nated again. The experimental animals died due to the cardio-respiratory arrest. The blood sam­ples revealed haemolysis and hyperkalemia, fall of hematocrit and rise in potassium plasma con­centration for four times. Pathomorphological examination showed pulmonary edema with hem­orrhages and early necrosis of cardiomyocytes. The lethality of actinoporins is due to cardiores­piratory arrest. Equinatoxin I differentiates from the other actinoporins in the special activity on the excitability of the atrium, as the P waves in ECG disappeared. The induced hyperkalemia was not sufficient to explain the lethality of the toxin. Equinatoxin I induces acute necrosis of myocardi­um. Together with pulmonary edema this is the most important mechanism that leads to the death of experimental animals.