Abstract

Pyrethroids are extensively used for the control of insect pests and disease vectors. Pyrethroids are regarded safe due to their selective toxicity: they are effective against insects but relatively harmless to mammals and birds. Unfortunately, pyrethroids are very toxic to fishes. The high toxicity of pyrethroids to fishes is only partly explained by slow metabolic elimination of pyrethroids, suggesting that some molecular targets in vital organs of the fish body are sensitive to pyrethroids. To this end we tested the effect of deltamethrin (DM) on fish (crucian carp, Carassius carassius) heart function in vitro. In sinoatrial preparations of the crucian carp heart DM (10μM) caused irregularities in rate and rhythm of atrial beating and strong reductions in force of atrial contraction, thus indicating that DM is arrhythmogenic to the fish heart. Consistent with this, DM (10.0μM) induced irregularities in electrical activity (surface electrocardiogram) of spontaneous beating hearts in vitro. In isolated ventricular myocytes, DM (0.1–30.0μM) modified Na+ current by slowing channel closing and shifting reversal potential and steady-state activation of the current to more negative voltages. Maximally about 48% of the cardiac Na+ channels were affected by DM with a half-maximal effect occurring at the concentration of 1.3μM. These findings indicate that DM can be cardiotoxic to the crucian carp and that these effects could be due to DM related changes in Na+ channel function. These findings indicate that in addition to their neurotoxicity effects pyrethroid could also be cardiotoxic to fishes.

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