1. Transport by the gill-like opercular epithelium of the teleost, Fundulus heteroclitus, was affected by pardaxin, a protein that is toxic to fish, isolated from the Red Sea flatfish Pardachirus marmoratus.

  2. Administration of pardaxin to the mucosal (seawater) side of the isolated short-circuited opercular epithelium, caused a transient stimulation of the active transport of ions (Isc), followed by an inhibition. The Isc stimulation was abolished by ouabain or/and in Na+-free Ringer but not in Cl-or HCO3-Ringer. When applied to the serosal (blood) side, pardaxin did not affect the Isc.

  3. Pardaxin produced a net transient Na+ current from the mucosal side to the serosal side of 2·2μequivcm−2h−1. It is concluded that this Na+ influx caused the Isc stimulation. The influx is suggested to be the mechanism of pardaxin’s toxicity in fish.

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