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Pardaxin Produces Sodium Influx in the Teleost Gill-like Opercular Epithelia
1 Department of Physiology and Biophysics, New York University Medical Center, 550 First Avenue, New York, New York 10016, U.S.A. and Osborn Laboratories of Marine Sciences, New York Aquarium, New York Zoological Society, Brooklyn, New York 11224, U.S.A.; Osborn Laboratories of Marine Sciences, New York Aquarium, New York Zoological Society, Brooklyn, New York 11224 U.S.A.
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 2.2 µequiv cm-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.
Key words: Pardaxin, fish toxin, ion-osmoregulation, skin epithelium.
Submitted on August 16, 1982
Accepted on January 31, 1983