Using isolated heads perfused at constant pressure, at rates close to those occurring in vivo, the permeability of the gills of the trout Salmo gairdneri to a range of solutes was measured. Under epinephrine-free conditions, butanol and water showed similar high branchial permeability coefficients. Urea, inulin and dextrans (mol. wt 3000 and 20 000) were 7–12 times less permeant, and mannitol 60-70 times less permeant than water or butanol. Epinephrine, at 10(−6) M, greatly increased the permeability of the gills to the small hydrophilic molecules, water and urea, and to the lipophilic substance, butanol, but did not affect the penetration of the large hydrophilic solutes, mannitol, inulin and dextrans. In the presence of 10(−6) M propanolol, a beta-blocker, epinephrine had no effect on the permeation of any of the test substances except that the permeability to urea decreased somewhat. The results suggest that epinephrine increases the permeability of the membranes of the branchial cells but does not affect the permeation of substances that cross the gill walls by paracellular routes or via an intracellular ‘bulk-transport’ mechanism. Such an action would be expected to increase the branchial transfer of oxygen.
The model Ah-receptor agonist β-naphthoflavone inhibits aflatoxin B1—DNA binding in vivo in rainbow trout at dietary levels that do not induce CYP1A enzymes
