Plasma prolactin, cortisol, and thyroid responses of the brown trout (Salmo trutta) exposed to lethal and sublethal aluminium in acidic soft waters.

Brown trout, with indwelling dorsal aortic cannulae, were exposed to various concentrations of aluminium (Al; 50 μg liter−1, 100% mortality over 48 hr; 25 μg liter−1, 50% mortality over 120 hr; 12.5 μg liter−1, 0% mortality over 120 hr) in acidic (pH 5.0) soft water. The plasma concentrations of prolactin (PRL), cortisol, thyroxine (T4), and triiodothyronine (T3) were monitored. Plasma PRL concentrations were transiently depressed (to less than 20% of resting concentrations) after 12 hr in trout in the two highest water Al concentrations, but were unchanged in the trout exposed to 12.5 μg liter−1Al. Plasma cortisol concentrations were elevated in response to all water Al levels and remained elevated in trout in the lethal conditions. The sublethally exposed trout showed a recovery in plasma cortisol concentrations by 120 hr. Plasma T4concentrations were significantly elevated in trout exposed to both the lethal and the sublethal Al concentrations (from mean resting concentrations of 1–2 ng ml−1to peaks of 8.9 and 9.0 ng ml−1in the 50 and 12.5 μg liter−1Al groups, respectively), although a recovery in plasma concentrations was evident in the sublethally exposed trout from 72 hr onwards. Plasma T3concentrations were relatively stable in the trout exposed to the two highest doses of Al, whereas the trout under the lowest, sublethal, Al conditions exhibited a sustained (12–72 hr) elevation in plasma T3concentrations (from a mean resting concentration of 0.9 ng ml−1to a peak of 4.2 ng ml−1at 48 hr). No clear relationship was apparent between the plasma PRL concentrations and the previously reported ionoregulatory status of the trout.