Abstract

In tilapia exposed for 3 months to water of pH 4.5, prolactin cell activity, as estimated by ultrastructural morphometry and determination of prolactin synthesis in vitro, was significantly higher than in controls from neutral water. Sodium influx from the water was 50% lower than in the controls, indicating impaired branchial sodium uptake mechanisms. In contrast to predictions based on the results of short-term exposure to acid water—which is known to induce an increase of sodium efflux—the sodium efflux rate was reduced to 70% of the control value. It is concluded that tilapia are able to acclimate to acid water by successful control—probably via prolactin—of diffusional sodium losses across the integument, in particular the gill surface. This compensates for the impaired sodium uptake, and enables the fish to reestablish a positive sodium balance in acid water.

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