The Roles of Calcium and Salinity in Protecting Against Physiological Symptoms of Waterborne Zinc Toxicity in the Euryhaline Killifish (fundulus Heteroclitus)

In fresh water, environmental Ca ameliorates Zn toxicity because Ca2+ and Zn2+ compete for uptake at the gills. Zn toxicity is also lower in sea water, but it is unclear whether this is due to increased Ca2+ concentration, and/or to the other ions present at higher salinity. Using the euryhaline killifish, we evaluated the relative roles of Ca2+ (as CaNO3) versus the other ions contributing to salinity in protecting against physiological symptoms of Zn2+ toxicity. Killifish were exposed to a sublethal level of Zn (500 mu g/L, as ZnSO4) for 96 h in either fresh water (0 % salinity) at low (1 mmol/L) and High Ca (10 mmol/L) or 35 ppt sea water (100 % salinity) at low (1 mmol/L) and High Ca (10 mmol/L). At 0 % salinity, High Ca partly or completely protected against the following effects of Zn seen at Low Ca: elevated plasma Zn, hypocalcaemia, inhibited unidirectional Ca2+ influx, inhibited branchial Na+/K(+ )ATPase and Ca(2+ )ATPase activities, and oxidative stress in gills, liver, intestine, and muscle. At 100 % salinity, in the presence of 1 mmol/L (Low Ca), Zn caused no disturbances in most of these same parameters, showing that the "non-Ca " components of sea water alone provided complete protection. However, for a few endpoints (inhibited intestinal Ca(2+ )ATPase activity, oxidative stress in gill and liver), High Ca (10 mmol/L) was needed to provide full protection against Zn in 100 % salinity. There was no instance where the combination of 100 % salinity and High Ca failed to provide complete protection against Zn-induced disturbances in sea water.