The protective role of dietary calcium against cadmium uptake and toxicity in freshwater fish: An Important role for the stomach

Waterborne cadmium causes toxicity in freshwater fish by inducing hypocalcaemia. Research on the rainbow trout (Oncorhynchus mykiss), a sensitive model species, has demonstrated that this occurs because Cd²⁺ ions compete with waterborne Ca²⁺ ions for the active branchial uptake pathway which normally ensures internal homeostasis of calcium levels. Therefore, increases in waterborne calcium concentrations (?hardness') protect against waterborne cadmium uptake and toxicity in both acute and chronic exposures. Increases in dietary calcium concentration also protect against waterborne exposure, because elevated gastrointestinal calcium uptake down-regulates the Ca²⁺ uptake pathway at the gills, thereby simultaneously reducing Cd²⁺ entry. Furthermore, dietary calcium also protects against dietborne cadmium exposure, although the physiological mechanisms appear to differ from those at the gills. Surprisingly, the principal site of this inhibitory action of dietary calcium on gastrointestinal cadmium uptake appears to be the stomach, which is also the major site of gastrointestinal calcium uptake, rather than the intestine as in mammals. These results underline the importance of considering not only water chemistry but also dietary chemistry in the environmental regulation of cadmium, and suggest that fish in the wild under chronic cadmium stress would benefit by switching to a more calcium-rich diet. While diet switching has been seen in the wild in fish under metal stress, its etiology remains unknown; to date, laboratory experiments have not been able to show that voluntary diet-switching of an adaptive nature actually occurs.