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The Protective Role of Dietary Calcium Against Cadmium Uptake and Toxicity in Freshwater Fish: an Important Role for the Stomach

Chris M. Wood A D , Natasha M. Franklin A B and Som Niyogi A C
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A Department of Biology, McMaster University, Hamilton, ON L8S 4K1, Canada.

B Present Address: CSIRO Land and Water, Bangor, NSW 2234, Australia.

C Present Address: Department of Biology, University of Saskatchewan, Saskatoon, SK S7N 5E2, Canada.

D Corresponding author. Email: woodcm@mcmaster.ca

Environmental Chemistry 3(6) 389-394 https://doi.org/10.1071/EN06056
Submitted: 3 October 2006  Accepted: 1 November 2006   Published: 13 December 2006

Environmental Context. Contamination of freshwater ecosystems by cadmium is of increasing concern with accumulation and toxicity in aquatic animals occurring through both waterborne and dietary routes. Increases in water calcium (‘hardness’) levels protect against waterborne uptake. Physiological research on freshwater fish has demonstrated that this occurs because cadmium moves through the calcium uptake pathway at the gills. Surprisingly, elevated dietary calcium also protects against waterborne exposure by down-regulating the calcium uptake pathway at the gills, and against dietary exposure by reducing cadmium uptake through the gastrointestinal tract. In both cases, the stomach is the critical site of action.

Abstract. 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.

Keywords. : aquatic chemistry — cadmium — calcium — fish — hardness — metal uptake


Acknowledgements

The research summarized here has been supported by the NSERC (Canada) CRD, Strategic, MITE-RN, MITHE-RN, and Discovery Programs in collaboration with funding from the International Copper Association, the International Lead Zinc Research Organization, the Nickel Producers Environmental Research Association, Noranda-Falconbridge, Teck-Comino, and Inco. CMW is supported by the Canada Research Chair Program. We thank Rebecca Kent and Joanne Kam for their contributions.


References


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