|Food selection, growth and physiology in relation to dietary sodium chloride content in rainbow trout (Oncorhynchus mykiss) under chronic waterborne Cu exposure|Niyogi, S.; Kamunde, C.N.; Wood, C.M. (2006). Food selection, growth and physiology in relation to dietary sodium chloride content in rainbow trout (Oncorhynchus mykiss) under chronic waterborne Cu exposure. Aquat. Toxicol. 77(2): 210-221. dx.doi.org/10.1016/j.aquatox.2005.12.005
In: Aquatic Toxicology. Elsevier Science: Tokyo; New York; London; Amsterdam. ISSN 0166-445X, more
Diets; Feeding behaviour; Oncorhynchus mykiss (Walbaum, 1792) [WoRMS]; Marine
|Authors|| || Top |
- Niyogi, S.
- Kamunde, C.N.
- Wood, C.M.
Waterborne Cu is toxic to Na+ and Cl− regulation in freshwater fish, and Cu is taken up, at least in part, via the Na+-transport pathway in the gills. Therefore, we hypothesized that freshwater fish may mitigate the toxic effects of waterborne Cu by selecting a NaCl-enriched diet over a normal diet. We tested this hypothesis in juvenile rainbow trout (Oncorhynchus mykiss) by offering them the choice between NaCl-enriched (1.9 mmol g−1 Na+) and normal (0.2 mmol g−1 Na+) diets under a chronic waterborne Cu exposure of 55 μg L−1 for a period of 28 days. Contrary to expectation, trout exhibited a preference for NaCl-enriched diet under control conditions, while exposure to chronic waterborne Cu severely disrupted their normal feeding pattern with an accompanying loss of preference for the NaCl-enriched diet. Waterborne Cu exposure also severely affected appetite and growth. Both appetite and growth gradually recovered with time, but remained significantly impaired relative to Cu-unexposed fish until the end of the exposure. Waterborne Cu exposure also significantly increased Cu accumulations in target organs (gill, liver, and gut), plasma and whole body. However, Cu accumulation decreased substantially towards the end of the exposure in target organs and whole body as well as in plasma in Cu-exposed fish with dietary choice relative to Cu-exposed fish with normal diet. These adjustments were concurrent with the gradual recovery of appetite, which also led to increased ingestion of the NaCl-enriched diet. Interestingly, this elevated dietary uptake of NaCl produced significant stimulation of Na+ efflux in Cu-exposed fish. Subsequently, it also led to significant elevation of Na+ levels in target organs and whole body, and restored the decrease of plasma Na+ and Cl− levels in Cu-exposed fish. The NaCl supplemented diet appeared to be beneficial in compensating Na+ and Cl− losses from the body induced by waterborne Cu. Overall, these results demonstrate that a NaCl-enriched diet, although consumed in relatively reduced quantities due to the impairment of food selection and appetite, can help to protect freshwater fish against chronic waterborne Cu toxicity.