Abstract

Interest in the interactions between dietary constituents in the gut is increasing, but information remains sparse. In this study rainbow trout were fed non-enriched (186.7±19.0μgZng−1 (dw)), enriched (20% increase) and hyper-enriched Zn (200% increase) diet for 21d followed by a single meal of Cd-spiked food (188.6±9.9μgCdg−1 (dw)). Intestinal, hepatic and renal Zn burdens were measured on Days 7, 14 and 21 and Cd concentrations in the same tissue were measured 48h-post Cd exposure. Oxidative stress was measured as lipid peroxidation in dissected tissues and intestinal mucus was quantified as sialic acid using the thiobarbituric acid assay. Rainbow trout maintained on the hyper-enriched Zn diet experienced significantly increased intestinal mucus secretion (p<0.01), were the only treatment group not to accumulate Cd in the intestine, and there was also no increase in intestinal oxidative damage. Conversely, fish fed the non-enriched and enriched Zn diets did not produce greater than basal levels of intestinal mucus and accumulated significantly greater concentrations of Cd in the intestine (p<0.01) leading to significant localised Cd-induced lipid peroxidation (p<0.01). High levels of mucus production correlated to lower incidences of lipid peroxidation (r2=0.54, p<0.05). These results demonstrate that mucus production stimulated by a high Zn diet have an inhibitory effect on Cd accumulation in the intestine and on Cd-induced lipid peroxidation. Mechanistically, it is likely that the elevated mucus production provides a barrier to Cd uptake. This study describes how one dietary constituent directly modifies the gut environment which indirectly influences the fate of another ingested cation.

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