This study examined the impact of elevated dietary Ca2+ on the responses to chronic dietary Pb exposure in juvenile rainbow trout. Trout were fed reference (0.3 μg Pb/g, ∼20 mg Ca2+/g) and Pb-enriched diets (∼50 or 500 μg Pb/g) in the presence of background Ca2+ (∼20 mg Ca2+/g) or (∼60 mg Ca2+/g) of added Ca2+ (as CaCO3) for 42 days. The quantitative order of Pb accumulation in tissues reflected the exposure pathway of Pb via the diet (per tissue wet weight): gut > bone > kidney > liver > spleen > gill > carcass > brain > white muscle. The anterior intestine accumulated the most Pb per tissue wet weight, while the bone accumulated the most Pb per fish weight. Pb concentrations were much higher in the posterior kidney than the anterior kidney. Simultaneous addition of Ca2+ to the diet had an overall protective effect in all the tissues analysed in reducing Pb accumulation. The RBCs accumulated 100 times more Pb when compared to the plasma, while the whole blood δ-aminolevulinic acid dehydratase was inhibited in the high treatment group without added Ca2+, by the end of the exposure. Neither plasma Cl-, K+, Mg2+ nor Na+, K+-ATPase activities in the gills, mid- and posterior intestine were affected. However, there were mild disruptions in plasma Na+ and Ca2+ levels in the elevated Pb and Ca2+ treatment groups, and a significant up-regulation in Na+, K+-ATPase activity at the anterior intestine in fish fed the high Pb diets with background or added Ca2+. By day 42, Pb levels in most tissues had either stabilized or started to decrease, indicating some capacity for regulation of accumulated loads. We conclude that elevated dietary Ca2+ levels will be protective in reducing Pb burdens in freshwater juvenile rainbow trout exposed to environments contaminated with waterborne Pb.
- δ-Aminolevulinic acid dehydratase (ALAD)
- Calcium (Ca)
- Lead (Pb)
ASJC Scopus subject areas
- Aquatic Science