Dietary Pb Accumulation in Juvenile Freshwater Rainbow Trout (Oncorhynchus mykiss)

Three different diets amended with lead (Pb) nitrate Pb(NO3)2 (7, 77, and 520 μg Pb/g dry weight) and a Pb-free control diet (0.06 μg Pb/g dry weight) were fed to juvenile freshwater rainbow trout for 21 days. Accounting for measured food consumption, the calculated doses per fish were 0.02, 3.7, 39.6, and 221.5 μg/day, for the control, low, intermediate, and high Pb treatments, respectively. The patterns of Pb accumulation over time were determined in various tissues (gills, liver, kidney, intestine, carcass), red blood cells (RBC), and plasma, as well as feeding, growth, hematological, and ionoregulatory parameters. Pb accumulation occurred in a dose-dependent manner in all tissues except the plasma, where accumulation was minimal. Overall, when fed the highest Pb diet, the intestine exhibited the greatest Pb burden (17.8 μg Pb/g tissue wet weight), with high concentrations also found in the kidney (2.4 μg Pb/g tissue wet weight) and liver (1.9 μg Pb/g) at the highest dietary Pb treatment by day 21. The RBCs accumulated a substantial amount of Pb (1.5 μg Pb/g) when compared to the plasma (0.012 μg Pb/g) in the high treatment group. The percentage of Pb retained in the fish decreased with increasing dietary Pb concentrations. Growth, survival, plasma protein, and hematocrit were not significantly affected by dietary Pb. Plasma Ca2+ levels decreased at the beginning of the experiment, whereas Mg2+ levels decreased during the middle of the experiment in both the intermediate and high dietary treatments. Both the Ca2+ and Mg2+ levels stabilized by day 21. Branchial Ca2+ and Na+ influx rates were not affected by dietary Pb, except on day 8 where Na+ influx rates were significantly elevated. The results of this study show that Pb does accumulate internally from the diet when present at levels within the range reported in contaminated benthic invertebrates in nature. We further identify the intestine as a potential target site of chronic toxicity of Pb via the diet, and RBCs as a reservoir of dietary Pb.