The effects of feeding diets containing 500 or 1500 ppm added lead as lead sulfate on zinc and zinc-65 metabolism in Holstein bull calves were investigated. Zinc absorption was slightly (not significantly) reduced in the calves fed lead. Fecal zinc excretion was increased by the lead diets by day 24 of the experiment. Dietary lead had no significant effect on zinc in blood. Except for the tibia, muscle, and brain, stable zinc decreased in all tissues of calves fed the 1500 ppm lead diets, and differences were significant in pancreas, heart, and testicle. A significant decrease was noted in pancreatic zinc in pancreas of calves fed 500 ppm lead. Tissue zinc-65 concentrations were decreased significantly by lead in the tibia and muscle. Intestinal tissue zinc was not affected materially by lead. Dietary lead had very little effect on cellular distribution of zinc in the liver and kidney. In the mucosal cells of the small intestine, lead increased zinc-65 in the cytosol while decreasing it in the crude nuclear fraction. This effect occurred in a linear fashion in all three sections of the small intestine as dietary lead increased.

Sixteen 10-wk-old, phosphorus (P)-depleted Holstein bull calves were fed for 6 wk a control diet containing .08% P or P-supplemented diets containing .14, .20 or .32% P with supplemental P from two sources (CDP and Dynafos). The diets contained .45, .56, .66 and .87% Ca. After 5 wk of the experiment, the calves were dosed orally with 65Zn, and daily total fecal collections were initiated. At the end of the experimental period, the calves were killed and tissue samples were taken for total Zn and 65Zn analyses. Growth, feed intake and feed efficiency improved with increasing dietary P levels. Level of dietary P and Ca had little or no effect (P greater than .05) on total Zn content of rib, tibia, liver, heart, kidney, muscle or blood. Likewise, 65Zn absorption and content in most tissues were not affected (P greater than .05). The results do not preclude the possibility of some minor effects of P levels on Zn metabolism. However, it is apparent that when adequate Zn is fed, any effects are likely to be of little or no practical importance.

Sixteen Holstein intact male calves averaging 85 kg and 74 days of age were assigned randomly to four dietary lead treatments according to body weight. They were fed for ad libitum consumption a control diet containing no added lead or the control diet supplemented with 500, 1500, or 4500 ppm lead as lead sulfate. One calf fed 1500 ppm lead and all four calves fed 4500 ppm lead died within 6 to 10 days after initiation of treatments. Death was sudden with few or no clinical signs prior to death. Those clinical signs that did appear included muscular tremors, gnashing of teeth, bellowing, and convulsions. Four control, four 500 ppm lead, and two 1500 ppm lead-fed calves survived the 7-wk experimental period. Feed consumption, body weight changes, glutamic oxaloacetic transminase and alkaline phosphatase activity in blood plasma, and hemoglobin were not affected significantly by lead treatments. Packed cell volume in calves fed 500 and 1500 ppm added lead was reduced. Lead concentrations in blood, kidney, liver, bone, brain, and muscle were elevated in lead supplemented calves above those of controls. The highest concentrations of lead were in kidney and liver.