Benefits of feeding pharmacological concentrations of zinc (Zn) provided by Zn oxide (ZnO) to 21-d conventionally weaned pigs in the nursery have been documented; however, several management questions remain. We conducted two experiments to evaluate the effect on growth from feeding 3,000 ppm Zn as ZnO during different weeks of the nursery period. In Exp. 1 (n = 138, 11.5 d of age, 3.8 kg BW) and Exp. 2 (n = 246, 24.5 d of age, 7.2 kg BW), pigs were fed either basal diets containing 100 ppm supplemental Zn (adequate) or the same diet with an additional 3,000 ppm Zn (high) supplied as ZnO. Pigs were fed four or two dietary phases in Exp. 1 and 2, respectively, that changed in dietary ingredients and nutrient content (lysine and crude protein) to meet the changing physiological needs of the pigs for the 28-d nursery period. Dietary Zn treatments were 1) adequate Zn fed wk 1 to 4, 2) high Zn fed wk 1, 3) high Zn fed wk 2, 4) high Zn fed wk 1 and 2, 5) high Zn fed wk 2 and 3, and 6) high Zn fed wk 1 to 4. In Exp. 1 and 2, pigs fed high Zn for wk 1 and 2 or the entire 28-d nursery period had the greatest (P < .05) ADG. During any week, pigs fed high Zn had greater concentrations of hepatic metallothionein and Zn in plasma, liver, and kidney than those pigs fed adequate Zn (P < .05). In summary, both early- and traditionally weaned pigs need to be fed pharmacological concentrations of Zn provided as ZnO for a minimum of 2 wk immediately after weaning to enhance growth.

An experiment was conducted to evaluate the effects of supplementing increasing concentrations of Fe to the diet of nursery pigs on growth performance and indices of hematological and mineral status. Pigs (n = 225; 6.5 kg; 19 +/- 3 d) were allotted randomly by BW, litter, and gender to one of five dietary treatments (five pigs per pen; nine pens per treatment). Basal diets for each phase (Phase 1: d 0 to 7; Phase 2: d 7 to 21; Phase 3: d 21 to 35) were formulated to contain minimal Fe concentration and then supplemented with 0, 25, 50, 100, and 150 mg Fe/kg of diet (as-fed basis) from ferrous sulfate. Three pigs per pen (n = 135) were chosen and bled throughout (d 0, 7, 21, and 35) to determine hemoglobin (Hb), hematocrit (Hct), transferrin (Tf), and plasma Fe (PFe). In addition, pigs (n = 5; 5.9 kg; 19 +/- 3 d) from the contemporary group were killed at d 0 to establish baseline (BL), and 30 pigs (six pigs/treatment) were killed at d 35 to determine whole-body and liver mineral concentrations. The improvements in growth performance during Phase 2 (ADG = linear, P = 0.04; ADFI = linear, P = 0.10; G:F = quadratic, P = 0.07) were of sufficient magnitude that dietary treatments tended to increase ADG (linear, P = 0.08), ADFI (quadratic, P = 0.09), and G:F (quadratic, P = 0.10) for the 35-d experiment. Hematological variables were not affected until d 21, at which time dietary Fe supplementation resulted in a linear increase (P = 0.03) in Hb, Hct, and PFe. This linear increase (P = 0.001) was maintained until d 35 of the experiment; however, dietary treatments resulted in a linear decrease (P = 0.01) in Tf on d 35. Whole-body Fe concentration increased (linear, P = 0.01) in pigs due to increasing dietary Fe concentrations. Moreover, pigs fed for 35 d had greater (P = 0.02) whole-body Fe, Zn, Mg, Mn, Ca, and P concentrations and lower (P = 0.001) whole-body Cu concentration than BL. Hepatic Fe concentration increased (linear, P = 0.001) in pigs due to dietary treatments; however, the hepatic Fe concentration of all pigs killed on d 35 was lower (P = 0.001) than the BL. Results suggest that Fe contributed by feed ingredients was not sufficient to maintain indices of Fe status. The decrease in Fe stores of the pigs was not severe enough to reduce growth performance. Even so, the lessening of a pig's Fe stores during this rapid growth period may result in the occurrence of anemia during the subsequent grower and finisher periods.

Egg injection studies were performed to confirm a proposed model of relative sensitivity of birds to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In this model, species are classified as belonging to one of three categories of sensitivity based on amino acid substitutions in the ligand-binding domain of the aryl hydrocarbon receptor. Embryo lethality and relative potencies of 2,3,7,8-tetrachlorodibenzofuran (TCDF) and 2,3,4,7,8-pentachlorodibenzofuran (PeCDF) were compared with TCDD for Japanese quail (Coturnix japonica; least sensitive), Common pheasant (Phasianus colchicus; moderately sensitive), and White Leghorn chicken (Gallus gallus domesticus; most sensitive). Doses ranging from 0.044 to 37 pmol/g egg (0.015-12 ng/g egg) were injected into the air cell of eggs prior to incubation. LD(50) (95% confidence intervals) values, based on rate of hatching for TCDD, PeCDF, and TCDF, were 30 (25-36), 4.9 (2.3-9.2), and 15 (11-24) pmol/g egg for the quail, 3.5 (2.3-6.3), 0.61 (0.28-1.2), and 1.2 (0.62-2.2) pmol/g egg for pheasant, and 0.66 (0.47-0.90), 0.75 (0.64-0.87), and 0.33 (0.23-0.45) pmol/g egg for chicken, respectively. LD(50)-based relative potencies of PeCDF and TCDF were 6.1 and 2.0 for quail, 5.7 and 2.9 for pheasant, and 0.88 and 2.0 for chicken, respectively. TCDD was not the most potent compound among the species tested, with PeCDF and TCDF being more potent than TCDD in the quail and pheasant. TCDF was the most potent in chicken. Species sensitivity was as expected for TCDD and TCDF, whereas for PeCDF, the chicken and pheasant were similar in sensitivity and both were more sensitive than the quail. Results from companion in vitro studies are generally similar to those reported here with a few exceptions.

Two experiments were conducted to evaluate the effects of dietary Zn and Fe supplementation on mineral excretion, body composition, and mineral status of nursery pigs. In Exp. 1 (n = 24; 6.5 kg; 16 to 20 d of age) and 2 (n = 24; 7.2 kg; 19 to 21 d of age), littermate crossbred barrows were weaned and allotted randomly by BW, within litter, to dietary treatments and housed individually in stainless steel pens. In Exp. 1, Phases 1 (d 0 to 7) and 2 (d 7 to 14) diets (as-fed basis) were: 1) NC (negative control, no added Zn source); 2) ZnO (NC + 2,000 mg/kg as Zn oxide); and 3) ZnM (NC + 2,000 mg/kg as Zn Met). In Exp. 2, diets for each phase (Phase 1 = d 0 to 7; Phase 2 = d 7 to 21; Phase 3 = d 21 to 35) were the basal diet supplemented with 0, 25, 50, 100, and 150 mg/kg Fe (as-fed basis) as ferrous sulfate. Orts, feces, and urine were collected daily in Exp. 1; whereas pigs had a 4-d adjustment period followed by a 3-d total collection period (Period 1 = d 5 to 7; Period 2 = d 12 to 14; Period 3 = d 26 to 28) during each phase in Exp. 2. Blood samples were obtained from pigs on d 0, 7, and 14 in Exp. 1 and d 0, 7, 21, and 35 in Exp. 2 to determine hemoglobin (Hb), hematocrit (Hct), and plasma Cu, (PCu), Fe (PFe), and Zn (PZn). Pigs in Exp. 1 were killed at d 14 (mean BW = 8.7 kg) to determine whole-body, liver, and kidney mineral concentrations. There were no differences in growth performance in Exp. 1 or 2. In Exp. 1, pigs fed ZnO or ZnM diets had greater (P < 0.001) dietary Zn intake during the 14-d study and greater fecal Zn excretion during Phase 2 compared with pigs fed the NC diet. Pigs fed 2,000 mg/kg, regardless of Zn source, had greater (P < 0.010) PZn on d 7 and 14 than pigs fed the NC diet. Whole-body Zn, liver Fe and Zn, and kidney Cu concentrations were greater (P < 0.010), whereas kidney Fe and Zn concentrations were less (P < 0.010) in pigs fed pharmacological Zn diets than pigs fed the NC diet. In Exp. 2, dietary Fe supplementation tended to increase (linear, P = 0.075) dietary DMI, resulting in a linear increase (P < 0.050) in dietary Fe, Cu, Mg, Mn, P, and Zn intake. Subsequently, a linear increase (P < 0.010) in fecal Fe and Zn excretion was observed. Increasing dietary Fe resulted in a linear increase in Hb, Hct, and PFe on d 21 (P < 0.050) and 35 (P < 0.010). Results suggest that dietary Zn or Fe additions increase mineral status of nursery pigs. Once tissue mineral stores are loaded, dietary minerals in excess of the body's requirement are excreted.

Deoxynivalenol (DON, vomitoxin), a trichothecene mycotoxin produced by Fusarium sp. that frequently occurs in cereal grains, has been associated with human and animal food poisoning. Although a common hallmark of DON-induced toxicity is the rapid onset of emesis, the mechanisms for this adverse effect are not fully understood. Recently, our laboratory has demonstrated that the mink (Neovison vison) is a suitable small animal model for investigating trichothecene-induced emesis. The goal of this study was to use this model to determine the roles of two gut satiety hormones, peptide YY3-36 (PYY3-36) and cholecystokinin (CCK), and the neurotransmitter 5-hydroxytryptamine (5-HT) in DON-induced emesis. Following ip exposure to DON at 0.1 and 0.25mg/kg bw, emesis induction ensued within 15-30min and then persisted up to 120min. Plasma DON measurement revealed that this emesis period correlated with the rapid distribution and clearance of the toxin. Significant elevations in both plasma PYY3-36 (30-60min) and 5-HT (60min) but not CCK were observed during emesis. Pretreatment with the neuropeptide Y2 receptor antagonist JNJ-31020028 attenuated DON- and PYY-induced emesis, whereas the CCK1 receptor antagonist devezapide did not alter DON's emetic effects. The 5-HT3 receptor antagonist granisetron completely suppressed induction of vomiting by DON and the 5-HT inducer cisplatin. Granisetron pretreatment also partially blocked PYY3-36-induced emesis, suggesting a potential upstream role for this gut satiety hormone in 5-HT release. Taken together, the results suggest that both PYY3-36 and 5-HT play contributory roles in DON-induced emesis.