No abstract

Owing to the methane (CH 4 ) produced by rumen fermentation, ruminants are a source of greenhouse gas (GHG) and are perceived as a problem. We propose that with appropriate regenerative crop and grazing management, ruminants not only reduce overall GHG emissions, but also facilitate provision of essential ecosystem services, increase soil carbon (C) sequestration, and reduce environmental damage. We tested our hypothesis by examining biophysical impacts and the magnitude of all GHG emissions from key agricultural production activities, including comparisons of arable-and pastoral-based agroecosystems. Our assessment shows that globally, GHG emissions from domestic ruminants represent 11.6% (1.58 Gt C y -1

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.

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.

Although Se is essential for antioxidant and thyroid hormone function, factors influencing its requirement are not well understood. A survey and two experiments were conducted to determine the influence of cattle breed and age on selenoprotein activity and the effect of maternal Se supplementation on cow and calf selenoprotein activity and neonatal thyroid hormone production. In our survey, four cowherds of different ages representing three breeds were bled to determine the influence of breed and age on erythrocyte glutathione peroxidase activity (RBC GPX-1). All females were nonlactating, pregnant, and consumed total mixed diets (Holstein) or grazed pasture (Angus and Hereford). In our survey of beef breeds, yearlings had greater average RBC GPX-1 activity than mature cows. In Exp. 1, neonatal Holstein heifers (n = 8) were bled daily from 0 to 6 d of age to determine thyroid hormone profile. An injection of Se and vitamin E (BO-SE) was given after the initial bleeding. Thyroxine (T4) and triiodothyronine (T3) concentrations were greatest on d 0 and decreased (P < 0.05) continuously until d 5 postpartum (156.13 to 65.88 and 6.69 to 1.95 nmol/L, d 0 to 5 for T4 and T3, respectively). Reverse T3 concentrations were 3.1 nmol/L on d 0 and decreased (P < 0.05) to 0.52 nmol/ L by d 5. In Exp. 2, multiparous Hereford cows were drenched weekly with either a placebo containing 10 mL of double-deionized H2O (n = 14) or 20 mg of Se as sodium selenite (n = 13). After 2 mo of treatment, Se-drenched cows had greater (P < 0.01) plasma concentrations than control cows (84.92 vs. 67.08 ng/mL), and at parturition, they had plasma Se concentrations twofold greater than (P < 0.05) control cows (95.51 vs. 47.14 ng Se/mL). After 4 mo, cows receiving Se had greater (P < 0.05) RBC GPX-1 activity than controls; this trend continued until parturition. Colostrum Se concentration was twofold greater (P < 0.05) in Se-drenched cows than control cows (169.97 vs. 87.00 ng/mL). Calves born to cows drenched with Se had greater (P < 0.05) plasma Se concentration, RBC GPX-1, and plasma glutathione peroxidase activity on d 0 compared with calves born to control cows. By d 7, no differences in plasma glutathione peroxidase activity in calves were observed. Maternal Se supplementation did not influence calf thyroid hormone concentrations. Selenium provided by salt and forages is not adequate for cattle in Se-deficient states.