Twelve Holstein steers in a completely randomized block design were fed either a basal diet (concentrate:silage or hay at a DM ratio of 35:65) plus Cu sulfate at 20 ppm of Cu (Cu-supplemented diet) or a basal diet plus ammonium molybdate to obtain 10 ppm of Mo (Cu-depleting diet) on a DM basis in the whole diet for 8 mo. Supplemental Mo was utilized in the Cu-depleting diet to develop a Cu-deficient group. Molybdenum slowly accumulated in the liver in the group fed the Cu-depleting diet. Copper concentrations in the liver and polymorphonuclear neutrophils decreased in the Cu-deficient group compared with the Cu-sufficient group. Plasma Cu concentration did not change during the trial for the Cu-sufficient group. In the Cu-deficient group, plasma Cu concentrations increased during the first 3 mo of the trial, then declined, and remained unchanged for the last 5 mo. Superoxide dismutase activities in red blood cells, polymorphonuclear neutrophils, and whole blood decreased in the Cu-deficient group. Phagocytic capacity was not affected by Cu status, but killing capacity was decreased by low Cu status in the Cu-deficient group by the end of the trial. Glutathione peroxidase activity was unaffected by Cu status. Clinical symptoms of Cu-deficiency were not observed in this trial; there was no evidence of blood hemoglobin or BW gain difference between the two groups. In this study, Cu status affected its distribution in the tissues and related enzyme activities as well as bactericidal function of neutrophils.

Ten Holstein cows averaging 120 d in lactation were arranged in replicated 5 x 5 Latin squares with 3-wk periods to evaluate the role of sulfur (S) in the dietary cation-anion balance equation. Diets were based on corn silage in Exp. 1 and sorghum silage in Exp. 2. Supplemental S and chloride (Cl) from the double sulfate of potassium and magnesium and CaCl2 were used to manipulate dietary cation-anion balance from 0 to +30 meq when expressed as meq [(Na + K)-(Cl + S)]/100 g diet DM and from +19 to +49 meq when expressed as meq [(Na + K)-Cl]/100 g diet DM. Blood pH was not affected by cation-anion balance, although both S and Cl supplementation tended to lower pH. Blood HCO3- and urine pH decreased and plasma calcium (Ca) and urinary Ca excretion increased as anion was added to the diet. Milk fat production tended to be increased by the low S supplementation. Dietary Cl and S had similar effects on acid-base status. Therefore, we suggest that S be included with Cl in the dietary cation-anion balance equation for lactating dairy cows as follows: meq [(Na + K)-(Cl + S)]/100 g diet DM. Although response of acid-base status to S and Cl was similar, as more data comparing the acidogenicity of S vs Cl become available, it may be necessary to include a modifying coefficient for S in the equation to adjust for differences between S and Cl in acid-generating potential. This coefficient may be further dependent on the dietary source of S.

Eighteen multiparous Holstein cows were assigned randomly to three treatments at the beginning of the dry period (8 wk before expected parturition). Treatments were: 1) the basal diet containing 5.5 ppm of Cu (control), 2) the basal diet supplemented with 10 ppm of Cu, and 3) the basal diet supplemented with 20 ppm of Cu. The objectives were to measure the changes of Cu and other trace mineral element concentrations in blood and liver from the onset of the dry period (approximately 8 wk prepartum) to 8 wk postpartum and to assess the requirement of Cu during this time. Liver Cu concentration in the control group declined continuously during the 8-wk dry period, and the nadir occurred at parturition. This decline was prevented by dietary Cu supplementation of 10 or 20 ppm. Liver Cu concentration in the control group started to increase slowly after the dramatic decline. Liver Zn concentration changed cubically as a function of week during the treatment period. Plasma Cu and Zn exhibited a quadratic pattern as a function of week. The plasma Cu concentration was lowest 5 wk prior to parturition.

Gluconic acid is a carboxylic acid naturally occurring in plants and honey. In nonruminant animals, gluconic acid has been shown to increase gastrointestinal butyrate concentrations and improve growth performance, but a ruminant application remains undescribed. This experiment examined the effects of postruminal calcium gluconate (CaG) on milk production, fecal volatile fatty acid concentrations, and plasma metabolite concentrations in lactating dairy cows. Six rumen cannulated multiparous Holstein cows (60 ± 6 d in milk) were randomly assigned to 6 treatment sequences within a 6 × 6 Latin square design in which each experimental period consisted of 5 d of continuous postruminal infusion followed by a 2 d wash-out period. Test treatments included a negative control (CON; 0.90% NaCl wt/vol), positive control (Na-butyrate, 135 g/d), and 4 doses of CaG (44, 93, 140, and 187 g/d). Cows received a total mixed ration (31% corn silage, 28% alfalfa silage, 5% hay, 36% concentrate) with dry matter intake fixed (25.3 ± 1.7 kg/d) throughout the experiment. On d 5 of each infusion period, samples of milk, feces, and blood were collected from each animal. Calcium gluconate treatments increased milk fat concentration, and a tendency was observed for increased milk fat yield and energy-corrected milk yield above levels achieved by CON, with maximal treatment responses of 4.43% (CON 3.81%), 2.089 kg/d (CON 1.760 kg/d), and 51.8 kg/d (CON 47.1 kg/d), respectively. Concentrations of iso-butyric acid in feces were greater in cows infused with CaG (13.3 µmol/g) treatments compared with CON (9.7 µmol/g). Arterial concentrations of glucose and nonesterified fatty acids were lower (glucose: CaG 2.98 mmol/L, CON 3.29 mmol/L and nonesterified fatty acids: CaG 0.130 mmol/L vs. 0.148 mmol/L) and β-hydroxybutyrate higher (CaG 1.703 vs. CON 0.812) in cows infused with CaG than CON. Together, these results suggest that postruminal infusion of CaG may alter metabolic mechanisms to support a milk fat production response.