Vitamin E and aspirin depress prostaglandins in protection of chickens against Escherichia coli infection.

The hypothesis was tested that vitamin E protects chickens from a lethal Escherichia coli infection by inhibiting the biosynthesis of prostaglandins, thereby activating humoral immunity and phagocytosis. When chickens were fed supplement vitamin E at the level of 300 mg/kg diet, which is six times the presently used dietary level, endogenous PGE1, PGE2, and PGF2 alpha levels decreased in the immunopoietic organs, bursa, and spleen. Antibody titers to E. coli lipopolysaccharide and phagocytosis increased at the same time. Infection slightly increased prostaglandin levels and vitamin E appeared to compensate for this increase. Aspirin, a known prostaglandin inhibitor acted synergistically with vitamin E in depressing endogenous PG levels in bursa and decreasing mortality from E. coli infection.

Effects of Escherichia coli on iron, copper, and zinc metabolism in chicks.

The present report describes the effects of Escherichia coli endotoxin and infection on kinetic changes of copper (Cu), iron (Fe), and zinc (Zn) levels in the transport (serum), storage (liver), and immune organs (spleen and bursa of Fabricius) of the chicken. During infection and endotoxin challenge, increased serum and bursal Cu were noted. Infection and endotoxin both led to a redistribution of Fe with a decrease in serum and an increase in the spleen. Infection decreased serum Zn and concomitantly increased hepatic and splenic Zn. Seven days postinfection, when recovery was well underway, hepatic and splenic Cu and splenic Zn were elevated. Hepatic Fe decreased with recovery, whereas splenic Fe increased. Endotoxin and infection changed trace element kinetics. The endotoxin produced tissue elemental alterations similar to the early stages of infection. This indicated that in early infection, some of the disease responses may be due to endotoxin, whereas the later responses may be due to other aspects of infection such as stress.

Effect of beta carotene on disease protection and humoral immunity in chickens.

The effect of beta carotene on disease protection and humoral immunity in chickens was investigated in comparison with the effect of other lipid-soluble antioxidant vitamins, vitamin E and A, which are both proven immunoenhancers and contributors to disease protection. Beta carotene alone was not as effective as either vitamin in protecting chickens from Escherichia coli infection, nor did it significantly enhance humoral immunity. In combination with vitamin E, however, beta carotene significantly increased disease protection and reduced hepatomegaly caused by E. coli infection.

Cattle blood plasma and red blood cell alpha-tocopherol levels in response to different chemical forms and routes of administration of vitamin E.

The chemical form and site of administration of vitamin E were assessed in cattle by measuring area under the time curve alpha-tocopherol levels in plasma and red blood cells (RBC). In Exp. 1, four groups of Holstein calves, 4 to 6 d old, received daily one of the following forms equivalent to 228 mg of alpha-tocopherol: D-alpha-tocopheryl acetate (DTA); DL-alpha-tocopheryl acetate (DLTA); D-alpha-tocopheryl polyethylene glycol 1,000 succinate (TPGS); and an experimental blend (EB) containing DTA and TPGS. A control group received no supplement. Temporal alpha-tocopherol responses were determined in blood samples collected for 35 d. Relative to controls whose plasma and RBC alpha-tocopherol levels remained unchanged, all supplementation increased (P less than .05) alpha-tocopherol levels in plasma and RBC in calves; the highest levels occurred in those that received either DTA or EB. In a second experiment, five Hereford steers with ruminal and duodenal cannulas were used in a crossover design to determine whether site of vitamin E administration affected plasma alpha-tocopherol levels. A single dose of 810 mg of DTA was placed daily into the rumen, and the same amount divided into five equal doses was given (into the duodenum) during a 12-h period. Plasma alpha-tocopherol levels were higher (P less than .05) when steers were ruminally dosed than when they were dosed duodenally. The results suggest that the alpha-tocopherol concentration of plasma and red blood cells in cattle depends on both the chemical form and on the site of administration.

Stress induction affects copper and zinc balance in calves fed organic and inorganic copper and zinc sources.

This study determined whether Cu and Zn balance was affected by feeding either Zn methionine (ZnMet) + Cu lysine (CuLys) or Zn sulfate (ZnSO4) + Cu sulfate (CuSO4) before and after stressing calves. Eight Charolais crossbred steer calves weighting 167 +/- 5 kg were randomly assigned to two treatments in a crossover experimental design. The millet hay and soybean meal diet when supplemented with the inorganic salts provided 9.2 ppm of Cu and 36.6 ppm of Zn or when fortified with the metal complexes contained 10.5 ppm of Cu and 36.6 ppm of Zn. Gentled calves were fed their respective diets for 28 d before an 18-d mineral balance trial was conducted. Collection consisted of five periods: 1) a 5-d baseline period, 2) 3 d of no Cu and Zn supplement, 3) 3 d of stress consisting of feed and water restriction and ACTH (80 IU) injections i.m. every 8 h, 4) 3 d of refeeding with no Cu and Zn supplement, and 5) 4 d of Cu and Zn repletion. Calves fed CuLys had 53% greater apparent Cu absorption and increased Cu retention (P < .05) during repletion compared with calves fed CuSO4. The 18-d mean retention of Cu from CuLys was greater (P < .05) than that from CuSO4. No differences (P > .05) in apparent absorption or retention of Zn were found between Zn sources, although during the 18-d trial mean retention was 58% higher when ZnMet was fed. Urinary Cu and Zn excretion decreased (P < .01) during stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Vitamin E supplementation and stress affect tissue alpha-tocopherol content of beef heifers.

The effect of stress on tissue alpha-tocopherol was investigated in 16 crossbred heifers fed a corn/corn silage-based diet. For 28 d, eight heifers (379 +/- 10 kg BW) received a dietary supplement of 1,000 IU of dl-alpha-tocopheryl acetate, whereas the controls (375 +/- 10 kg BW) received no supplemental vitamin E. Tissue samples of plasma, red blood cells, liver, trapezius, and longissimus muscles and subcutaneous fat immediately dorsal to each muscle were taken on d 1 for determination of alpha-tocopherol concentration. On d 2 through 4 each heifer was restricted to 2.61 kg of grass hay and allowed water. On d 5, 6, and 7 no feed or water was given, 100 IU of ACTH and .0024 mg of epinephrine/kg BW were given every 8 h, and biopsies for alpha-tocopherol content were again taken on d 7. The stress reduced (P < .01) mean BW, increased (P < .01) serum cortisol, creatine kinase, and urea. After stress, supplemental vitamin E reduced (P < .13) the increase in creatine kinase relative to that in heifers not supplemented with vitamin E. Stress also increased (P < .04) serum Se in heifers fortified with the vitamin E. Alpha-tocopherol content of plasma, red blood cells, liver, and subcutaneous fat dorsal to the trapezius muscle was increased (P < .01) by supplemental vitamin E. The stress treatment reduced (P < .01) alpha-tocopherol content of plasma in those fed the vitamin E and increased it (P < .05) in the nonsupplemented vitamin E-deficient heifers. Stress also decreased red blood cell (P < .01) and liver (P < .05) alpha-tocopherol content in cattle supplemented with vitamin E. Tissue alpha-tocopherol concentrations were reduced by stress only when a diet adequate in vitamin E was fed. In addition, in most sampled tissues, stress did not affect alpha-tocopherol concentrations.

Effects of transportation on early embryonic death in mares.

Incidence of early embryonic death (EED) and associated changes in serum cortisol, progesterone and plasma ascorbic acid (AA) in transported mares were investigated. Mares were transported for 472 km (9 h) during either d 16 to 22 (T-3 wk, n = 15) or d 32 to 38 (T-5 wk, n = 15) of gestation. Blood samples were drawn from control, nontransported mares (NT-3 wk, NT-5 wk, n = 24) and transported mares pre-trip, midtrip, and at 0, 12, 24, 48 and 72 h post-transport and daily for the next 2 wk. Incidence of EED between transported and nontransported mares was not different (P greater than .05). Serum cortisol in all transported mares increased (P less than .05) relative to pre-trip values at midtrip and 0 h post-transport. Relative to NT mares, serum cortisol was higher (P less than .05) at midtrip in T-3 wk mares and 0 h post-transport in T-5 wk mares. Serum progesterone in all T mares increased (P less than .05) at midtrip relative to pre-trip values and was higher (P less than .05) in T-3 wk mares than in NT-3 wk mares at midtrip and 0 h post-transport. Post-transport decreases (P less than .05) in concentrations of progesterone were observed in mares that aborted. Plasma AA in transported mares increased (P less than .05) at midtrip in T-5 wk mares and decreased (P less than .05) relative to pre-trip values at 24 and 48 h post-transport (T-3 wk and T-5 wk mares, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Zinc repletion with organic or inorganic forms of zinc and protein turnover in marginally zinc-deficient calves.

We conducted two experiments using marginally Zn-deficient (-Zn) calves to determine which supplemental chemical form of Zn would most rapidly reverse certain Zn deficiency signs and to determine whether a change in protein turnover had occurred in Zn deficiency. In Exp. 1, 40 crossbred beef heifers were allocated by BW to four groups. The control group received 23 mg Zn/kg diet DM from ZnSO4 supplemented to the -Zn diet (17 mg Zn/kg diet DM). The three other groups received the -Zn diet. After 21 d, based on a decreased (P < .05) feed efficiency, they were deemed -Zn. Cell-mediated immune (CMI) response to phytohemagglutinin (PHA) was reduced (P < .05) but plasma and liver Zn were unaffected in the -Zn calves. Zinc was repleted by feeding iso-Zn amounts (23 mg Zn/kg diet DM) from Zn lysine, Zn methionine, or ZnSO4. At 8 h after injection of PHA, control CMI response values were similar to Zn Methionine, and Zn lysine was lower (P < .05). In Exp. 2, 10 Holstein steers were allocated by BW to two groups. One group received the -Zn diet, and the other received the +Zn diet. Urine collections were obtained from both groups of calves when the -Zn calves showed a decrease (P < .05) in feed efficiency relative to the controls and when they were repleted with 23 mg Zn/kg diet DM from ZnSO4 and their feed efficiency had returned to that of the controls. Urinary 3-methylhistidine indicated that -Zn calves had less (P < .05) daily protein degradation than the controls. Refeeding Zn to the -Zn group did not change BW or daily protein degradation. Results indicated that a marginal Zn deficiency decreased fractional accretion rate, increased (P < .05) urine excretion, and tended to increase (P < .19) Na and decrease (P < .12) K concentrations in the urine.

Endocrine and metabolic changes during altered growth rates in beef cattle.

Eight steers from a group of 14 were fed ad libitum from 240 to 510 kg live weight, gaining at 1.4 +/- .2 kg/d. The six other steers were diet-restricted and grew at .37 +/- .09 kg/d from 240 to 307 kg, prior to ad libitum realimentation on the same diet to a final weight of 510 kg. Blood samples taken during the growth phases from both treatments were analyzed for insulin-like growth factor-I (IGF-I), triiodothyronine (T3), thyroxine (T4), glucose (GLU), nonesterified fatty acids (NEFA), and blood urea nitrogen (BUN) and (or) growth hormone (GH). During restricted growth, mean serum concentrations of GH were elevated (45.6 vs 23.4 ng/ml; P less than .05), serum concentrations of IGF-I decreased (108 vs 167 ng/ml; P less than .05) compared with control steers with ad libitum access to feed. Levels of T4 and GLU also were lower (P less than .05) during restricted than during normal growth. During early realimentation, levels of GLU (P less than .05), IGF-I (P less than .01), T4 and BUN (P less than .01) increased. Levels of T3 remained unchanged, whereas concentration of NEFA declined (P less than .001). Blood urea nitrogen decreased during early realimentation despite a large increase in diet protein intake and in protein storage, suggesting an increased efficiency of nitrogen use for protein synthesis. During realimentation, IGF-I levels rose above those of control steers and remained higher at the final weight of 510 kg (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Differences in diagnostic test results and hematologic data between aged and young horses.

Hematologic data and results of diagnostic tests were compared between aged (greater than or equal to 20 years old) and young (less than or equal to 5 years old) horses to identify hematologic and metabolic changes associated with aging. Initial data were obtained from 8 aged and 6 young mares (group 1). Similar data were collected from a second group of aged (3 mares and 3 geldings) and young (1 mare and 5 geldings) horses (group 2). Dexamethasone suppression tests (DST) and necropsies were performed on 6 additional mares and mare 8 from group 1 (group 3). Complete blood counts and serum biochemical profiles were compared between young and aged horses of groups 1 and 2. Mean corpuscular volume was higher (P less than 0.05) in aged horses. Oral glucose tolerance and insulin response to orally administered glucose were measured in 13 aged horses (groups 1 and 2) and 6 young mares of group 1. In group 1, plasma ascorbic acid values were lower (P less than 0.05) in aged horses than in young horses maintained under the same conditions and feeding regimens. An apparent age-related hyperinsulinemic response to orally administered glucose identified in group-1 mares was probably a result of a high occurrence of subclinical hypophyseal and/or thyroid adenomas. Of 13 aged horses necropsied (groups 2 and 3), 10 had hypophyseal and/or thyroid adenomas that, in group 2, were consistently associated (P less than 0.05) with hyperinsulinemic responses to orally administered glucose. All horses in groups 2 and 3 were given a 24-hour DST.(ABSTRACT TRUNCATED AT 250 WORDS)

Vitamin E enhancement of Venezuelan equine encephalomyelitis antibody response in guinea pigs.

Immune response potentiation by vitamin E was studied in guinea pigs with Venezuelan equine encephalomyelitis attenuated live-virus vaccine as the antigenic stimulus; antibodies were measured by the hemagglutination-inhibition (HI) test. Significantly higher (P less than 0.01) HI antibody titers resulted when guinea pigs were given intramuscular injections of dl-alpha-tocopherol, 33 IU/kg of body weight, before and after immunization. The HI antibody titers to Venezuelan equine encephalomyelitis virus were not increased when guinea pigs were given dl-alpha-tocopheryl acetate orally. This is the first report on vitamin E humoral immune response enhancement to an attenuated live-virus vaccine.

Effects of shipping, handling, adrenocorticotropic hormone, and epinephrine on alpha-tocopherol content of bovine blood.

In 2 studies, plasma, erythrocyte, and neutrophil alpha-tocopherol concentrations were monitored in beef cattle after shipping, handling, and sample collection. On the basis of alpha-tocopherol results, an additional 2 studies were designed to measure the effects of administration of adrenocorticotropic hormone (ACTH) and epinephrine on the alpha-tocopherol concentration in the aforementioned blood constituents and on creatine kinase (CK) activity in Holstein calves. In the first of these studies, 15 beef cattle that had recently arrived at the feedlot consumed feed supplemented daily with 1,000 IU of dl-alpha-tocopheryl acetate. Values for initial blood samples indicated that CK activity was high. Although plasma alpha-tocopherol concentration indicated that vitamin supplementation was adequate, RBC and neutrophil alpha-tocopherol values were generally nondetectable. After 4 weeks of supplementation, plasma alpha-tocopherol concentration increased (P < 0.05), and neutrophil and RBC alpha-tocopherol values became measurable in most of the cattle. In the second study, 6 beef heifers had decreased (P < 0.05) plasma, RBC, and neutrophil alpha-tocopherol values after multiple periods of handling and blood sample collection. In the third and fourth studies, 10 tamed Holstein heifer calves, 5 of which were administered ACTH and epinephrine to simulate stress effects on blood alpha-tocopherol concentrations and CK activity. In study 3, the vitamin E-adequate heifers had increased blood CK (P < 0.001) activity and cortisol (P < 0.01) concentration, and decreased (P < 0.05) neutrophil alpha-tocopherol concentration after hormone injections.(ABSTRACT TRUNCATED AT 250 WORDS)

The role of vitamins in modulating disease resistance.

Many of the metabolic incursions resulting from stress and oxidative damage are detrimental to disease resistance. Vitamins A, E, and C and carotenoids are able to protect cells from free radical oxidation, reduce the detrimental effects of certain eicosanoids, and enhance humoral and cellular immune responses in disease. The regulation of cell differentiation by vitamin A in maintaining an epithelial barrier to pathogen entry and the differentiation of precursor cells to functional lymphocytes by 1,25-dihydroxycholecalciferol are essential to disease resistance. Nutritionists must redefine the levels of vitamins necessary to maximize health-supportive systems. The animal's metabolism must constantly be adjusting to its environmental stress or disease and may require increased vitamins.

The effects of stress, Escherichia coli, dietary ethylenediaminetetraacetic acid, and their interaction on tissue trace elements in chicks.

The present study determined effects of Escherichia coli infection, crowding stress, and EDTA supplementation on Cu, Fe, and Zn levels in the serum, liver, bursa of Fabricius, and spleen of chickens. Organ weights as a percentage of BW were affected by treatments prior to and after infection. Liver and spleen weights as a percentage of BW increased with infection but bursa weight decreased. One week of stress increased hepatic Cu, but 3 wk of EDTA ingestion increased serum Cu and serum, hepatic, bursal, and splenic Fe. These elemental changes resulting from EDTA may have predisposed the chicks to a higher mortality rate from E. coli compared with controls. Peak mortality occurred 2 days after infection, coincident with an increased serum Cu, decreased serum and bursal Fe and Zn, and increased hepatic and splenic Zn. At 7 days postinfection, recovering chicks experienced decreased hepatic Fe, elevated hepatic Zn, decreased bursal Cu, Fe, and Zn, and increased splenic Cu, Fe, and Zn. The current study demonstrates the interactive effects of EDTA, stress, and E. coli infection on serum and organ trace element concentration.

Vitamin E or vitamin A protects chickens against E. coli infection.

The supplementation of either vitamin E (300 mg./kg. diet) or vitamin A (60,000 I.U./kg. diet) to a standard chick ration increased the protection of six week old immunized chickens against E coli infection, decreasing mortality from about 40% to 5%. The combination of the two vitamins, however, did not give as much protection as either vitamin alone. Vitamin E or A did not protect chicks from weight loss and severe morbidity due to infection, but slightly increased the rate of recovery.

Effect of excessive dietary vitamin E on the chick.

Day-old male broiler chicks were fed a broiler ration for five weeks to which was added one of the following levels of dl-alpha tocopheryl acetate; 0; 2,000; 4,000; 8,000; 16,000; 32,000, and 64,000 I.U./kg. The chicks fed diets containing 4,000 I.U./kg. or more of vitamin E showed decreased pigmentation in their beaks, feet and shanks, and liver as a percent of body weight was significantly increased. Feeding at least 8,000 I.U./kg of the vitamin significantly reduced chick body weight and resulted in waxy appearing feathers. Dietary inclusion of 16,000 I.U./kg. or more of vitamin E significantly increased feather, spleen, liver, and plasma vitamin E content.

Maternal vitamin E alters passively acquired immunity of chicks.

Passively transferred antibody levels were significantly increased in plasma of two- and seven-day-old chicks when the dams were fed 150 and 450 p.p.m. vitamin E prior to immunization with Brucella abortus. However, if the hens were fed 90, 300 and 900 p.p.m. vitamin E before immunization, the chicks evidenced no increase in antibody titers relative to controls. This nonlinear antibody response by the reticulo-endothelial system to vitamin E confirms in Gallus domesticus similar results reported for other species.