Effects of high-sulfur water and clinoptilolite on health and growth performance of steers fed forage-based diets.

Sulfur-induced polioencephalomalacia (sPEM), a neurological disorder affecting ruminants, is associated with consumption of diets with increased S (high-S). High-S water is commonly found in many western states and is a major source of dietary S for grazing cattle. Consumption of high-S water has been associated with sPEM and decreased performance. Identification of a feed supplement that would counteract the negative effects of high-S water would decrease the incidence of sPEM and prevent performance reductions in regions with problematic water sources. The objectives of this study were to 1) determine the effects of administering high-S drinking water to forage-fed feedlot steers on health and performance, and 2) determine the effectiveness of clinoptilolite, a clay mineral with increased cation-exchange capacity, in negating the effects of high-S drinking water. Yearling steers (n = 96; 318.2 +/- 2.1 kg of BW) were randomly assigned to 1 of 4 treatments for a 77-d trial period: control with low-S water (566 mg of SO(4)/L), high-S water (3,651 mg of SO(4)/L), or high-S water plus clinoptilolite supplemented at 2.5 or 5.0% of the diet DM. Feed and water consumption were measured daily, and all steers were weighed on d -2, -1, 29, 53, 76, and 77. Plasma samples were collected on d 0, 58, and 77, and liver samples on d 0 and 77. There was a greater (P or= 0.546) in ADG or G:F were observed. Plasma Cu decreased (P = 0.029) to a greater magnitude in high-S water steers than the control steers over the 77-d trial period. Mineral analyses of hepatic tissue from randomly selected healthy steers from each treatment group (n = 10 per treatment) showed an interaction (P

Dextromethorphan is protective against sensitized N-methyl-D-aspartate receptor-mediated excitotoxic brain damage in the developing mouse brain.

Enhanced glutamate release and inflammation play an important role in the pathogenesis of developmental brain injury. Although N-methyl-d-aspartate receptor (NMDAR) antagonists potently attenuate neonatal brain damage in several animal models, they can also impact trophic functions in the developing brain. As a consequence, high-affinity NMDAR antagonists have been shown to trigger widespread apoptotic neurodegeneration in the newborn brain. Dextromethorphan (DM), a low-affinity NMDAR antagonist with anti-inflammatory properties, may be neuroprotective against excitotoxic and inflammation-enhanced excitotoxic brain injury, without the associated stimulation of apoptotic degeneration. Using an established newborn mouse model of excitotoxic brain damage, we determined whether systemic injection of DM significantly attenuates excitotoxic lesion size. We investigated several doses and time regimens; a dose of 5 microg/g DM given in a combination of both pre-injury and repetitive post-injury treatment proved most effective. DM treatment significantly reduced lesion size in gray and white matter by reducing cell death as shown by a decreased Fluoro-Jade B staining and caspase-3 activation. Pre-treatment with interleukin-1beta and lipopolysaccharide enhanced NMDAR-mediated excitotoxic brain injury and microglial cell activation. This sensitizing effect was abolished by DM treatment, as the effectiveness of DM in reducing lesion size and microglial cell activation was similar to phosphate-buffered saline-pre-treated controls. In all cases, no gender-specific differences were detected. DM treatment did not trigger any apoptotic neurodegeneration (caspase-3 cleavage, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, Fluoro-Jade B staining). Although functional parameters were not measured, our data corroborate reports that DM is neuroprotective and that it may therefore improve functional outcome following perinatal brain injury.

Application of research findings and summary of research needs: Bud Britton Memorial Symposium on Metabolic Disorders of Feedlot Cattle.

Updated research findings with acidosis, feedlot bloat, liver abscesses, and sudden death syndromes were presented at the Bud Britton Memorial Symposium on Metabolic Disorders of Feedlot Cattle. Possible industry applications include the need to establish guidelines for use of clostridial vaccines in feedlot cattle, further assessment of the relationship between acidosis and polioencephalomalacia, examination of the effects of various ionophores on the incidence of metabolic disorders, and evaluation of the effects of feed bunk management and limit- and restricted-feeding programs on the incidence of metabolic disorders. A multidisciplinary approach among researchers, consulting nutritionists and veterinarians, and feedlot managers will be required for effective progress in research and in the application of research findings. Areas suggested for further research include 1) assessment of feed consumption patterns and social behavior of cattle in large-pen, feedlot settings; 2) evaluation of the relationship between feed intake management systems (feed bunk management programs, limit- and programmed-feeding) and the incidence of metabolic disorders, including delineation of the role of variability in feed intake in the etiology of such disorders; 3) efforts to improve antemortem and postmortem diagnosis, and to establish standardized regional or national epidemiological databases for various metabolic disorders; 4) ascertaining the accuracy of diagnosis of metabolic disorders and determining the relationship of previous health history of animals to the incidence of metabolic disorders; 5) further defining ruminal and intestinal microbiology as it relates to metabolic disorders and deeper evaluation of metabolic changes that occur with such disorders; 6) continued appraisal of the effects of grain processing and specific feed ingredients and nutrients on metabolic disorders, and development of new feed additives to control or prevent these disorders; and 7) application of biotechnology to develop grain varieties with altered nutrient degradation profiles that decrease the propensity for disastrous acid loads in the rumen, feed-grade enzymes and probiotics that modify nutrient digestion or microbial profiles in the rumen and intestine, and specific strains of ruminal bacteria and protozoa that alter ruminal and metabolic conditions that may precipitate metabolic disorders.

Biopotency of vitamin E in lucerne meal for chickens.

In order to estimate the biopotency of vitamin E in lucerne/alfalfa meal in comparison to that of dl-alpha-tocopheryl acetate (dl-alpha-Ta; all-rac-alpha-Ta) a study was conducted with newly hatched White Leghorn male chicks. An increase in the vitamin E level in the liver and plasma, and the prevention of nutritional encephalomalacia (NE) were used as criteria for biopotency. After a vitamin E depletion period of one week posthatching, the chicks continued on a semipurified, vitamin E free basal diet without vitamin E supplementation, or were repleted with graded levels of that vitamin for six weeks, provided as extracted lucerne oil or as dl-alpha-Ta. High performance liquid chromatography (HPLC) with fluorescence detection was used for the analysis of the vitamin E homologues. The diagnosis of NE was based on clinical and histopathological observations. A significant increase (P < 0.05) in vitamin E content in the liver and plasma was observed in response to dietary supplementation with both vitamin E sources. The linear increase both in the liver and plasma storage assays was associated with a reduced incidence of NE. The disease was totally prevented by a dietary supplement of 7.50 and 5.40 mg vitamin E/Kg feed provided as dl-alpha-Ta or lucerne oil, respectively. The natural biopotency of the vitamin E in lucerne meal compared with that of dl-alpha-Ta in the liver and plasma storage assays and in the prevention of NE was 123, 105 and 99%, respectively, as calculated by the slope ratio technique.

Ovine polioencephalomalacia associated with dietary sulphur intake.

Fifty-six female crossbred two-month-old lambs were housed in individual cages, and fed a basic ration of barley (59%), soybean meal (5%), and alfalfa (32%) prepared to meet NRC nutrient requirements. Four percent of the diet contained a standard salt mix to which the factors inorganic sulphur (S) and thiamine (B1) were added. Four treatment groups were used: low sulphur and normal thiamine (0.19% S, 13.7 mg/kg B1) low sulphur and high thiamine (0.19% S, 243 mg/kg B1), high sulphur and normal thiamine (0.63% S, 13.7 mg/kg B1), high sulphur and high thiamine (0.63% S, 243 mg/kg B1). All animals had free access to water and were offered 1 kg/animal/day of diet for 14 weeks, when necropsy was undertaken. Seven lambs fed unsupplemented (normal B1) diets containing added sulphur developed clinical symptoms of polioencephalomalacia (PEM) between the 3rd and 7th week of the trial. Morbidity (P less than 0.013) and mortality (P = 0.08) differences were attributed to S administration. None of the B1 supplemented lambs developed clinical signs of PEM. Body weight and relative organ weights did not differ among treatment groups. Serial sections of all brains were examined grossly and microscopically. Nonparametric statistical analysis revealed sulphur related effects in the cerebrum, midbrain and hindbrain (P less than 0.0001), no thiamine-related effects or interaction between the factors were seen, except in the amygdaloid body. It was concluded that inorganic sulphur was associated with polioencephalomalacia, and that dietary thiamine may decrease the severity of lesions in some affected areas of the central nervous system.

Biopotency of vitamin E in barley.

Investigations were carried out to establish the total biopotency of the natural vitamin E isomers in barley compared with that of DL-alpha-tocopheryl acetate. The chick was used as an experimental animal. Prevention of nutritional encephalomalacia (NE) and chick liver-storage and plasma-storage assays of vitamin E were the methods used in the study. The individual tocopherols and tocotrienols, both in the tissue samples and in the grain and barley oil, were analysed using high-pressure liquid chromatography (HPLC) with fluorescence detection. The diagnosis of NE was based on careful clinical and histopathological observations. It can be concluded from the results that full protection against NE in the chicks was obtained with a supplementation level of 7.5 mg DL-alpha-tocopheryl acetate/kg diet (i.e. a total vitamin E content of 11.20 mg/kg diet) or with a supplement of 8.7 g barley oil/kg diet (i.e. a total vitamin E content of 22.99 mg from barley oil/kg diet). This gave a biopotency factor of 0.49 for barley for prevention of NE of the chicks, as compared to that of DL-alpha-tocopheryl acetate. Using regression analysis a statistically linear relationship could be observed between the total dietary vitamin E level and the response, as measured by the total vitamin E content in the liver and plasma, both in the groups supplemented with DL-alpha-tocopheryl acetate and in the groups supplemented with corresponding amounts of vitamin E in barley oil. The liver and plasma responses to the total vitamin E in the barley-oil diet compared with those of the DL-alpha-tocopheryl acetate reference diet gave identical values for the regression coefficients, i.e. in both liver-storage and plasma-storage assays the value for slopes of dose-response lines was 0.37. This means that the biopotency of the total vitamin E in barley was 37% of that of dietary DL-alpha-tocopheryl acetate. Thus, barley is not as rich a source of vitamin E as could be supposed on the basis of the chemical determination of its total vitamin E content. It was possible to verify this experimentally established biopotency of 0.37 for the total vitamin E in barley by converting the chemically determined amounts of the vitamin E isomers in barley into DL-alpha-tocopheryl acetate equivalents by multiplying them with internationally accepted potency factors for the individual natural isomers (DL-alpha-tocopheryl acetate 1.00, D-alpha-tocopherol 1.49, D-beta-tocopherol 0.60, D-gamma-tocopherol 0.15, D-alpha-tocotrienol 0.37).(ABSTRACT TRUNCATED AT 400 WORDS)

Dietary factors affecting experimental models of nutritional encephalomalacia.

Various factors affecting the experimental development of nutritional encephalomalacia (NE) were studied in young chicks. The effects of these factors were evaluated by calculation of the age at which one-half were affected (T1/2). The incidence of ataxia and mortality and statistical analysis of the intensity of the disease were also calculated. No differences were found among the safflower oil samples oxidized for periods ranging from 12 to 48 hr in their potency to induce NE, while oil oxidized for 72 hr was less effective. No difference was observed between the effects of oxidized safflower oil and freshly distilled methyl esters of safflower oil on the development of NE. This disorder was more severe in chicks fed a fat-free diet deficient in vitamin E for the first week and then the NE-inducing diet than in chicks fed the NE-inducing diet from hatching. Feeding chicks vitamin E for the first week delayed the development of encephalomalacia but did not prevent it. In order to prevent NE in young chicks fed oxidized safflower oil, a ratio of .3 mg alpha-tocopherol per gram oil was required.

[Etiopathogenesis and prevention of encephalomalacia in chickens]. / Prouchvania vurkhu etiopatogenezata i profilaktikata na entsefalomalatsiiata po piletata.

Studies were carried out on the dissemination of encephalomalation with chickens. The quality of the feeding-mixes, meant for the different categories of fowls, was also studied with regard to the contents of vitamins, fats, aldehyde and peroxide number and antioxidizers. The contents of vitamin E was also determined, as well as its biological activity in a biological material. The prophylactic effect of different vitamin preparations was tested in combination with other means of prophylaxis of broilers against encephalomalation. It was proved that the increase of aldehydes and peroxides in feeding-mixes could lead to the appearance of encephalomalation with chickens. The quantity of santokvin--200 g/t of fodder enabled the good conservation and preservation of the biological activity of vitamin E. The index 'biological activity' is a more appropriate criterium for a supply of chickens with vitamin E, rather than its quantitative contents in biological substrates. On the basis of the experiments made, a disgram is offered about the prophylaxis of encephalomalation with chickens.

[Protective effect of alpha-linolenic acid in encephalomalacia in chickens]. / L'effet protecteur de l'acide alpha-linolénique sur l'encéphalomalacie chez le poulet.

Encephalomacia is a vitamin E deficiency syndrome which affects the cerebellum of young chicks. The lesion includes degenerative alterations of cellular and fibrillar elements, apparently as the result of the ischaemia caused by thrombotic events in the microvascular system. A supply of linoleic acid, as fatty acid methyl esters prepared from safflower oil (Carthamus tinctorius), caused a high incidence of encephalomalacia. On the other hand, linseed oil esters, rich in alpha-linolenic acid, did not induce any symptoms and protected the chicks to a large extend against the development of signs produced by linoleic acid. Fatty acid esters of cod liver oil, rich in long-chain derivatives of alpha-linolenic acid, exerted a relatively weak protective effect. The analytical results show that a supply of alpha-linolenic acid led to an accumulation of eicosapentaenoic acid, 20:5 omega 3, and a reduced concentration of arachidonic acid in the phospholipds of liver and plasma. The results suggest that, under the conditions leading to encephalomalacia, the prostacyclin-thromboxane balance is shifted in direction of an excessive production of TXA2, causing thrombus formation in the capillaries of the cerebellum, alpha-linolenic acid, by modifying the PUFA profile, exerts a multiple action the main result of which appears to be an antithrombotic effect at the level of the microvascular system of the cerebellum.

Preventive effect of selenium, methionine and antioxidants against encephalomalacia of chicks induced by dilauryl succinate.

The protective effect of supplemental selenium, methionine, ascorbic acid, menaquinone and five antioxidants against encephalomalacia of chicks fed a diet containing dilauryl succinate was examined. Diauryl succinate induces vitamin E deficiency signs such as fragility of the erythrocytes and encephalomalacia. Supplementation of selenium and methionine with or without simultaneous supplementation of a low level of dl-alpha-tocopheryl acetate had little effect on preventing encephalomalacia. The preventive effect of ascorbic acid, methylene blue, ethoyquine, 2,6-ditertiary-butyl-p-cresol and butylated hydroxyanisole was roughly in proportion to their dietary level, and a high level of any of them could almost completely protect the chicks from encephalomalacia, while diphenyl-p-phenylenediamine was not as effective and the effect was not proportional to the dose. Menaquinone had little effect. No difference was observed in the plasma tocopherol levels and peroxide levels in the adipose tissueof the chick fed eith er dilauryl succinate or cornstarch. The effect of dilauryl succinate appears to be independent of peroxides generated in the chick.