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Concerns about beef production are growing among consumers, questioning the use of antibiotics, hormones, and metaphylactic treatments, as well as its environmental footprint. Therefore, beef production systems need to be more efficient to increase productivity while using less resources to become sustainable and reduce environmental impact. There is a need to develop and apply non-pharmaceutical alternatives to improve health, feed efficiency and performance of beef cattle. We investigated four different targeted strategies to enhance performance of beef cattle: 1) The effect of an injectable multi-mineral complex supplementation for grazing beef cows on overall mineral status, fertility, and subsequent offspring performance. Two doses of the trace mineral injection increased in pregnancy rate after artificial insemination, with a greater impact on cows with poor body condition score; 2) Inclusion of a yeast-derived product combining live yeast (probiotics) and cell wall components (prebiotics), on performance and physiological responses of beef steers during backgrounding and finishing phases. Including a yeast-derived product into a finishing diet containing monensin did not improve performance, physiological responses, and carcass quality of feedlot cattle. Nonetheless, inclusion of the yeast derived product as a substitute of monensin during the backgrounding and finishing phases decreased feed intake without affecting growth, with an overall improvement in feed efficiency; 3) Use of phytotherapy (condensed tannins) to reduce protozoa parasites load and prevent coccidiosis in peripartum beef heifers and their newborn calves. Daily supplementation of condensed tannins reduced coccidia load in heifers and newborn calves, although this reduction was transient; and 4) following the smart farming approach, validate the use of an automated scale system for grazing or feedlot beef cattle, which was able to accurately measures body weight in grazing and feedlot systems for growing and mature beef cattle while reducing cattle handling, without disrupting feeding behavior, decreasing the probability of animal lesions, accidents and optimizing labor. / Doctor of Philosophy / Diet diversification is a response of a growing economy, growing population, and urbanization, which increases the demand of meat products, especially beef, in substitution of staple foods. However, concerns around beef production and its impact on the environment are becoming more relevant for consumers. The need to produce more with less resources requires a sustainable intensification process. Specifically, beef cattle production systems are less efficient when compared to poultry or swine in terms of time and amount of feed required. Beef production systems need to focus on environmental and socially conscious strategies to satisfy the demand, increase animal health, productivity, and profitability. One approach is based on nutritional strategies and applied technologies to enhance productivity, efficiency, welfare, and health. In this dissertation we present three different strategies to improve efficiency of beef production systems: 1) using injectable trace minerals supplementation to ensure adequate mineral nutrition in grazing cows, improving their pregnancy rate to artificial insemination, particularly when cows are in poor body condition; 2) use of yeast as natural additives to successfully substitute antibiotics as growth promotants in feedlot diets with an improvement in feed efficiency; 3) use of secondary plant compounds, such as tannins, to substitute prophylactic antibiotic utilization for coccidiosis in cows and newborn calves. We demonstrate three successful strategies that can improve health, feed efficiency and reproductive performance of beef cattle, all of which are important to achieve greater productivity and profitability in beef production systems.

O primeiro artigo desse estudo apresenta a ocorrência de um surto de intoxicação por monensina em búfalos de um rebanho misto com bovinos, os quais não foram afetados. Tal fato sugeriu a possibilidade de que búfalos fossem menos tolerantes à monensina que bovinos. Embora com número reduzido de animais experimentais, dados preliminares foram compatíveis com essa hipótese. O segundo artigo desse trabalho descreve detalhadamente achados clínicopatológicos da intoxicação por monensina em búfalos, confirma a maior susceptibilidade dos búfalos (em comparação com bovinos) à monensina e determina a mínima dose tóxica de monensina para búfalos. Sinais clínicos e lesões característicos de intoxicação por monensina foram induzidos em búfalos dosados (1 dia) com 15, 10, 7,5 e 5 mg/kg de monensina. Apenas os búfalos dosados com 2,5 (1 dia) e 1 mg/kg (7 dias) de monensina não morreram. Os sinais clínicos iniciaram aproximadamente 6 h após dosagem com monensina e incluíram apatia, anorexia, diarréia, sialorréia, fraqueza muscular, taquicardia, dificuldade locomotora, dispnéia, distensão da jugular, decúbito e morte. As dosagens de creatinina quinase (CK) dos búfalos aumentaram acentuadamente após dosagem com monensina. As alterações macroscópicas foram ascite, hidrotórax, hidropericárdio, cardiomegalia, hepatomegalia e áreas pálidas focais no miocárdio e nos músculos esqueléticos. Degeneração e necrose de miofibras foram os principais achados histopatológicos. Os búfalos intoxicados naturalmente no surto desenvolveram predominantemente lesões nos músculos esqueléticos e os búfalos experimentais tiveram lesões cardíacas mais pronunciadas. Por outro lado, nenhuma evidência de doença, nem mesmo alteração nos níveis de CK, foram observados nos bovinos dosados com as mesmas dosagens de monensina, confirmando observações preliminares que esses animais são mais resistentes à monensina que os búfalos. / The first article of this study reports the occurrence of an outbreak of monensin toxicosis in water buffaloes from a feedlot in which buffaloes and cattle were kept together but only the former were affected. This suggested that buffaloes were less tolerant to monensin than cattle. Although tested with small number of experimental animals, preliminary data were consistent with this hypothesis. The second manuscript describes the clinicopathological findings in monensin toxicosis in water buffaloes, confirms that buffaloes are more susceptible to monensin than cattle, and presents the minimal toxic dosage of monensin to buffaloes. Typical clinical signs and lesions of monensin intoxication were induced in water buffaloes dosed with single doses of 15, 10, 7.5, and 5 mg/kg of monensin. Only buffaloes dosed with 2.5 mg/kg (1 d) and 1 mg/kg (7 d) survived. Clinical signs initiated approximately 6 h postdosing and included apathy, anorexia, diarrhea, drooling, muscular weakness, locomotion disorders, dyspnea, tachycardia, jugular distension and pulse, recumbency and death. The creatine kinase (CK) levels were highly augmented in blood samples of buffaloes dosed with monensin. Most prominent gross changes were ascites, hydrothorax, hydropericardium, cardiomegaly, hepatomegaly, and focal pale areas in the myocardium and in skeletal muscles. Degeneration and necrosis of myofibers were the main histopathological findings. Conversely, no evidence of disease, neither change in CK levels were observed in the beef cattle steers dosed with same doses, confirming preliminary findings that buffaloes are more susceptible to monensin than cattle. Buffaloes in field cases predominantly developed lesions in skeletal muscles, and those from the trial had cardiac lesions as the most pronounced changes. In addition, this report presents the minimal toxic dosage of monensin to buffaloes and suggests that CK tests may serve as monitoring tools in the management of buffalo herds supplemented with monensin.

O primeiro artigo desse estudo apresenta a ocorrência de um surto de intoxicação por monensina em búfalos de um rebanho misto com bovinos, os quais não foram afetados. Tal fato sugeriu a possibilidade de que búfalos fossem menos tolerantes à monensina que bovinos. Embora com número reduzido de animais experimentais, dados preliminares foram compatíveis com essa hipótese. O segundo artigo desse trabalho descreve detalhadamente achados clínicopatológicos da intoxicação por monensina em búfalos, confirma a maior susceptibilidade dos búfalos (em comparação com bovinos) à monensina e determina a mínima dose tóxica de monensina para búfalos. Sinais clínicos e lesões característicos de intoxicação por monensina foram induzidos em búfalos dosados (1 dia) com 15, 10, 7,5 e 5 mg/kg de monensina. Apenas os búfalos dosados com 2,5 (1 dia) e 1 mg/kg (7 dias) de monensina não morreram. Os sinais clínicos iniciaram aproximadamente 6 h após dosagem com monensina e incluíram apatia, anorexia, diarréia, sialorréia, fraqueza muscular, taquicardia, dificuldade locomotora, dispnéia, distensão da jugular, decúbito e morte. As dosagens de creatinina quinase (CK) dos búfalos aumentaram acentuadamente após dosagem com monensina. As alterações macroscópicas foram ascite, hidrotórax, hidropericárdio, cardiomegalia, hepatomegalia e áreas pálidas focais no miocárdio e nos músculos esqueléticos. Degeneração e necrose de miofibras foram os principais achados histopatológicos. Os búfalos intoxicados naturalmente no surto desenvolveram predominantemente lesões nos músculos esqueléticos e os búfalos experimentais tiveram lesões cardíacas mais pronunciadas. Por outro lado, nenhuma evidência de doença, nem mesmo alteração nos níveis de CK, foram observados nos bovinos dosados com as mesmas dosagens de monensina, confirmando observações preliminares que esses animais são mais resistentes à monensina que os búfalos. / The first article of this study reports the occurrence of an outbreak of monensin toxicosis in water buffaloes from a feedlot in which buffaloes and cattle were kept together but only the former were affected. This suggested that buffaloes were less tolerant to monensin than cattle. Although tested with small number of experimental animals, preliminary data were consistent with this hypothesis. The second manuscript describes the clinicopathological findings in monensin toxicosis in water buffaloes, confirms that buffaloes are more susceptible to monensin than cattle, and presents the minimal toxic dosage of monensin to buffaloes. Typical clinical signs and lesions of monensin intoxication were induced in water buffaloes dosed with single doses of 15, 10, 7.5, and 5 mg/kg of monensin. Only buffaloes dosed with 2.5 mg/kg (1 d) and 1 mg/kg (7 d) survived. Clinical signs initiated approximately 6 h postdosing and included apathy, anorexia, diarrhea, drooling, muscular weakness, locomotion disorders, dyspnea, tachycardia, jugular distension and pulse, recumbency and death. The creatine kinase (CK) levels were highly augmented in blood samples of buffaloes dosed with monensin. Most prominent gross changes were ascites, hydrothorax, hydropericardium, cardiomegaly, hepatomegaly, and focal pale areas in the myocardium and in skeletal muscles. Degeneration and necrosis of myofibers were the main histopathological findings. Conversely, no evidence of disease, neither change in CK levels were observed in the beef cattle steers dosed with same doses, confirming preliminary findings that buffaloes are more susceptible to monensin than cattle. Buffaloes in field cases predominantly developed lesions in skeletal muscles, and those from the trial had cardiac lesions as the most pronounced changes. In addition, this report presents the minimal toxic dosage of monensin to buffaloes and suggests that CK tests may serve as monitoring tools in the management of buffalo herds supplemented with monensin.

O primeiro artigo desse estudo apresenta a ocorrência de um surto de intoxicação por monensina em búfalos de um rebanho misto com bovinos, os quais não foram afetados. Tal fato sugeriu a possibilidade de que búfalos fossem menos tolerantes à monensina que bovinos. Embora com número reduzido de animais experimentais, dados preliminares foram compatíveis com essa hipótese. O segundo artigo desse trabalho descreve detalhadamente achados clínicopatológicos da intoxicação por monensina em búfalos, confirma a maior susceptibilidade dos búfalos (em comparação com bovinos) à monensina e determina a mínima dose tóxica de monensina para búfalos. Sinais clínicos e lesões característicos de intoxicação por monensina foram induzidos em búfalos dosados (1 dia) com 15, 10, 7,5 e 5 mg/kg de monensina. Apenas os búfalos dosados com 2,5 (1 dia) e 1 mg/kg (7 dias) de monensina não morreram. Os sinais clínicos iniciaram aproximadamente 6 h após dosagem com monensina e incluíram apatia, anorexia, diarréia, sialorréia, fraqueza muscular, taquicardia, dificuldade locomotora, dispnéia, distensão da jugular, decúbito e morte. As dosagens de creatinina quinase (CK) dos búfalos aumentaram acentuadamente após dosagem com monensina. As alterações macroscópicas foram ascite, hidrotórax, hidropericárdio, cardiomegalia, hepatomegalia e áreas pálidas focais no miocárdio e nos músculos esqueléticos. Degeneração e necrose de miofibras foram os principais achados histopatológicos. Os búfalos intoxicados naturalmente no surto desenvolveram predominantemente lesões nos músculos esqueléticos e os búfalos experimentais tiveram lesões cardíacas mais pronunciadas. Por outro lado, nenhuma evidência de doença, nem mesmo alteração nos níveis de CK, foram observados nos bovinos dosados com as mesmas dosagens de monensina, confirmando observações preliminares que esses animais são mais resistentes à monensina que os búfalos. / The first article of this study reports the occurrence of an outbreak of monensin toxicosis in water buffaloes from a feedlot in which buffaloes and cattle were kept together but only the former were affected. This suggested that buffaloes were less tolerant to monensin than cattle. Although tested with small number of experimental animals, preliminary data were consistent with this hypothesis. The second manuscript describes the clinicopathological findings in monensin toxicosis in water buffaloes, confirms that buffaloes are more susceptible to monensin than cattle, and presents the minimal toxic dosage of monensin to buffaloes. Typical clinical signs and lesions of monensin intoxication were induced in water buffaloes dosed with single doses of 15, 10, 7.5, and 5 mg/kg of monensin. Only buffaloes dosed with 2.5 mg/kg (1 d) and 1 mg/kg (7 d) survived. Clinical signs initiated approximately 6 h postdosing and included apathy, anorexia, diarrhea, drooling, muscular weakness, locomotion disorders, dyspnea, tachycardia, jugular distension and pulse, recumbency and death. The creatine kinase (CK) levels were highly augmented in blood samples of buffaloes dosed with monensin. Most prominent gross changes were ascites, hydrothorax, hydropericardium, cardiomegaly, hepatomegaly, and focal pale areas in the myocardium and in skeletal muscles. Degeneration and necrosis of myofibers were the main histopathological findings. Conversely, no evidence of disease, neither change in CK levels were observed in the beef cattle steers dosed with same doses, confirming preliminary findings that buffaloes are more susceptible to monensin than cattle. Buffaloes in field cases predominantly developed lesions in skeletal muscles, and those from the trial had cardiac lesions as the most pronounced changes. In addition, this report presents the minimal toxic dosage of monensin to buffaloes and suggests that CK tests may serve as monitoring tools in the management of buffalo herds supplemented with monensin.

Les cellules de mélanome humain expriment différents antigènes tumoraux qui sont reconnus par les lymphocytes T cytotoxiques CD8 + (CTL) induisant des réponses spécifiques de la tumeur in vivo. Cependant, chez les patients atteints de mélanome l'efficacité de la réponse naturelle des CTL ou stimulée par thérapie est limitée. Les mécanismes sous-jacents de l'échec de la phase effectrice des CTL contre les mélanomes sont encore largement méconnus. Notre hypothèse est que l'efficacité limitée des CTL dans leur combat contre les tumeurs est le résultat d'une balance défavorable entre la capacité des CTL à tuer les tumeurs et une résistance tumorale intrinsèque à l'activité cytolytique des CTL. Au cours de ma thèse je me suis concentrée sur la dynamique moléculaire qui se produit à la synapse lytique afin de pouvoir identifier un mécanisme précoce mis en place par les cellules de mélanome face à l'attaque des CTL. En combinant l'utilisation d'approches de microscopie de pointe et des outils moléculaires, j'ai pu montrer que, lors de l'interaction avec les CTL, les cellules de mélanome humain subissent une activation de leur trafic vésiculaire endosomal et lysosomal, lequel est intensifié à la synapse lytique et corrèle avec la dégradation par la cathepsine de la perforine et un défaut de pénétration d'entrée du granzyme B. De plus, j'ai démontré que le blocage du trafic lysosomal dépendant de SNAP23, la modification du pH (intra-vésiculaire) et l'inhibition de l'activité lysosomale protéotlytique des cellules de mélanome permet de restaurer leur sensibilité à l'attaque des CTL. Nos résultats révèlent une stratégie sans précédent d' " auto-défense " des cellules de mélanome à la synapse immunologique basée sur une sécrétion lysosomale massive et sur la dégradation de la perforine sécrétée par les CTL. Ainsi pouvoir interférer avec cette stratégie synaptique d'auto-défense des cellules de mélanome pourrait contribuer à potentialiser les réponses des CTL et les immunothérapies chez les patients atteints de mélanome. / Human melanoma cells express various tumor antigens that are recognized by CD8+ cytotoxic T lymphocytes (CTL) and elicit tumor-specific responses in vivo. However, natural and therapeutically enhanced CTL responses in melanoma patients are of limited efficacy. The mechanisms underlying the failure of CTL effector phase against melanomas are still largely elusive. Our hypothesis is that the limited efficacy of CTL in their fight against tumors is the result of an unfavorable balance between CTL ability to kill tumors and an intrinsic tumor resistance to CTL cytolytic activity. During my thesis I focused on the molecular dynamics occurring at the lytic synapse in order to identify possible "early response-mechanism" of melanoma cells to CTL attack. Using a combination of cutting edge microscopy approaches and molecular tools, I showed that upon conjugation with CTL, human melanoma cells undergo an exacerbated late endosome/lysosome trafficking, which is intensified at the lytic synapse and is paralleled by cathepsin-mediated perforin degradation and deficient granzyme B penetration. Abortion of SNAP-23-dependent lysosomal trafficking, pH perturbation or impairment of lysosomal proteolytic activity restores susceptibility to CTL attack. Our results reveal an unprecedented strategy of melanoma cell "self-defense" at the immunologic synapse based on a lysosome secretory burst and perforin degradation at the lytic synapse. Interfering with this synaptic self-defense strategy might be instrumental to potentiate CTL-mediated therapies in melanoma patients.

The relationship between measures of temperament, growth performance, and social hierarchy in finishing beef cattle were explored in two experiments. In experiment 1, high OCS (objective chute score) steers had periods of significantly higher ADG (P < 0.01), but OCS had no relationship with dominance ranking (P > 0.47). Conversely, slow exit velocity (EV) correlated with higher ranking (P ≤ 0.06), but EV had no relationship with performance (P > 0.37) in a competitive environment. Rank showed no relationship with performance (P > .58). In experiment 2, steers with fast EV had periods of decreased growth (P ≤ .06), intake (P ≤ .06), and gain:feed (G:F; P = 0.02). There were no interactions between EV, OCS, and monensin or between EV and monensin. Monensin and EV together, however, significantly impacted overall (days 0 – end) G:F (P = 0.02) and gain (P = 0.05). Overall, these studies further confirm the idea that EV affects performance as does OCS in concert with monensin. Moreover, it further confirms that different measures of temperament correlated to different aspects of performance and should not be lumped together under the general term “temperament” when describing its relationship with performance.

Doctor of Philosophy / Department of Animal Sciences and Industry / Barry J. Bradford / The mechanisms behind the metabolic changes observed when transition cows are administered monensin, as well as the effects of supplementing mid-lactation cows with two commercial amino acid products were investigated. Traditionally, the effects of monensin are attributed to increased gluconeogenic precursor supply, but recent research indicated that the effects of monensin extend beyond gluconeogenic flux. Thus, the primary objectives of Experiment 1 were to determine if monensin modulates transition cow feeding behavior, ruminal pH, and/or expression of key metabolic genes. Overall, monensin decreased time between meals prepartum (126 vs. 143 ± 5.0 min; P < 0.03) with a trend appearing postpartum (81.4 vs. 88.8 ± 2.9 min; P < 0.08), which could be related to the smaller ruminal pH standard deviation during the first day cows received the lactation ration (0.31 vs. 0.26 ± 0.015; P < 0.02). Monensin also increased liver mRNA abundance of carnitine palmitoyltransferase 1a (0.15 vs. 0.10 ± 0.002 arbitrary units; P < 0.04), which corresponded to a slower rate of liver triglyceride (TG) accumulation from 7 days before calving through 7 days post calving (412 vs. 128 ± 83 mg TG/g protein over this time period; P = 0.03). No significant effects of monensin supplementation were observed on other metabolic parameters or milk production. Overall, these results confirm that the effects of monensin on transition cows extend beyond altered propionate flux. In Experiment 2, mid-lactation cows consuming a control diet containing 26% wet corn gluten feed (dry matter basis) were compared to cows consuming the same diet supplemented with lysine embedded within Ca salts of fatty acids and the isopropyl ester of 2-hydroxy-4-(methylthio) butanoic acid, a methionine precursor. This trial was conducted because the NRC (2001) model indicated a lysine deficiency prior to supplementation; however amino acid supplementation had no effects. This trial was then extended to decrease dietary CP from 17.9% to 17.1%, and further increase lysine and methionine supply in the treatment diet. No production or intake effects were observed during this period, but MUN was decreased in the treated group (10.8 vs. 12.5 ± 0.2 mg/dL; P < 0.001).

Problemática mundial levantada nas últimas duas décadas, a geração de gases de efeito estufa (GEE) tem parte devida à emissão de metano por ruminantes. O metano, um potente GEE, é produto final do processo fermentativo de bovinos e, por constituir perda no potencial produtivo destes, tem sido objeto de estudo por nutricionistas do mundo todo. Na busca por estratégias para diminuírem essas perdas, diferentes dietas, aditivos e manejos nutricionais têm sido empregados. Portanto, o objetivo deste trabalho foi avaliar o efeito dos aditivos alimentares, monensina ou tanino, sobre a produção de metano ruminal em bovinos, utilizando-se a técnica de fermentação ruminal ex situ (micro-rúmen), e sobre os parâmetros da fermentação ruminal, a digestibilidade aparente total e a excreção de nutrientes da dieta. Seis vacas (873 ± 81 kg) canuladas no rúmen foram utilizadas e distribuídas a três dietas, que diferiram quanto ao aditivo utilizado, seguindo-se delineamento experimental em quadrado latino 3x3 replicado (n= 18 unidades experimentais): Controle (CON): sem aditivo; Monensina (MON): adição de 300 mg de monensina sódica por animal por dia; Tanino (TAN): adição de 100 g de extrato concentrado de tanino condensado obtido da Acácia-negra (Acacia mearnsii) por animal por dia. Cada período experimental foi constituído de 21 dias, sendo que, entre o dia 5 e o dia 15, 2 g do marcador óxido crômico por kg de MS de alimento consumido foi administrado via cânula ruminal, para determinação da digestibilidade aparente total da MS e suas frações, bem como da excreção dos nutrientes da dieta. O ensaio de digestibilidade foi constituído por duas fases, sendo os cinco primeiros dias para adaptação ao marcador e os cinco últimos para coleta de fezes. A excreção da MS e dos nutrientes, bem como a excreção de nitrogênio, foi calculada a partir dos dados de coeficiente de digestibilidade da MS e suas frações. Para cada período experimental, os últimos 6 dias foram destinados para coleta de dados do consumo de matéria seca (CMS). No dia 21 coletou-se líquido ruminal, antes, 3, 6, 9 e 12 h após a alimentação matinal, para determinação da concentração de ácidos graxos de cadeia curta (AGCC) e metano (CH4). As concentrações de CH4 e AGCC foram determinadas por cromatografia gasosa. O pH ruminal foi mensurado por um dispositivo contínuo de mensuração, durante 24 horas no 21º dia de cada período experimental. A técnica de fermentação ex situ consiste em incubar frascos tipo penicilina com conteúdo ruminal sólido e líquido, em banho termostático por 30 minutos, com posterior mensuração da produção de metano por cromatografia gasosa, sendo estimada a perda de energia relativa (PER). A PER avalia a eficiência da fermentação dos alimentos, ou seja, verifica a perda de metano quando comparada aos outros produtos da fermentação, tais como, acído acético, propiônico e butírico. Os dados foram analisados pelo programa SAS (Versão 9.2, 2010) através do procedimento MIXED. No modelo, o efeito de tratamento foi considerado fixo e os efeitos de período, quadrado e animal dentro de quadrado considerados aleatórios. Não houve diferenças significativas (P0,05) entre os tratamentos para o consumo, digestibilidade aparente total e excreção da MS, PB, EB, FDN, FDA, EE, ENN, MO ou P, nem na digestibilidade do NDT e na excreção de N. Não houve efeito signifivativo dos aditivos (P>0,05) sobre a concentração de N-NH3, pH ruminal, para os ácidos acético, propiônico e butírico, nem para o AGCC total. Para a variável metano houve diferença significativa (P<0,05), sendo que o tratamento com monensina foi responsável por reduzir a produção de metano em 10,7%, já o tanino reduziu em 8,0%, quando comparados ao tratamento controle. Observou-se que a PER foi diminuída significativamente em 20,3% e 23,8% (P=0,0387) com a administração dos aditivos monensina e tanino, quando comparadas ao tratamento controle. Portanto, a utilização de monensina ou tanino, em dietas com proporção de volumoso e concentrado de 50%, demonstra ser uma interessante opção em dietas para bovinos, com vistas a eficiência energética dos animais, não interferindo sobre o consumo, digestibilidade e excreção dos nutrientes com consequente redução nas emissões de metano. / Worldwide problem raised in the last two decades, the generation of greenhouse gases (GHG) is partly due to methane emission by ruminants. Methane, a powerful greenhouse gas, is the end product of the fermentation process in cattle, and as is considered a potential loss in their productive potential has been studied by nutritionists worldwide. In the search for strategies to decrease these losses, different diets, additives and nutritional management have been employed. Therefore, the aim of this study was to evaluate the effect of feed additives monensin or tannins on ruminal methane production in cattle evaluated by the technique of ex situ ruminal fermentation (micro-rumen), and on rumen fermentation parameters, as well as, total tract apparent digestibility and excretion of nutrients. Six ruminally cannulated cows (873 ± 81 kg) were distributed to three diets that differed on the additive used, in a replicated 3x3 Latin square experimental design (n=18 experimental units): Control (CON): no additive; Monensin (MON) addition of 300 mg of monensin per animal per day; Tannin (TAN): addition of 100 g of concentrated extract condensed tannin obtained from black wattle (Acacia mearnsii) per animal per day. Each experimental period consisted of 21 days, and between day 5 and day 15, 2 g per kg DM consumed of the marker chromic oxide was administered via rumen cannula for determination of DM and its fractions apparent digestibility as well as, excretion of nutrients. Digestibility trial consisted of two phases, the first five days for adaptation to the marker and the last five for feces sampling. The excretion of DM and nutrients, as well as, nitrogen excretion was calculated from the data of DM digestibility and its fractions. In each trial, the last 6 days were used for data collection of dry matter intake (DMI). On day 21, ruminal fluid was collected before, 3, 6, 9 and 12 h after morning feeding to determine the concentration of short chain fatty acids (SCFA) and methane (CH4). The concentration of SCFA and CH4 were determined by gas chromatography. Rumen pH was measured by a continuous measurement device for 24 hours on day 21 of each experimental period. The fermentation technique consists of ex situ incubation of penicillin flasks with liquid and solid rumen contents in water bath for 30 minutes, with subsequent measurement of methane production by gas chromatography, with final estimation of relative energy loss (REL). The REL evaluates the efficiency of feed fermentation , in other words, verifies methane loss when compared to the other fermentation products such as acetic, propionic and butyric acids. Data were analyzed using the MIXED procedure of SAS (Version 9.2, 2010). In the model, the effect of treatment was considered fixed and the effects of period, square, and animal within square were considered random. No significant differences (P0.05) between treatments were observed for dry matter intake, apparent digestibility and excretion of DM, CP, GE, NDF, ADF, EE, NFE, MO or P, nor TDN digestibility and N excretion. There was no significant effect (P>0.05) of additives on rumen pH, concentration of total SCFA, acetic, propionic and butyric acids, as well as, NH3- N. Monensin reduced (P<0.05) methane production by 10.7%, whereas tannin reduced by 8.0%, when compared to control treatment. Relative energy loss was significantly decreased by 20.3% and 23.8% (P=0.0387) with administration of monensin and tannin when compared to control. Therefore, the use of monensin or tannin in diets with forage to concentrate ratio of 50%, shows to be an interesting option in catlle diets aiming to improve energy efficiency in animals, not interfering on intake, digestibility and nutrient excretion with consequent reduction in methane emissions.

Objetivou-se compreender melhor o modelo de indução de acidose láctica ruminal (ALR) com sacarose destacando-se aspectos básicos da fermentação ruminal e suas consequências, assim como avaliação comparativa da eficácia de dois aditivos (Virginiamicina VM e Monensina MON), associados ou não, na prevenção desta enfermidade em bovinos adultos de corte. Para tal, foram utilizados 30 fêmeas da raça Nelore, providas de cânula ruminal, com cerca de 413 kg de peso corpóreo. Os animais foram mantidos em baias individuais e alimentados com dieta basal composta de 75% de feno de capim de coast-cross e de 25% de ração concentrada comercial, por 30 dias antes da indução de ALR. Durante esse período os bovinos foram distribuídos em cinco grupos iguais de seis animais cada, assim constituídos: controle (CON); MON 30 ppm; VM 25 ppm; VM 34 ppm e MON 30 ppm + VM 25 ppm. Os aditivos foram administrados numa mistura de 500 g fubá, antes do oferecimento do alimento. Em seguida, foi realizada indução individual de ALR com uso de sacarose de acordo com peso metabólico corrigido, administrada pela cânula ruminal. Foram obtidas amostras de conteúdo ruminal, sangue, urina e fezes, assim como realizado exame físico nos seguintes momentos: zero (basal) e após três, seis, 12 e 18 horas da indução. Foi realizada análise de variância (Teste F) dos dados que obedeceram à distribuição paramétrica, e utilizado o comando Proc mix para medidas repetidas no tempo de duas vias considerando os fatores tratamento, tempo e interação entre tratamento e tempo. Alguns dados foram submetidos ao teste T de Student. Os dados que não obedeceram a distribuição paramétrica foram avaliados pelos testes de Kruskal-Wallis e qui-quadrado. Para o estudo da relação entre duas variáveis foi determinado os índices de correlação e determinação. Ocorreu acidose ruminal intensa, por grande produção inicial de ácidos graxos de cadeia curta (AGCC), seguido de ácido láctico, com predomínio do isômero L sobre o D, os quais com a glicose gerada na fermentação provocaram aumento de osmolaridade nesse conteúdo. A acidose sistêmica foi de grau moderado em pequena parte dos bovinos, com presença de desidratação num expressivo número de animais. Boa parte dos bovinos tratados (n =15) apresentavam depressão nervosa e desidratação. Ocorreu pontualmente um quadro de hipertermia no auge da fermentação ruminal. Os melhores resultados preventivos da ALR foram obtidos com a associação VM + MON, a qual postergou a produção de ácido láctico, quer seja pela menor produção deste, como pela conversão de ácido láctico L em ácidos acético e propiônico. Ao término do experimento essa associação promoveu maior pH e menor acúmulo de ácido láctico L, assim como viabilizou que um menor número de animais necessitassem ser tratados, em relação ao grupo controle. As duas diferentes doses de VM tiveram resultados intermediários, seguidos da MON, a qual não se recomenda como único aditivo com fins de prevenção da ALR. / The objective was to better understand the induction model of rumen lactic acidosis (RLA) with sucrose, highlighting the basic aspects of ruminal fermentation and its consequences, as well as comparative evaluation of the efficacy of two additives (Virginiamycin VM and Monensin MON), associated or not, in the prevention of acidosis in adult beef cattle. For this purpose, 30 Nellore ruminally-cannulated females were used, with average body weight of about 413 kg. The animals were kept in individual stalls and fed a basal diet composed of 75% coast-cross grass hay and 25% commercial concentrated feed for 30 days prior to RLA induction. During this period the cattle were distributed into five equal groups of six animals each, as follows: control (CON); MON 30 ppm; VM 25 ppm; VM 34 ppm and MON 30 ppm + VM 25 ppm. The additives were provided in a 500 g corn meal before the feed was offered. Subsequently, individual RLA induction with sucrose was performed according to corrected metabolic weight, via ruminal cannula. Samples of rumen contents, blood, urine and feces were collected, and physical examination at: zero (baseline) and after three, six, 12 and 18 h after induction. Variance analysis (Test F) of the data that obeyed the parametric distribution was performed, and the Proc mix command was used for repeated measurements in two-way time considering the factors treatment, time and interaction between treatment and time. Some data were submitted to Student\'s t-test. The data that did not obey the parametric distribution were evaluated by the Kruskal-Wallis and chi-square tests. The correlation and determination indices were determined for the study of the relationship between two variables.. A severe ruminal acidosis occurred due to the large initial production of short chain fatty acids (SCFA), followed by lactic acid, with predominance of the L over D-isomer, which with the glucose generated in the fermentation caused an increase in osmolarity in this content. Systemic acidosis was moderate in a small number of cattle, with dehydration in an expressive number of animals. Most treated cattle (n =15) presented nervous depression and dehydration. A temporary hyperthermia occurred at the peak of ruminal fermentation. The best results of RLA prevention were obtained from VM + MON association, which postponed the lactic acid production, either by its lower production, or by the conversion of L-lactic acid in in acetic and propionic acids. At the end of the experiment, this association promoted greater pH and lower L-lactic acid accumulation, and a smaller number of animals needed to be treated, compared to the control group. The two different doses of VM had intermediate results, followed by MON, which is not recommended as a single additive for the RLA prevention.