O projeto avaliou os efeitos da aflatoxina B1 (AFB1) e fumonisina B1 (FB1), isoladas e associadas, sobre a produtividade e a qualidade dos ovos de codornas poedeiras (Coturnix coturnix japonica). Duzentas e oitenta e oito aves, adquiridas com idade de 8 semanas, foram subdivididas em 6 grupos experimentais (48 aves por grupo) e submetidas a 6 tipos de tratamentos, constituídos por rações contendo AFB1 e FB1 nas concentrações: (0 AFB1+0 FB1), (0 AFB1+10 mg/kg FB1), (50 &microg/kg AFB1+0 FB1), (50 µg/kg AFB1+10 mg/kg FB1), (200 µg/kg AFB1+0 FB1), e (200 µg/kg AFB1+10 mg/kg FB1). As aves foram alimentadas durante 140 dias (5 ciclos de 28 dias). Os parâmetros de produtividade foram avaliados semanalmente, através do consumo de ração, peso dos ovos, índice de conversão alimentar e curva de produção. A qualidade dos ovos foi avaliada a cada ciclo de 28 dias, cada ovo produzido nesse dia foi analisado individualmente para a determinação do valor de unidade Haugh, gravidade específica e percentual do peso da casca. Ao final do 5º período experimental, o peso médio dos ovos foi significativamente menor (p < 0,05) nas aves alimentadas com 10 mg FB1/kg, 50 &microg/kg AFB1, 200 µg/kg AFB1 e com o tratamento de associação de 10 mg FB1/kg + 50 µg/kg AFB1. Em relação à produção de ovos, as codornas alimentadas com 10 mg FB1/kg apresentaram uma diminuição significativa (p < 0,05), ao final do 3º, 4º e 5º ciclos. O consumo médio diário de ração foi significativamente menor (p< 0,05) nas aves alimentadas com 10 mg FB1/kg, ao final do 4º e 5º ciclos, enquanto que os níveis de 50 ou 200 µg/kg AFB1 provocaram uma diminuição significativa (p < 0,05), ao final do 5º período experimental. Ao final do 1º, 2º e 5º ciclos, o consumo médio de ração foi significativamente menor (p< 0,05) nas aves tratadas com 10 mg FB1/kg + 50 µg/kg AFB1. Os índices de conversão alimentar e os valores de Unidades Haugh não foram afetados (p > 0,05) pelos tratamentos. A gravidade específica dos ovos foi significativamente menor (p < 0,05) ao final do 5º ciclo, nas aves tratadas com 10 mg FB1/kg + 200 µg/kg AFB1. Observou-se uma diminuição significativa (p < 0,05) na porcentagem do peso de casca, nas aves tratadas com 10 mg FB1/kg ao final do 1º ciclo, entretanto, houve um aumento significativo (p < 0,05) nos tratamentos com 200 µg/kg AFB1 e também com 10 mg/kg FB1 + 50 µg/kg AFB1 ao final do 1º ciclo. Já ao final do 5º ciclo, o aumento na porcentagem de peso de casca (p < 0,05) ocorreu somente nas aves tratadas com 10 mg/kg FB1 + 200 µg/kg AFB1. Os resultados demonstraram que a administração prolongada de FB1 e AFB1, isoladas ou associadas nos níveis utilizados no presente experimento, pode causar prejuízos econômicos aos produtores de ovos de codornas. / This study evaluated the individual and combined effects of aflatoxin B1 (AFB1) and fumonisin B1 (FB1) on egg quality and performance of laying Japanese quail (Coturnix coturnix japonica). Two hundred twenty-eight birds were purchased at 8 week of age and randomly distributed into 6 experimental groups and given rations containing AFB1 and FB1 at the following levels: (0 AFB1+0 FB1), (0 AFB1+10 mg/kg FB1), (50 &microg/kg AFB1+0 FB1), (50 &microg/kg AFB1+10 mg/kg FB1), (200 &microg/kg AFB1+0 FB1), e (200 &microg/kg AFB1+10 mg/kg FB1). The birds were fed for 140 days (5 28-day laying periods). Each treatment consisted of four replicates of twelve quail. Egg production and individual egg weight were checked daily. Feed consumption and feed utilization were determined weekly. Eggs laid in the last day of each 28-day laying period were collected and submitted to individual analysis for specific gravity, Haugh units and percent egg shell. Results showed that average egg weight at the end of the fifth cycle was significantly lower (p < 0,05) for groups fed 10 mg FB1/kg, 50 &microg/kg AFB1, 200 &microg/kg AFB1 and also for the group fed 10 mg FB1/kg + 50 &microg/kg AFB1. Average egg production significantly decreased (p < 0,05) for groups fed 10 mg FB1/kg by the end of the third, fourth and fifth cycles. Feed consumption was significantly lower (p < 0,05) for group exposed to 10 mg FB1/kg, by the end of fourth and fifth cycles, whereas birds fed 50 or 200 &microg/kg AFB1 showed a significant decrease (p < 0,05) on feed consumption, by the end of fifth cycle. Birds exposed to 10 mg FB1/kg + 50 &microg/kg AFB1 also showed lower values (p < 0,05) of feed consumption, by the end of first, second and fifth cycles. Feed utilization and Haugh units were not affected (p > 0,05) by AFB1 and FB1. Average egg specific gravity was significantly lower (p < 0,05) for group fed 10 mg FB1/kg + 200 &microg/kg AFB1, by the end of fifth cycle. Percent egg shell was significantly lower (p < 0,05) for group exposed to 10 mg FB1/kg, by the end of the first cycle, however, birds exposed to 200 &microg/kg AFB1 and also to 10 mg/kg FB1 + 50 &microg/kg AFB1, showed a significantly increase (p < 0,05) of percent egg shell, by the of the first cycle. Percent egg shell was significantly higher (p < 0,05) for group fed 10 mg/kg FB1 + 200 &microg/kg AFB1 , by the end of fifth cycle. The results obtained in the present study showed that the prolonged administration of FB1 and AFB1, singly or combined at the levels checked, may cause economic losses to the quail egg producers.

Thiamine is an important nutrient found in significant amounts in wheat flours. This vitamin is heat labile thus destruction occurs during bread baking. Using a kinetic approach, the effect of heat and pH on thiamine degradation in a model system were studied. In order to compare the stability of thiamine from natural (whole wheat) and synthetic (enriched white) sources, thermal destruction of thiamine in the two breads was investigated. Destruction rates of thiamine hydrochloride in phosphate buffer at pH 6.0 and temperatures between 80 and 120°C were measured. The breakdown reaction could be described by first order kinetics. An energy of activation of 34.2. kcal/mole was obtained. Destruction rates of thiamine hydrochloride in phosphate buffer at 120°C were measured for pH values between 4.0 and 7.0. The reaction rate increased as the system was made more alkaline, with greater destruction at pH 6.0 and above. Thiamine losses in an enriched white flour system baked at a nominal temperature of 246°C (475°F) for 60, 75 and 90 min were found to be 2.4, 27.9 and 29.2%, respectively. Two experiments were carried out with 450 g (1 lb) enriched white loaves baked at 221°C (430°F). Baking times were 30 min for the first experiment, and 15, 37 and 60 min for the second experiment. No appreciable thiamine destruction were found in either experiment. The main investigation was with a semi-model system of 12g bread loaves made from enriched white and whole wheat flours. Four different nominal oven temperatures of 177, 221, 246 and 288°C (350, 425, 475 and 550°F) were used with four different baking times for each run. The pH of the dough and baked bread were determined. Oven, crust and loaf center temperatures were monitored. The mass average temperature data of the bread during baking showed a changing rate of temperature rise, and because of this, it was not possible to obtain kinetic data. However, a linear relationship was obtained when the logarithm of the percent thiamine retention was plotted against time. This experiment showed a lower thiamine stability with higher oven temperature. Thiamine was less stable in whole wheat bread than in enriched white bread. This might be explained by higher pH and ash content in whole wheat bread. Thiamine losses during normal baking of whole wheat and enriched white bread were found to be in the range of 28.3 to 47.8%. / Land and Food Systems, Faculty of / Graduate

The lactic dehydrogenase activity in plasma and tissues was measured in the thiamine-deprived, the oxythiamine-treated and the pyrithiamine-treated rats as well as the control rats. The lactic dehydrogenase levels of brain and kidney were significantly increased by oxythiamine treatment. The enzyme activity in heart was markedly decreased only in the thiamine-deprived rats. Unlike the above tissues, the enzyme levels in liver were decreased by 29-44 per cent in all three types of thiamine deficiency, However, the enzyme activity in plasma was significantly increased only by pyrithiamine administration. The distribution patterns of lactic dehydrogenase isozymes were electrophoretically examined in these deficiencies. No significant difference among the three thiamine-deficient groups was observed in brain, kidney, and heart. All five isozymes were observed in proportions that are highly specific for the tissues involved. Two extra bands, in addition to five major bands, were found in liver. In thiamine deprivation liver LDH_3 was noticeably more abundant than LDH_2 in some cases, which is opposite to that found in the control. One extra band between LDH_2 and LDH_3 was absent in liver after pyrithiamine treatment. No noticeable difference in the isozyme distribution of plasma was found among the three thiamine-deficient groups. Blood pyruvate along with lactate was significantly increased by oxythiamine treatment. Pyrithiamine administration also caused a marked increase of blood pyruvate along with lactate only in the phase of the polyneuritic convulsion. Remarkable increases in weight of the adrenal glands were observed in all three cases.

O estudo investigou a influência do fator de transformação de crescimento beta1 (TGFb1) sobre células osteogênicas induzidas com fatores mineralizantes (dexametasona Dex), comparando a viabilidade e a proliferação celular, a mineralização, e a expressão de proteínas não colágenas da matriz osteopontina (OPN), sialoproteína óssea (BSP) e fibronectina (FN). A morfologia foi examinada por microscopia eletrônica de transmissão (MET). O TGFb1 diminuiu a viabilidade e a proliferação celular, mesmo com Dex. A mineralização da matriz foi positivo apenas no grupo tratado com Dex, e negativo nos grupos tratados TGFb1 e TGFb1+Dex. OPN e BSP não foram imunoreativas apenas para o controle negativo, já a FN foi imunoexpressa em todos os grupos. A mineralização foi confirmada, tanto no controle positivo quanto no tratado com Dex, e alterações morfológicas foram observadas nas células tratadas com TGFb1 e TGFb1+Dex, através da MET. Esse estudo mostrou que TGFb1 inibe a mineralização, alterando a viabilidade e proliferação, bem como a morfologia celular, mesmo quando tratadas com Dex. / The study investigated the influence of transforming growth factor beta1 (TGFb1) on osteogenic cells induced with mineralizing factors (dexamethasone Dex), comparing the viability and proliferation cellular, the formation of mineral nodules in vitro, and the expression of the noncollagenous matrix proteins osteopontin (OPN), bone sialoprotein (BSP), and fibronectin (FN). The morphology was examined by transmission electron microscopy (TEM). The TGFb1 decreased the viability and proliferation cellular, even when combined with Dex. The mineralization of matrix was positive only in the group treated with Dex, and negative in the groups treated with TGFb1 and TGFb1+Dex. OPN and BSP were not immunoreactive only negative, already the FN was immunoreactive in all groups.The mineralizing was confirmed in the positive control and Dex, through TEM. Some morphological changes were seen in cells treated with TGFb1 and TGFb1+Dex. This study showed that TGFb1 inhibits the mineralization, changing the viability, proliferation and cell morphology, even when treated with Dex.

Les mycotoxines telles que la fumonisine B1 (FB1) produites par les champignons du genre Fusarium sont particulièrement préoccupantes pour la filière maïsicole. L’ensilage de maïs est un processus de fermentation naturel susceptible de favoriser l’évolution des teneurs en FB1. La maîtrise du risque de contamination par la FB1 et la recherche de moyens permettant la décontamination des ensilages est donc nécessaire. L’objectif de ce travail est de caractériser le devenir de la FB1 dans les ensilages de maïs grain et de mettre en évidence l’existence d’agents microbiens capables de dégrader cette toxine. Pour cela, des mini-silos contenant du maïs grain naturellement contaminé en FB1 provenant de différents parcelles et issus des deux années de récolte ont été préparés. La stratégie analytique basée sur le dosage de la FB1 libre et la FB1 complexée par HPLC-MS/MS a révélé une diminution significative de la teneur en FB1 totale qui ne peut être attribuée à un mécanisme de complexation et résulte d’un mécanisme de dégradation. La recherche du microbiote associé à la dégradation de la FB1 a été réalisée par deux approches complémentaires : Une analyse métagénomique combinant l’extraction sélective de l’ADN microbien et le séquençage haut débit «shotgun» afin de comparer la diversité taxonomique et fonctionnelle d’un ensilage dégradant la FB1 et d’un ensilage moins dégradant. En parallèle, un criblage de microorganismes cultivables capables de métaboliser la FB1 a été conduit et a permis de confirmer les résultats de l’analyse globale. Ce travail apporte une première image du microbiote potentiellement associé à la dégradation de la FB1, ainsi que des activités microbiennes responsables. / Fungi of the genus Fusarium are one of the major contaminants of maize that can produce mycotoxins, such as the fumonisin B1 (FB1). Maize silage which is based on the fermentation of whole crop plant or grains is considered the main source of monogastrics and cattle feeding in Europe. The ensiling process could favor changes in FB1 content; however this has scarcely been documented. This led to questioning regarding the possibility of managing the microbiota during ensiling in order to reduce the level of mycotoxins exposure and improve feed quality. The aim of this work is to study the fate of FB1 during ensiling process of high moisture maize grain and to identify an endemic microbiota capable of degrading FB1. Laboratory scale silages were prepared with naturally contaminated FB1 grains from two cropping years. An analytical procedure allowed assessing both free and matrix associated FB1 forms and showed a significant decrease in total FB1 content that are not linked to the presence of bound FB1. Additionally, our data showed that the FB1 content decrease was mainly due to a degradation process. Identification of a potential microbiota responsible for FB1 degradation was conducted. A metagenomics approach combining a selective microbial DNA extraction and high-throughput shotgun sequencing showed microbial specific patterns between FB1 degrading and weakly degrading silage. These results were also supported by the isolation of microbial strains able to metabolize FB1. Ultimately, this work evidenced a microbiota associated to FB1 degradation and the functional diversity involved in this activity. Bacteria and yeasts have been obtained for further studies on degradation activities and their usage as silage starter.

O estudo investigou a influência do fator de transformação de crescimento beta1 (TGFb1) sobre células osteogênicas induzidas com fatores mineralizantes (dexametasona Dex), comparando a viabilidade e a proliferação celular, a mineralização, e a expressão de proteínas não colágenas da matriz osteopontina (OPN), sialoproteína óssea (BSP) e fibronectina (FN). A morfologia foi examinada por microscopia eletrônica de transmissão (MET). O TGFb1 diminuiu a viabilidade e a proliferação celular, mesmo com Dex. A mineralização da matriz foi positivo apenas no grupo tratado com Dex, e negativo nos grupos tratados TGFb1 e TGFb1+Dex. OPN e BSP não foram imunoreativas apenas para o controle negativo, já a FN foi imunoexpressa em todos os grupos. A mineralização foi confirmada, tanto no controle positivo quanto no tratado com Dex, e alterações morfológicas foram observadas nas células tratadas com TGFb1 e TGFb1+Dex, através da MET. Esse estudo mostrou que TGFb1 inibe a mineralização, alterando a viabilidade e proliferação, bem como a morfologia celular, mesmo quando tratadas com Dex. / The study investigated the influence of transforming growth factor beta1 (TGFb1) on osteogenic cells induced with mineralizing factors (dexamethasone Dex), comparing the viability and proliferation cellular, the formation of mineral nodules in vitro, and the expression of the noncollagenous matrix proteins osteopontin (OPN), bone sialoprotein (BSP), and fibronectin (FN). The morphology was examined by transmission electron microscopy (TEM). The TGFb1 decreased the viability and proliferation cellular, even when combined with Dex. The mineralization of matrix was positive only in the group treated with Dex, and negative in the groups treated with TGFb1 and TGFb1+Dex. OPN and BSP were not immunoreactive only negative, already the FN was immunoreactive in all groups.The mineralizing was confirmed in the positive control and Dex, through TEM. Some morphological changes were seen in cells treated with TGFb1 and TGFb1+Dex. This study showed that TGFb1 inhibits the mineralization, changing the viability, proliferation and cell morphology, even when treated with Dex.

Call number: LD2668 .T4 1944 H62 / Master of Science

The blood thiamine concentration of 11 subjects was determined by means of the Friedemann and Kmieciak (1943) method every 5 days during a 30-day experimental period. Study I was conducted on 5 students in 1947 and Study II was conducted on 6 students in 1948. The subjects in both studies were on diets in which their intake of ascorbic acid only was controlled. A record was kept of each subjects food intake. The daily values for total Calories, non-fat Calories and thiamine in the diet were obtained from food tables. Non-fat Calories, the ratio of non-tat Calories to total Calories, thiamine to 1000 Calories and thiamine to non-fat Calories were calculated. The blood thiamine values for the subjects in Study I (all girls) ranged from 4.91 to 10.85 mcg per cent. There was a general decrease throughout the study in the mean intake of thiamine expressed in terms of mcg per 1000 Calories and mcg per 1000 non-fat Calories. The greater the decrease in thiamine intake in terms of mcg per 1000 non-fat Calories the greater was the loss of blood thiamine. The values for thiamine in the blood of the boys in Study II ranged from 8.00 to 15.32 mcg per cent and for the one girl in Study II from 8.35 to 13.93 mcg per cent. The blood thiamine values for the subjects in Study II did not indicate the same relationship to thiamine intake as did those in Study I. There was an increase in the concentration of the thiamine in the blood even though there was a decrease in the mean thiamine intake from the beginning to the end of the experiment. It would appear, therefore, that the boys obtained sufficient thiamine throughout the 30-day period. No data have been obtained which indicate whether or not there are variations from day to day in the concentration of thiamine in the blood when subjects are maintained on a constant intake of thiamine. A metabolism study using 5 adult women as subjects was planned in order to determine the daily values for thiamine in the blood when subjects were maintained on a controlled diet for a period of 52 days. An unpublished micro-method for the determination of thiamine in the blood developed by Dr. H. Burch (1948) was to be used. The experimental diet consisted of a basal diet providing approximately 1000 Calories and 300 mcg of thiamine with additions to the basal diet planned in units providing approximately 500 Calories and 150 mcg of thiamine. The values for protein, fat, carbohydrate and total Calories were obtained, from food tables. Non-fat Calories were calculated and the thiamine content of the food was determined by analysis. All 5 subjects ate the same food each day. In spite of the fact that considerable preliminary work was performed before the study started the blood thiamine values obtained in the nutrition laboratory were always significantly lower than results obtained by other workers. It was decided to freeze the blood samples after the protein had been removed and work on certain aspects of the method before any analyses of the blood thiamine were made. Further study of the Burch method included variation in the amounts of potassium acetate used, use of different trichloroacetic acid reagents, tests for enzyme activity, variations in the incubation procedure, variations in the procedure for the oxidation to thiochrome and in the extraction of thiochrome, reading samples sooner after transfer to optically matched tubes, variations in the irradiation procedure, use of all new reagents, use of another micro-photofluorometer, development of standard curves and the determination of the response of two subjects to an oral test dose of thiamine hydrochloride. None of these variations resulted in a solution of the problem. Suggestions for future work with the Burch method are discussed. / Graduation date: 1950

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