RESUMEN
Um experimento avaliou a adição de ractopamina e extratos cítricos a dietas de suínos em terminação. Foram utilizados 108 suínos (54 machos e 54 fêmeas) em um delineamento de blocos completos ao acaso, sendo o sexo o fator de bloqueamento e nove os tratamentos: T1. controle (C) (0ppm de ractopamina e 0ppm de extratos cítricos), T2. C+10RAC (ractopamina, em ppm), T3. C+20RAC, T4. C+250EC (extratos cítricos, em ppm), T5. C+500EC, T6. C+250EC+10RAC, T7. C+250EC+20RAC, T8. C+500EC+10RAC e T9. C+500EC+20RAC. O peso vivo final (109,9±3,6kg), consumo de ração (2,6±0,2kgd-1), ganho de peso (1,0±0,1kgd-1), conversão alimentar (2,7±0,2), comprimento de carcaça (97,0±2,7cm), profundidade de músculo (56,1±5,6mm) e pH (5,9±0,3) não foram influenciados pelos tratamentos. Sobre o peso de carcaça, o efeito foi somente do tratamento com 20ppm de ractopamina em relação a 10ppm de ractopamina, sendo 5,7 por cento superior. A espessura de toucinho do grupo controle foi 35 por cento superior aos níveis de ractopamina, e a interação foi 500ppm de extratos cítricos e 10ppm de ractopamina. A carne magra do controle foi 5,3 por cento inferior em relação aos níveis de ractopamina. A alimentação de suínos em terminação com dietas contendo ractopamina, extratos cítricos e suas interações não altera o desempenho, mas influencia algumas características de carcaça.
This study was carried out to evaluate the effect of the addition of the citrus extracts and ractopamine in finishing pig diets. A Hundred eight pigs were used (54 males and 54 females) in a completely randomized design, blocked by sex and distributed in nine treatments: T1. control (C) (0ppm of the ractopamine e 0ppm of the citrus extracts), T2. C+10RAC (ractopamine, ppm), T3. C+20RAC, T4. C+250EC (citrus extracts, ppm), T5. C+500EC, T6. C+250EC+10RAC, T7. C+250EC+20RAC, T8. C+500EC+10RAC and T9. C+500EC+20RAC. The final body weight (109.9±3.60kg), feed intake (2.6±0.24kg d-1), body weight gain (1.01±0.09kg d-1), feed conversion ratio (2.7±0.25), carcass length (97±2.71cm), depth muscle (56.1±5.63mm), and pH (5.9±0.33) were not affected by treatments. There was a significant effect for the treatment with 20ppm of ractopamine, which was 5.7 higher, in relation to the treatment with 10ppm of ractopamine. The backfat thickness of control group was 35 percent higher than the ractopamine levels and the interaction was of 10ppm of ractopamine and 500ppm of citrus extracts. The lean meat in the control group was on average, 5.3 percent lower in relation to the ractopamine levels. Feeding of finishing pigs with diets containing ractopamine, citrus extracts and their interactions didn't affect performance, however affected some carcass characteristics.
RESUMEN
Introducción. La anemia de Fanconi es una enfermedad genética con herencia autosómica recesiva caracterizada por aplasia medular, predisposición a leucemia mieloide aguda, tumores sólidos y aumento en la inestabilidad cromosómica. Este síndrome puede considerarse como modelo biológico para analizar sustancias naturales con posible efecto genotóxico, difíciles de evaluar en células normales. Los objetivos de este estudio son describir y cuantificar las alteraciones cromosómicas estructurales inducidas por cinco flavonas, dos isoflavonas y una droga quimioterapéutica inhibidora de la topoisomerasa II, en cultivos de linfocitos de anemia de Fanconi a fin de determinar si existe un incremento en el número y tipo de daño cromosómico respecto al control. Materiales y métodos. Se analizaron los cromosomas de linfocitos estimulados con fitohemaglutinina M de una paciente con anemia de Fanconi. Se evaluaron 100 metafases de cada uno de los cultivos expuestos a las sustancias y control basal. Las alteraciones cromosómicas fueron documentadas con fotografías convencionales y digitales mediante analizador de imágenes. Se utilizó la prueba de c2 para determinar diferencias significativas entre el daño cromosómico entre cultivos expuestos y no expuestos con un valor de P <0,05. Resultados. Se encontraron 431 alteraciones cromosómicas en 1000 metafases analizadas; la genisteína tuvo el mayor efecto genotóxico, seguida de la genistina, fisetina, kaenferol, quercetina, baicaleína y miricetina. Las anomalías más frecuentes fueron las rupturas cromatídicas, rupturas cromosómicas, brechas (gaps) cromatídicas y cromosómicas, intercambios cuadri-radiales, cromosomas dicéntricos y rearreglos complejos. Conclusión. Los bioflavonoides genisteína, genistina y fisetina, presentes comúnmente en la dieta, aumentaron el número de alteraciones cromosómicas de manera significativa respecto al control en linfocitos de anemia de Fanconi.
Introduction. Fanconi anemia is an autosomal recessive disease characterized by a variety of congenital abnormalities, progressive bone marrow failure, increased chromosomal instability and higher risk to acute myeloid leukemia, solid tumors. This entity can be considered an appropriate biological model to analyze natural substances with possible genotoxic effect. The aims of this study were to describe and quantify structural chromosomal aberrations induced by 5 flavones,² isoflavones and a topoisomerase II chemotherapeutic inhibitor in Fanconi anemia lymphocytes in order to determine chromosomal numbers changes and/ or type of chromosomal damage. Materials and methods. Chromosomes stimulated by phytohaemagglutinin M, from Fanconi anemia lymphocytes, were analysed by conventional cytogenetic culture. For each chemical substance and controls, one hundred metaphases were evaluated. Chromosomal alterations were documented by photography and imaging analyzer. To statistical analysis was used chi square test to identify significant differences between frequencies of chromosomal damage of basal and exposed cell cultured a P value less than 0.05. Results. There were 431 chromosomal alterations in 1000 metaphases analysed; genistein was the more genotoxic bioflavonoid, followed in descendent order by genistin, fisetin, kaempferol, quercetin, baicalein and miricetin. Chromosomal aberrations observed were: chromatid breaks, chromosomal breaks, cromatid and chromosomal gaps, quadriratials exchanges, dicentrics chromosome and complex rearrangements. Conclusion. Bioflavonoids as genistein, genistin and fisetin, which are commonly present in the human diet, showed statistical significance in the number of chromosomal aberrations in Fanconi anemia lymphocytes, regarding the basal damage.