The aim of this study was to determine the binding capacity of a hydrated sodium calcium aluminosilicate (HSCAS) for aflatoxin B(1) (AFB(1)), and the efficacy of the HSCAS to reduce the concentrations of residual AFB(1) and its metabolites in the liver and kidney of broilers fed AFB(1). One hundred 1-d-old male broilers (Ross 708) were maintained in chick batteries and allowed ad libitum access to feed and water. A completely randomized design was used with 5 replicate pens of 5 chicks assigned to each of 4 dietary treatments from hatch to 21 d. Dietary treatments included the following: A) basal diet (BD), with no HSCAS or AFB(1), B) BD supplemented with 0.5% HSCAS only, C) BD supplemented with 2.5 mg of AFB(1)/kg of feed, and D) BD supplemented with 2.5 mg of AFB(1)/kg of feed and 0.5% HSCAS. On d 21, 5 chicks from each treatment were anesthetized with carbon dioxide, killed by cervical dislocation, and samples of liver and kidney were collected for analysis of AFB(1) residues. The percentage of AFB(1) bound for each concentration of adsorbent (100, 10, 1, 0.5, 0.25, and 0.05 mg/10 mL) was 100, 91.1, 81.8, 75.4, 40.1, and 8.8%, respectively. Concentrations of aflatoxin residues (AFB(1), aflatoxicol, aflatoxins B(2) and G(1)) were lower (P < 0.05) in livers and kidneys of birds fed AFB(1) plus HSCAS (diet D), when compared with birds fed AFB(1) alone (diet C). However, histopathology data from the in vivo study indicated that HSCAS did not prevent lesions associated with aflatoxicosis. The decrease in the bioavailability of AFB(1) caused by the HSCAS reduced aflatoxin residues in liver and kidney, but not enough to completely prevent the toxic effects of AFB(1) in broilers.

A study was conducted to determine the toxicity of melamine in young broilers fed graded levels of melamine. An additional objective was to determine melamine residual levels in selected tissues. One hundred and seventy-five 1-d-old male Ross broiler chicks were sorted to a randomized block design in stainless steel battery pens. Chicks were assigned to 7 dietary treatments containing 0, 0.5, 1.0, 1.5, 2.0, 2.5, and 3.0% melamine. Each dietary treatment was fed to 5 replicate pens of 5 chicks for 21 d. Mortality increased quadratically (P<0.001) with increasing dietary concentrations of melamine. However, compared with controls, mortality was only higher (P<0.001) in birds fed≥2.5% melamine. Feed intake decreased linearly (P<0.001), whereas BW gain decreased quadratically (P<0.02) with increasing dietary concentrations of melamine. Compared with controls, both feed intake and BW gain were lower (P<0.001) only in birds fed≥1.0% melamine. Relative kidney weights increased linearly (P<0.001), whereas relative liver weights increased quadratically (P<0.05) with increasing dietary concentrations of melamine. Melamine residues in breast muscle and liver tissue increased linearly (P<0.001) with increasing dietary concentrations of melamine, whereas melamine residues in kidney and bile increased quadratically (P<0.02) with increasing dietary concentrations of melamine. Compared with controls, melamine concentrations in liver and kidney were higher (P<0.001) in birds fed all levels of melamine, whereas melamine concentrations in breast muscle and bile were only higher (P<0.001) in birds fed≥1.0% melamine. Serum albumin, total protein, globulin, and calcium increased quadratically (P<0.02) in birds as dietary melamine increased, whereas serum aspartate transaminase and gamma gluatamyltransferase increased linearly (P<0.01) with increasing levels of melamine in the diet. Renal histopathology revealed nonpolarizable melamine crystals in the collecting tubules and ducts of birds fed≥1.5% melamine. In summary, dietary melamine was toxic to broilers at concentrations≥1.0%.

My special thanks to my wife and best friend Marina S. Murarolli who gave me all the support and love during happy and hard times, always been by my side, helping me to make decisions. I also would like to thank my parents, Airton and Neide, for all the love and always supporting all my decisions. My brother, Vinicius, and my sister, Flaveli, for the love and friendship. My parents-in-law, Vera and Tomas, and my sister-inlaw, Marcela, always helping and advising us with their experience.Thanks to all my Brazilian friends, who makes me feel at home

O estudo foi realizado para verificar o efeito de diferentes relações dietéticas de energia metabolizável:proteína bruta e do peso inicial de pintos de corte de 01 sobre o desempenho e rendimento de carcaça em frangos de corte. Foram utilizados 640 pintos, fêmeas, de uma linhagem comercial para corte (Cobb). O delineamento experimental utilizado foi de blocos ao acaso, em esquema fatorial 2 x 2, sendo empregados dois níveis de peso de pintos de 01 dia (38g e 46g) e dois níveis de relação EM:PB (Alto - 149,8; 174,4 e; 194,4 e, Baixo - 130,0; 150,0 e; 166,7, para ração inicial, crescimento e final, respectivamente) totalizando, assim, 4 tratamentos, cada um com 4 repetições de 40 aves, criados até 48 dias de idade. Foram avaliados o Consumo de Ração (CR), Ganho de Peso (GP), Conversão Alimentar (CA) durante o período experimental e, Rendimento de Carcaça e Rendimento de Cortes (Asa, coxa+sobrecoxa, peito, cabeça, pé e dorso) no final do período experimental. Nas variáveis CR e GP não foram observados efeitos significativos (P>;0,05) em nenhum dos tratamentos e períodos. Na variável CA, observou-se efeito significativo (P<0,05) no período de 1 a 35 dias de idade onde as aves alimentadas com a dieta com Relação EM:PB baixa apresentaram uma pior conversão alimentar, independente do peso inicial. No rendimento de carcaça houve efeito significativo (P<0,05), onde as aves com maior peso inicial obtiveram uma melhor porcentagem de rendimento quando receberam, durante todo o período de criação, dietas com relação EM:PB alta.

Consumption of ochratoxin A (OTA) contaminated diets by broilers results in economic losses to the poultry industry. This experiment evaluated the effects of quantity and time of exposure to dietary OTA on performance, organ weights, serum biochemistry, and renal gene expression of chicks. Determination of genes expressed in response to OTA will allow for the identification of pathways that are influenced by OTA. 180-day old male broiler chicks were randomly assigned to a 3×3 factorial arrangement of treatments (3 levels of OTA; 0, 1 and 2 mg OTA/kg diet and 3 time periods; 7, 14 and 21 days) with 4 replicate pens of 5 birds each per treatment. For RNA-sequencing analysis (RNA-Seq), kidney samples were collected weekly from 3 controls and 3 chicks fed 1 mg OTA/kg. NextGENe software was used for read alignment and transcript quantification. Birds fed 2 mg OTA/kg diet had decreased feed intake and body weight gain, and increased serum uric acid on days 14 and 21. Compared to controls, birds fed 2 mg OTA/kg diet also had poorer feed conversion and increased kidney weights. On day 21, birds fed 1 mg OTA/kg diet had decreased albumin, and aspartate aminotransferase concentrations. Genes associated with carbohydrate and amino acid metabolism were downregulated, and genes associated with the immune system were upregulated at days 7 and 14. Genes associated with lipid metabolism and xenobiotic biodegradation were also downregulated on day 14. These changes disappeared on day 21 suggesting that the kidney and other related organs were repaired or the damage was contained. In conclusion, decreased performance and increased kidney weight and serum uric acid in birds fed 2 mg OTA/kg confirmed the effects of OTA. Supplementation of 1 mg OTA/kg diet caused time-dependent alterations in renal gene expression in chicks.