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This study aimed to determine the aflatoxin B1 (AFB1) binding capacity of a beer fermentation residue (BFR) containing Saccharomyces cerevisiae cells, and the efficacy of BFR to ameliorate the toxic effects of AFB1 on performance, serum biochemistry, and histology of broilers. The BFR was collected from a microbrewery, and the yeast cells were counted, dried, and milled before it was used in the study. In vitro evaluation of the BFR was conducted using different concentrations of AFB1 (2.0, 4.0, 8.0, 16.0, and 32.0 µg AFB1/mL) and 100 mg/10 mL of BFR at pH 3.0 or 6.0. Two hundred 1-day-old male broilers (Ross 308) were assigned to 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, which included: 1) basal diet (BD), with no BFR or AFB1; 2) BD supplemented with 1% BFR; 3) BD supplemented with 2 mg AFB1/kg of feed; and 4) BD supplemented with 2 mg AFB1/kg feed and 1% BFR. Performance variables were determined weekly, while serum analyses were performed on d 14 and 21. At the end of the study, chicks were anesthetized with carbon dioxide, euthanized by cervical dislocation, and the kidney, liver, and bursa of Fabricius were removed for determination of relative weights, and for histological evaluation. In vitro assays showed that the higher the initial AFB1 concentration in solution, the greater the AFB1 amount adsorbed by BFR at both pHs tested. Feed intake, BW gain, and concentrations of albumin, total protein, and globulin increased (P < 0.05) in broilers fed BFR+AFB1 (Diet 4), when compared to the birds receiving only AFB1 (Diet 2). Although BFR was not able to reduce or prevent the effects of AFB1 on relative weights of kidneys and liver, it reduced the severity of histological changes in the liver and kidney caused by AFB1.

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Aflatoxins (AF) and fumonisins (FU) are a major problem faced by poultry farmers, leading to huge economic losses. This experiment was conducted to determine the effects of AF (1 mg/kg of feed) and FU (25 mg/kg of feed), singly or in combination, on the lipid metabolism in commercial layers and investigate the efficacy of a commercial binder (2 kg/t of feed) on reducing the toxic effects of these mycotoxins. A total of 168 Hisex Brown layer hens, 37 wk of age, were randomized into a 3 × 2 + 1 factorial arrangement (3 diets with no binder containing AF, FU, and AF+FU; 3 diets with binder containing AF, FU, and AF+FU; and a control diet with no mycotoxins and binders), totaling 7 treatments. The hens contaminated with AF showed the characteristic effects of aflatoxicosis, such as a yellow liver, resulting from the accumulation of liver fat, lower values of plasma very low-density lipoprotein and triglycerides, and higher relative weight of the kidneys and liver. Hepatotoxic and nephrotoxic effects of FU were not observed in this study. On the other hand, the FU caused a reduction in small intestine length and an increase in abdominal fat deposition. The glucan-based binder prevented some of the deleterious effects of these mycotoxins, particularly the effects of AF on hepatic lipid metabolism, kidney relative weight, and FU in the small intestine.

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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.

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1. Our objective was to evaluate the toxic effects of aflatoxin B1 (AFB1) and fumonisin B1 (FB1), administered singly or in combination to broilers. 2. Feeds were prepared with concentrations equal to 0, 50 and 200 microg AFB1/kg, and/or 0, 50 and 200 mg FB1/kg, and offered to broiler chicks from 8 to 41 d of age. The experimental design was totally randomised, in a 3 x 3 factorial arrangement with 9 treatments and 12 birds per treatment. Animals were vaccinated against Newcastle disease on d 14 of life and killed at 41 d. 3. Compared with controls, all mycotoxin-treated groups at 41 d had lower body weight and weight gain, and higher relative heart weight. The relative weight of the liver increased only in birds fed diets containing 200 mg FB1, singly or in combination with AFB1. 4. At 35 d, all groups receiving mycotoxin-treated rations had reduced geometrical mean antibody titres, with birds from groups fed combinations of AFB1 and FB1/kg having even lower values, when compared to the other groups. 5. Histological changes were observed only in liver from birds fed mycotoxin-contaminated rations, and in kidneys of birds fed the diet containing 200 microg AFB1 and 200 mg FB1/kg. Main alterations included vacuolar degeneration and cell proliferation of bile ducts in the liver, and hydropic degeneration in renal tubules in the kidneys. 6. We concluded that AFB1 and FB1 in combination have primarily additive effects on body weight, liver structure and immunological response of broilers at the concentrations used.

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RESUMO O objetivo do presente trabalho foi avaliar os efeitos da aflatoxina B 1 (AFB1) e da fumonisina B1 (FB1) sobre os níveis séricos da enzima aspartato amino-transferase (AST) e de proteínas totais de frangos de corte alimentados com ração contendo as toxinas isoladas e em associação, nos níveis de 0, 50 e 200 ?g de AFB1/kg e 0, 50 e 200 mg de FB1/kg. O delineamento experimental foi o inteiramente casualizado em esquema fatorial 3 x 3, com 9 tratamentos e 12 repetições, totalizando 108 aves. As aves foram alimentadas com as rações contaminadas a partir do 8 o dia até o 41o dia de idade. Aos 41 dias de idade, houve um aumento (p < 0,05) nos níveis de AST das aves que receberam dietas contendo AFB1 e FB1, com exceção do grupo que recebeu somente 50 ?g de FB1/kg. Este aumento foi maior quanto mais elevados foram os níveis de AFB1, sendo que um efeito tóxico aditivo foi observado nos tratamentos de associação com 50 mg de AFB1/ kg e 50 ou 200 mg de FB1/kg. Aos 28 dias de idade, observou-se uma redução (p < 0,05) na concentração de proteína dos grupos que receberam ração com 200 ?g de AFB1/kg, com ou sem FB1, porém esta redução não foi observada aos 41 dias de idade. Conclui-se que a intoxicação de frangos de corte com AFB1 e FB1, isoladas ou associadas, causa um aumento na concentração sérica de AST e uma redução nos níveis de proteínas totais após 20 dias de exposição contínua através da ração.

ABSTRACT The aim of the present study was to evaluate the effects of dietary aflatoxin B1 (AFB1) and fumonisin B1 (FB1) on the seric levels of aspartate amino-transferase (AST) and total protein of broiler chicks. The mycotoxins were added to rations, singly and in combination, at levels of 0, 50 and 200 ?g AFB1/kg, and 0, 50 and 200 mg FB1/kg. A completely randomized 3 x 3 factorial design was used, with 9 treatments and 12 replications per treatment (total: 108 birds). Broilers were fed the contaminated rations from days-of-age 8 to 41. At 41 days of age, the concentration of AST increased (p < 0.05) in all groups receiving AFB1 and FB1, with the exception of birds fed 50 mg FB1/kg alone. Higher levels of AST were found in broilers fed the highest levels of AFB1, and an additive effect was observed in the association treatments 50 ?g AFB1/kg and 50 or 200 mg FB1/kg. Total protein decreased (p < 0.05) at 28 days of age in groups receiving 200 ?g AFB1/kg alone or in combination with FB1. However this reduction was not found at 41 days of age. In conclusion, AFB1 and FB1, singly or in combination at the levels studied, cause an increase in the serum levels of AST and a decrease of total proteins after 20 days of continuous exposition through the diet.

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In the present study, 288 8-wk-old Japanese quail were randomly distributed into 6 experimental groups (48 birds per group) and fed the following diets for 140 d: 1) 0 (control); 2) 10 mg of fumonisin B1 (FB1); 3) 50 microg of aflatoxin B1 (AFB1); 4) 50 microg of AFB1 + 10 mg of FB1; 5) 200 microg of AFB1; and 6) 200 microg of AFB1 + 10 mg of FB1/kg of feed. Each treatment consisted of 4 replicates of 12 quail. Egg production and individual egg weight were checked daily. Feed intake and feed conversion were determined weekly. Results showed that by the end of the fifth cycle, average egg weight was lower (P < 0.05) in groups fed 10 mg of FB1/kg, 50 microg of AFB1/kg, 200 microg of AFB1/kg, and 10 mg of FB1 + 50 microg of AFB1/kg of feed. Egg production decreased (P < 0.05) in birds fed 10 mg of FB1/kg by the third, fourth, and fifth cycles. Feed intake was lower (P < 0.05) in birds fed 10 mg of FB1/kg by the fourth and fifth cycles, and in birds fed 50 and 200 microg of AFB1/kg in the fifth cycle. Birds fed 10 mg of FB1 + 50 microg of AFB1/kg consumed less feed (P < 0.05) in the first, second, and fifth cycles. Results indicated that prolonged administration of FB1 and AFB1, singly or in combination at the levels evaluated, may cause economic losses to quail egg producers.

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1. A 28-d experiment was conducted to evaluate the effects of fumonisin B1 (FB1) on egg production and egg quality of young laying Japanese quail fed on fumonisin-contaminated rations. 2. To this end, 128 7-week-old birds were randomly distributed into 4 experimental groups (32 birds per group) and given rations containing 0 (control), 10, 50 and 250mg FB1/kg feed. Each treatment consisted of 4 replicates of 8 quail. Egg production and egg weight were checked daily. Feed consumption and feed conversion were determined weekly. Eggs laid on the last day of each 7-d period were collected and subjected to individual analysis for specific gravity, Haugh units and percentage eggshell. 3. Compared with controls, quail given > or = 50 mg FB1/kg had reduced feed intake and lower body weight gain. Feed conversion was reduced only in birds given 250 mg FB1/kg. 4. Mean egg production and egg weight were lower in birds given 250mg FB1/kg. Eggshell weight was reduced in birds given > or =50mg FB1/kg. However, mean specific gravity, Haugh units and percentage eggshell were not affected by FB1. 5. No histopathological changes were observed in liver, kidney or heart samples from any treatment group. 6. The results indicated that exposure to FB1 at concentrations > or = 50 mg/kg could adversely affect quail performance, emphasising the importance of controlling fumonisin contamination of quail rations.

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