The aim of this study was to evaluate the ability of AflaDetox (Adiveter, Agro-Reus, Reus, Tarragona, Spain) in counteracting the deleterious effects of aflatoxin B(1) (AFB(1)) in broiler chicks. A total of 120 Ross 308 one-day-old male broiler chicks were assigned to 8 treatments for 42 d. The experiment had a 2 x 4 factorial arrangement of treatments involving 0 and 1 mg of AFB(1)/kg feed and 0, 1, 2, and 5 g of AflaDetox/kg feed. Chicks were fed on the ground during the first 7 d and in cages (3 chicks/cage; 5 cages/treatment) from 7 to 42 d. Growth performance was measured from d 7 to 42 and whole-tract digestibility of gross energy and protein on d 40 to 41. Serum biochemical parameters, organ weights, histopathological examination of liver, and AFB(1) residues in liver and breast muscle tissues were determined on d 42. Aflatoxin B(1) significantly decreased the BW gain, feed intake, and impaired feed conversion rate (P < 0.05). The addition of AflaDetox in the contaminated diets significantly diminished the inhibitory effects of dietary AFB(1) (P < 0.05) on the growth performance with no differences compared to the control diet. Feeding AFB(1) alone decreased serum protein concentration, increased the serum activity of alkaline phosphatase, and caused significant increases in the relative weights of livers. Treatment with AflaDetox significantly alleviated the negative effects of AFB(1) on these parameters (P < 0.05) with no effect on uncontaminated diets. Liver tissue of broilers receiving AFB(1) alone had perilobular inflammation and vacuolar degeneration of hepatocytes as compared with the tissue from the control group (P < 0.05). Residues of AFB(1) were detected in the liver tissues of broilers fed on the AFB(1) diet (0.166 microg/kg). Supplementation of AflaDetox reduced the incidence and severity of the hepatic histopathology changes associated with aflatoxicosis and the amount of AFB(1) residue in liver. In conclusion, our results showed that addition of AflaDetox may reduce the adverse effects produced by the presence of AFB(1) in broiler chickens diets.

An experiment was conducted to evaluate the efficacy of a new ochratoxin-binding agent (Ocra-Tox, 5 g/kg of feed) in offsetting the toxic effects of ochratoxin A (OTA, 2 mg/kg of feed) in laying hen diets. Performance, serum biochemistry, OTA residue in the liver and eggs, and egg quality parameters were evaluated. Twenty-eight Hisex Brown laying hens, 47 wk of age, were allocated to 1 of 4 experimental treatments for 3 wk: control, OTA (containing 2 mg of OTA/kg of feed), OcraTox (containing 5 g of OcraTox/kg of feed), and OTA + OcraTox (containing 2 mg of OTA and 5 g of OcraTox/kg of feed). Laying hens fed OcraTox showed results similar to the control hens (P > 0.05). The OTA diet significantly (P < 0.05) reduced daily feed consumption, egg mass production, and serum triglyceride concentrations, and increased the relative liver weight, the serum activity of alkaline phosphatase, and the serum concentration of uric acid as compared with the control diet. Addition of OcraTox to the contaminated diet alleviated (P < 0.05) the negative effects resulting from OTA, reaching values not significantly different from the control diet for most of the parameters except the relative weight of the liver. Birds fed the OTA treatment showed a greater content of OTA in the liver (15.1 microg/kg) than those fed the control diet (<0.05 microg/kg). Supplementing the contaminated diet with OcraTox (OTA + OcraTox) reduced the values to 12.0 microg/kg. Residues of OTA were not detected above our detection limit (0.05 microg/kg) in any of the analyzed eggs. In conclusion, our results indicated that addition of OcraTox can counteract the deleterious effects caused by OTA in laying hens.

The plant extract mixture (XT) used in the present experiment, containing carvacrol, cinnamaldehyde, and capsicum oleoresin, has previously been shown to decrease diarrhea mortality and to modify the intestinal environment of pigs after weaning. However, results obtained among experiments have not been consistent. We hypothesized that dietary protein could be a main factor determining the effect of plant extracts on intestinal environment. Thus, in the present study we assessed the effects of XT in piglet diets with different protein sources and amounts. Pigs weaned at 20 +/- 1 d of age (n = 240) were allocated to 1 of 6 treatments, which followed a factorial arrangement, with 2 amounts (as-fed basis) of the XT (0 and 200 mg/kg) and 3 diets with various amounts of CP and protein sources. Diet FM18 contained 10% of low-temperature fish meal (LT-FM) and a CP level of 18%; diet SBM18 contained 5% of LT-FM plus 9% of full fat extruded soy and a CP level of 18%; and SBM20 diet contained 10% of LT-FM plus 6.3% of full fat extruded soy and a CP level of 20%. Growth performance of the animals was recorded for 14 d, but no differences were detected among treatments. Eight pigs per treatment were killed to examine variables describing aspects of gastrointestinal ecology. For diets containing 18% CP, FM18 and SBM18, XT tended to decrease ileal digestibility of OM (P = 0.064 and 0.071, respectively) and decreased starch digestibility (P = 0.032 and 0.014, respectively). It also reduced villi length (P = 0.003 and 0.013, respectively) and tended to decrease intraepithelial lymphocyte number (P = 0.051 and 0.100, respectively) in the proximal jejunum. The XT inclusion also increased ileal lactobacilli:enterobacteria (P = 0.017) ratio and decreased VFA production in the cecum (P = 0.045) for all diets. A decreased CP level appeared to favor the effects of the studied plant extracts in a positive or negative way depending on the variable measured. The microbial differences produced by XT could be the reason for improved digestive health observed by the authors in stronger challenging conditions (e.g., dirtier environments or long fasting periods after weaning).

Two experiments were conducted to evaluate the efficacy of an activated diatomaceous clay (ADC) in reducing the toxic effects of zearalenone (ZEA) in the diet of rats and piglets. In the rat experiment, 90 Sprague-Dawley female weanling rats with an initial BW of 45 ± 1.0 g were assigned to 1 of 6 dietary treatments for 28 d in a completely randomized design (CRD) with a 2 × 3 factorial arrangement (0 or 6 mg ZEA/kg feed and 0, 1, and 5 g ADC/kg feed). In the piglet experiment, 64 female piglets ([Large White × Landrace] × Pietrain with an initial BW of 14.9 ± 1.65 kg) were fed 1 of 8 experimental diets for 26 d in a CRD design with a 2 × 4 factorial arrangement (0 or 0.8 mg ZEA/kg feed and 0, 1, 2, and 5 g ADC/kg feed). The ADFI, ADG, and G:F were determined at the end of each experiment. At the conclusion of studies, serum samples were collected and rats and piglets were euthanized to determine visceral organ weights. The diet contaminated with ZEA did not alter the growth of rats and the relative weight of liver and kidneys. However, ZEA increased ( < 0.05) the relative weight of uterus, ovaries, and spleen and decreased ( < 0.05) the serum activities of alkaline phosphatase and alanine aminotransferase compared to the control group. Supplementation of ADC in the rat diets counteracted ( < 0.05) the observed toxic effects of ZEA on the uterus and ovaries weight. The diet contaminated with ZEA (0.8 mg/kg feed) increased ( < 0.05) the weight of the uterus and ovaries in piglets but did not modify the serum biochemical variables or the relative weight of other visceral organs. The addition of 5 g ADC/kg to the contaminated feed reduced the toxic effects of ZEA on uterus and ovary weights to that of the control group. Zearalenone (10.5 μg/kg bile) and α-zearalenol (5.6 μg/kg bile) residues were detected in the bile of piglets fed the ZEA treatment. Supplementation of ADC to diets contaminated with ZEA reduced ( = 0.001) ZEA content in bile compared to the ZEA treatments. The results of these experiments indicate that a long-term consumption of ZEA-contaminated diets stimulated growth of the reproductive tract in rats and piglets and the presence of ZEA residue in bile in piglets. These effects may be counteracted by the addition of ADC to the diet.

The present study was conducted to determine the toxic dose response of a chronic dietary Zearalenone (ZEA) in weaned young rats. Sixty, 21-day-old, Sprague Dawley female rats were randomly allocated to five groups of four replicate cages containing three rats. Rats were fed diets with increasing amounts of ZEA (0, 0.5, 0.9, 1.8 and 3.6 mg/kg) for 4 weeks. Daily feed intake was reduced (P < .05) by feeding the ZEA diets with 0.9 and 3.6 mg ZEA/kg feed. Rats fed the diet containing 1.8 mg ZEA/kg increased (P < .05) the body weight gain (BWG) and reduced (P < .05) feed conversion rate (FCR) as compared to the control group. The two highest levels of dietary ZEA also increased (P < .05) the weight of the uterus. However, ovaries' weight, timing of vaginal opening and the inter-oestrous interval were not affected by increasing the doses of dietary ZEA (P > .05). Similarly, serum concentrations of total protein, follicle-stimulating hormone and alanine aminotransferase, aspartate aminotransferase and alkaline phosphate activities were not altered by the ZEA treatments. In conclusion, our results indicated that a chronic dietary consumption of ZEA at concentrations of 1.8 mg ZEA/kg increases the BWG and the uterus weight of weaning female rats.