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Fusarium mycotoxins (FUS) occur frequently in poultry diets, and regulatory limits are laid down in several countries. However, the limits were established for exposure to a single mycotoxin, whereas multiple contamination is more realistic, and different studies have demonstrated that it is not possible to predict interactions between mycotoxins. The purpose of this study was thus to compare the toxic effect of deoxynivalenol (DON), fumonisins (FB) and zearalenone (ZON), alone and in combination on broiler chickens, at the maximum tolerated level established by the EU for poultry feed. Experimental corn-soybean diets incorporated ground cultured toxigenic Fusarium strains. One feed was formulated for chickens 0 to 10 days old and another for chickens 11 to 35 days old. The control diets were mycotoxin free, the DON diets contained 5 mg DON/kg, the FB diet contained 20 mg FB1 + FB2/kg, and the ZON diet contained 0.5mg ZON/kg. The DONFBZON diet contained 5, 20, and 0.5 mg/kg of DON, FB1 + FB2, and ZON, respectively. Diets were distributed ad libitum to 70 broilers (male Ross PM3) separated into five groups of 14 chickens each reared in individual cages from one to 35 days of age. On day 35, after a starvation period of 8 h, a blood sample was collected, and all the animals were killed and autopsied. No difference between groups that could be attributed to FUS was observed in performances, the relative weight of organs, biochemistry, histopathology, intestinal morphometry, variables of oxidative damage, and markers of testicle toxicity. A significant increase in sphinganine and in the sphinganine to sphingosine ratio was observed in broilers fed FB. Taken together, these results suggest that the regulatory guidelines established for single contamination of broiler chickens fed with DON, FB, and ZON can also be used in the case of multiple contamination with these toxins.

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BackgroundReproductive hens are subjected to a restricted diet to limit the decline in fertility associated with change in body mass. However, endocrine and tissue responses to diet restriction need to be documented.ObjectiveWe evaluated the effect of different levels of feed restriction, with or without fish oil supplementation, on metabolic parameters and adipokine levels in plasma and metabolic tissues of reproductive hens.MethodsWe designed an in vivo protocol involving 4 groups of hens; RNS: restricted (Rt) unsupplemented, ANS: ad libitum (Ad, receiving an amount of feed 1.7 times greater than animals on the restricted diet) unsupplemented, RS: Rt supplemented, and AS: Ad supplemented. The fish oil supplement was used at 1% of the total diet composition.ResultsHens fed with the Rt diet had a significantly (P < 0.0001) lower growth than Ad hens, while the fish oil supplementation had no effect on these parameters. Furthermore, the bioelectrical impedance analysis (BIA) and the fat ultrasonographic examinations produced similar results to the other methods that required animals to be killed (carcass analysis and weight of adipose tissue). In addition, the Rt diet significantly (P < 0.05) decreased plasma levels of triglycerides, phospholipids, glucose and ADIPOQ, and fish oil supplementation decreased plasma levels of RARRES2. We also showed a positive correlation between insulin values and ADIPOQ or NAMPT or RARRES2 values, and a negative correlation of fat percentage to RARRES2 values. Moreover, the effects of the Rt diet and fish oil supplementation on the mRNA expression depended on the factors tested and the hen age.ConclusionsRt diet and fish oil supplementation are able to modulate metabolic parameters and the expression of adipokines and their receptors in metabolic tissue.

Kinetics of the two isomers suggests that γ-HBCD is rapidly biotransformed and eliminated, and partly isomerized into the more persistent α-HBCD. Carry-over rate of ingested γ-HBCD to egg yolk was estimated at 1.2%. Estimated half-lives of γ-HBCD in egg yolk, in abdominal fat, and in liver were 2.9, 13, and 0.41 days, respectively.

The aim of the current study was to describe the fate of ingested α-hexabromocyclododecane (α-HBCDD) in laying hens. Individuals were exposed to two dietary concentrations of α-HBCDD (50 and 5 ng g(-1) feed) for 18 or 11 weeks followed by a 7-week decontamination period. The results show that no isomerization of α- to β- or γ-HBCDD forms occurred, whereas OH-HBCDD was identified as a product of α-HBCDD metabolism. Irrespective of the level of feed contamination, estimates of steady-state accumulation ratios were 5.2, 3.6, and 9.2 and half-lives were estimated at 17.4, 22.8, and 35.3 days in egg yolk, liver tissue, and abdominal fat, respectively. The steady-state carry-over rate to eggs was 22.9%. Thus, α-HBCDD ingested by laying hens is readily transferred to eggs and significantly accumulates in adipose tissue.

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