Interactions between plant-derived oestrogenic substances and the mycoestrogen zearalenone in a bioassay with MCF-7 cells.

Human and animal diets may contain several non-steroidal oestrogenic compounds which originate either from plants (phytoestrogens) or from fungi that infect plants (mycoestrogens such as zearalenone (ZEN)). Phytoestrogens may compete with ZEN in binding to the oestrogen receptor ß and thereby may counteract the oestrogenic activity of ZEN. Using a modified version of the E-screen assay, plant-derived oestrogenic substances were tested for their proliferative or anti-proliferative effect on oestrogen-dependent MCF-7 cells. The samples were additionally tested for their ability to influence the oestrogenic activity of ZEN (1 µM). Among the individual substances tested, 8-prenylnaringenin had the strongest effect, as cell proliferation was increased by 78% at the lowest concentration (0.23 µM), and by 167% at the highest concentration (29.4 µM). Coumestrol (5.83 µM) increased cell proliferation by 39%, and genistein (370 µM) by 61%, respectively. Xanthohumol and enterolactone did not stimulate cell proliferation significantly. In the co-incubation experiments with ZEN, none of the single substances was able to decrease the oestrogenic activity of ZEN. Only for 8-prenylnaringenin (14.7 and 29.4 µM) was a trend towards an increase in the ZEN-induced cell proliferation up to 72% observed. In conclusion, with the exception of 8-prenylnaringenin, no substantial interaction between phytoestrogens and the mycotoxin ZEN could be detected using a bioassays with MCF-7 cells.

Mycotoxin-contaminated diets and deactivating compound in laying hens: 1. effects on performance characteristics and relative organ weight.

The current experiment was conducted to determine the effect of mycotoxin-contaminated diets with aflatoxin (AFLA) and deoxynivalenol (DON) and dietary inclusion of deactivation compound on layer hen performance during a 10-wk trial. The experimental design consisted of a 4 × 2 factorial with 4 toxin levels: control, low (0.5 mg/kg AFLA + 1.0 mg/kg DON), medium (1.5 mg/kg AFLA + 1.5 mg/kg DON), and high (2.0 mg/kg AFLA + 2.0 mg/kg DON) with or without the inclusion of deactivation compound. Three hundred eighty-four 25-wk-old laying hens were randomly assigned to 1 of the 8 treatment groups. Birds were fed contaminated diets for a 6-wk phase of toxin administration followed by a 4-wk recovery phase, when all birds were fed mycotoxin-free diets. Twelve hens from each treatment were subjected to necropsy following each phase. Relative liver and kidney weights were increased (P < 0.05) at the medium and high toxin levels following the toxin phase, but the deactivation compound reduced (P < 0.05) relative liver and kidney weights following the recovery period. The high toxin level decreased (P < 0.05) feed consumption and egg production during the toxin period, whereas the deactivation compound increased (P < 0.05) egg production during the first 2 wk of the toxin phase. Egg weights were reduced (P < 0.05) in hens fed medium and high levels of toxin. An interaction existed between toxin level and deactivation compound inclusion with regard to feed conversion (g of feed/g of egg). High inclusion level of toxins increased feed conversion compared with the control diet, whereas deactivation compound inclusion reduced feed conversion to a level comparable with the control. These data indicate that deactivation compound can reduce or eliminate adverse effects of mycotoxicoses in peak-performing laying hens.

Effects of mycotoxin-contaminated diets and deactivating compound in laying hens: 2. effects on white shell egg quality and characteristics.

An experiment was conducted to determine the effect of dietary inclusion of Mycofix Select (Biomin GmbH, Herzogenburg, Austria) on discrete egg parameters and quality characteristics of hens fed mycotoxin-contaminated diets (aflatoxin; AFLA) and deoxynivalenol (DON)) during a 10-wk trial. A 4 × 2 factorial design was used with 4 contamination levels: control, low (0.5 mg/kg of AFLA + 1.0 mg/kg of DON), medium (1.5 mg/kg of AFLA + 1.5 mg/kg of DON), and high (2.0 mg/kg of AFLA + 2.0 mg/kg of DON) with or without the inclusion of mycotoxin deactivating compound. Three hundred and eighty-four 25-wk-old laying hens were housed 3 per cage. Birds were fed contaminated diets for a 6-wk phase of toxin administration followed by a 4-wk recovery phase, when all birds were fed mycotoxin-free diets. Parameters evaluated included egg weight, Haugh unit value, specific gravity, eggshell thickness, egg shape index, and relative albumen and yolk weights. Albumen height and Haugh unit value were depressed (P < 0.05) at the high mycotoxin level 2 wk postinclusion. Egg weight was significantly reduced (P < 0.05) with the high toxins level by the third week of toxin administration and remained throughout the study during toxin administration. Egg shape index indicated a variation (P < 0.05) in shape with all toxin levels compared with the control. Relative yolk weight was decreased (P < 0.05) by the high toxin level. An interaction existed between the deactivating compound inclusion and toxins level with regard to specific gravity. Following the toxin phase, the deactivating compound inclusion increased (P < 0.05) egg specific gravity in the control and low toxin groups whereas a decrease (P < 0.05) was observed at the high toxin level. These data indicate that mycotoxins present in feed can reduce egg quality, size, yolk weight, and alter egg shape and that inclusion of a mycotoxin deactivating compound can ameliorate some of the negative effects of mycotoxin consumption.

Net effect of an acute phase response--partial alleviation with probiotic supplementation.

The acute phase response (APR) is characterized by inflammation, fever, and altered organ metabolism resulting in muscle catabolism and anorexia. Lipopolysaccharide (LPS)-induced APR may reflect depressed growth and appetite loss. Therefore, a 1-wk growth experiment was conducted to examine whether dietary supplementation of a multispecies probiotic (PoultryStar) would alleviate growth suppression and anorexia caused by LPS-induced APR. The experiment was designed with 4 treatments (n = 8 cages/treatment; 6 birds/cage) starting at 14 d of age. Before (0 to 14 d of age) and for the experiment (14 to 21 d of age), male broiler chicks were fed diets devoid of probiotic or were supplemented with 1.7 x 10(8) cfu/kg of probiotic. At 14 d of age, birds fed the diet devoid of probiotic were further divided into 3 treatments: an unchallenged positive control, LPS-challenged negative control (LPS-NC), and a treatment that was pair-fed to LPS-NC. The probiotic-fed birds were also then challenged with LPS. The LPS (Escherichia coli 055:B5) was injected intraperitoneally 4 times at 48-h intervals at 1 mg/kg of BW. The LPS challenge dramatically depressed BW gain from 14 to 21 d of age by 22% (P < 0.001). However, 41% of growth depression was attributable to factors other than feed intake reduction when compared with the pair-fed treatment. Probiotic supplementation recovered 17% of depressed growth (vs. LPS-NC; P = 0.068), but this improved growth was not due to improvements in feed intake (P = 0.47). However, recovery of feed intake of the probiotic + LPS birds occurred 48-h earlier than the LPS-NC birds. Growth depression induced by LPS administration resulted in an overall relative feed intake (vs. positive control) of 0.83 and also decreased net energy and protein accretion. Probiotic supplementation did not alleviate the reduction in net energy or protein accretion induced by LPS. In conclusion, APR (induced by LPS administration) diverted a large portion of consumed nutrients from tissue accretion. Probiotic supplementation lessened the anorexic effects of LPS resulting in a trend toward BW gain improvement versus the LPS-NC.