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Poult Sci 2006. 85:2117-2123
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ENVIRONMENT, WELL-BEING, AND BEHAVIOR

Effects of Feeding Grains Naturally Contaminated with Fusarium Mycotoxins on Brain Regional Neurochemistry of Laying Hens, Turkey Poults, and Broiler Breeder Hens

M. Yegani*, S. R. Chowdhury*, N. Oinas{dagger}, E. J. MacDonald{dagger} and T. K. Smith*,1

* Department of Animal and Poultry Science, University of Guelph, Ontario, Canada N1G2W1; and {dagger} Department of Pharmacology and Toxicology, University of Kuopio, Fin-70211, Finland

1 Corresponding author: tsmith{at}uoguelph.ca


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Three experiments were conducted to compare the effects of feeding blends of grains naturally contaminated with Fusarium mycotoxins on brain regional neurochemistry of laying hens, turkey poults, and broiler breeder hens. In Experiment 1, thirty-six 45-wk-old laying hens were fed diets including the following for 4 wk: 1) control, 2) contaminated grains, and 3) contaminated grains + 0.2% polymeric glucomannan mycotoxin adsorbent (GMA). Concentrations of brain neurotransmitters and metabolites were analyzed in pons, hypothalamus, and cortex by HPLC with electrochemical detection. Neurotransmitters and the metabolites measured included dopamine, 3,4-dihydroxylphenyacetic acid, homovanillic acid, serotonin [5-hydroxytryptamine (5-HT)], 5-hydroxyindolacetic acid, epinephrine, and norepinephrine. The feeding of contaminated grains significantly increased concentrations of 5-HT and decreased the 5-hydroxyindolacetic acid:5-HT in the pons region in the brain stem. Dietary supplementation with GMA prevented these effects. There was no effect of diet on concentrations of other neurotransmitters or metabolites in the pons, hypothalamus, or cortex. In Experiment 2, thirty-six 1-d-old turkey poults were fed diets including the following for 4 wk: 1) control, 2) contaminated grains, and 3) contaminated grains + 0.2% GMA. Hypothalamic, pons, and cortex neurotransmitter concentrations were not affected by diet. In Experiment 3, forty-two 26-wk-old broiler breeder hens were fed diets including the following for 15 wk: 1) control, 2) contaminated grains, and 3) contaminated grains + 0.2% GMA. There was no effect of diet on neurotransmitter concentrations in the pons, hypothalamus, or cortex. It was concluded that differences in intraspecies effects of these mycotoxins on brain neurotransmitter concentrations might explain the intraspecies differences in the severity of Fusarium mycotoxin-induced reductions in feed intake.

Key Words: Fusarium mycotoxin • brain regional neurochemistry • laying hen • turkey poult • broiler breeder hen


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Fusarium mycotoxins, including trichothecenes, are produced by many species of Fusarium fungi (Hussein and Brasel, 2001). Interest in the neurotoxicological effects of trichothecenes and other Fusarium mycotoxins has been based on the reports indicating that the feeding of these compounds can reduce feed intake and induce vomiting in pigs (Prelusky and Trenholm, 1993). Although deoxynivalenol (DON) has been reported to be one of the least acutely toxic trichothecenes, the anorexic and emetic effects of DON are equal to or greater than those reported for more acutely toxic trichothecenes such as T-2 toxin (Rotter et al., 1996).

Trichothecenes are potent inhibitors of hepatic protein synthesis (Meloche and Smith, 1995), which can result in hyperaminoacidemia (Wannemacher and Dinterman, 1983). Tryptophan is the precursor of serotonin [5-hydroxytryptamine (5-HT)], and elevated levels of tryptophan in the blood can result in tryptophan crossing the blood-brain barrier and increasing tryptophan concentrations in the brain. Serotonergic neurons are important in mediating behaviors such as feed intake, sleep, and muscle coordination (Leathwood, 1987). It has been demonstrated that such neurons can play a role in both anorexic and emetic effects of DON in rats and pigs (Fitzpatrick et al., 1988b; Prelusky, 1993).

Although mechanisms responsible for feed refusal or reduced feed intake induced by Fusarium mycotoxins are not fully understood, it has been proposed that alterations in brain neurotransmitter concentrations represent one of the possible mechanisms. There are known to be species differences in the effects of these mycotoxins on brain regional neurochemistry (Boyd et al., 1988; Fitzpatrick et al., 1988a; Swamy et al., 2004b).

There are many reports in the literature concerning the changes in brain neurochemistry caused by the feeding of Fusarium mycotoxins to rats (Boyd et al., 1988; Fitzpatrick et al., 1988b; MacDonald et al., 1988), pigs (Smith and MacDonald, 1991; Prelusky et al., 1992; Prelusky, 1993; Swamy et al., 2002b; 2004b), and chickens (Chi et al., 1981; Boyd et al., 1988; Fitzpatrick et al., 1988a; Swamy et al., 2004b). In most of these studies, elevations in 5-HT concentrations were the major effect seen.

Mycotoxin adsorbents prevent mycotoxicoses by inhibiting intestinal absorption of mycotoxins and preventing transfer through the blood to target tissues (Ramos et al., 1996). It has been shown that the feeding of a polymeric glucomannan mycotoxin adsorbent (GMA), extracted from the cell wall of yeast, can prevent some of the adverse effects of Fusarium mycotoxins in broilers (Swamy et al., 2002a; 2004a), laying hens (Chowdhury and Smith, 2004), ducklings (Chowdhury et al., 2005), and broiler breeder hens (Yegani et al., 2006).

To the best of our knowledge, no study has reported the comparative effects of feeding Fusarium mycotoxins on brain neurochemistry of laying hens, turkey poults, and broiler breeder hens. The objectives of these studies were, therefore, to investigate the comparative effects of feeding diets containing blends of grains naturally contaminated with Fusarium mycotoxins on brain regional neurochemistry and to determine the efficacy of GMA in preventing these effects.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Experimental Designs
Laying Hens.
Thirty-six 45-wk-old laying hens (ISA Brown, Cambridge, Ontario, Canada) were weighed and randomly assigned to 6 replicates for each of 3 treatments (2 birds per replicate). Birds were housed in individual cages in an environmentally controlled room maintained at 21°C with 15 h of daily light. Feed and water were provided ad libitum.

Turkey Poults.
Thirty-six 1-d-old Hybrid male turkey poults (Hybrid Turkeys, Kitchener, Ontario, Canada) were individually weighed, wing-banded, and randomly distributed into groups of 4 poults per floor pen (3 pens per treatment). Poults were initially maintained at 32°C, and the temperature was gradually lowered by 3°C per week to reach 21°C by the end of wk 4. Feed and water were provided ad libitum.

Broiler Breeder Hens.
Forty-two 26-wk-old broiler breeder hens of a commercial strain (Ross 308, Horizon Poultry Products Inc., Hanover, Ontario, Canada) were weighed and randomly assigned to individual cages as 14 replicates for each of 3 treatment groups. The cages were kept in an environmentally controlled room maintained at 21°C with 16 h of daily light. Feed consumption of hens was restricted to 133 g/bird per day and was increased based on the recommendation of the primary breeder to 155 g/bird per day by the end of experiment. Unlimited access to water was provided from individual nipple drinkers. The birds were vaccinated at the time of placement (26 wk of age) with a killed-typed Newcastle-bronchitis vaccine (Intervet Canada Ltd., Whitby, Ontario, Canada).

These experiments were approved by the University of Guelph Animal Care Committee and met the guidelines of the Canadian Council on Animal Care.

Experimental Diets
All the birds in the 3 experiments were fed corn, wheat, and soybean meal-based conventional diets including the following: 1) control, 2) contaminated grains, and 3) contaminated grains + 0.2% GMA (MTB 100, Alltech Inc., Nicholasville, KY). In the contaminated grain diet, all corn and wheat was replaced by corn and wheat naturally contaminated with Fusarium mycotoxins. The diet containing GMA was similar, except that 0.2% GMA was added at the expense of corn. Nutrient concentrations in the control diet met or exceeded minimum requirements according to the NRC (1994).

Determination of Dietary Mycotoxin Concentrations
Dietary concentrations of 19 mycotoxins including DON, 3-acetyl-DON, 15-acetyl-DON, nivalenol, T-2 toxin, iso T-2 toxin, acetyl-T-2 toxin, HT-2 toxin, T-2 triol, T-2 tetraol, fusarenone-X, diacetoxyscirpenol, scirpentriol, 15-acetoxyscirpentriol, neosolaniol, zearalenone, zearalenol, aflatoxin, and fumonisin were analyzed by gas chromatography and mass spectrometry at the Veterinary Diagnostic Laboratory, North Dakota State University, Fargo (Raymond et al., 2003). The detection limits were 0.2 mg/kg, with the exception of aflatoxin and fumonisin, which were detected at 0.02 and 2 mg/kg, respectively.

Experimental Parameters Measured
Analysis of Brain Regional Neurotransmitter Concentrations.
Laying hens and turkey poults were killed by instantaneous cervical dislocation after 4 wk of feeding, and brain sections (hypothalamus, pons, and cortex) were excised and immediately frozen in liquid N and stored at –80°C until analyzed for neurotransmitter concentrations (Glowinski and Iversen, 1966). Broiler breeder hens were killed after 15 wk of feeding. Brain sections from the 3 avian species were analyzed for dopamine (DA), 3,4-dihydroxylphenyacetic acid (DOPAC), homovanillic acid (HVA), 5-HT, 5-hydroxyindolacetic acid (5-HIAA), epinephrine (EPI), and norepinephrine (NE) using HPLC with electrochemical detection. The method was partially validated on the basis of a Food and Drug Administration guideline (2001). After thawing on ice, brain tissue samples were homogenized (1:10, wt/vol) in 0.1 M perchloric acid in a glass Potter-Elveheim homogenizer with a Teflon pestle (Fisher Scientific Co., Toronto, Ontario, Canada). Tissue homogenates were centrifuged for 15 min at 15,000 x g at 4°C, transferred into plastic vials, and analyzed immediately. The HPLC consisted of a type 582 solvent delivery system, a type DG-1210 vacuum degasser, a 542 autosampler, a type 880 thermostatted chamber, an 8-channel CoulArray 5600 electrochemical array detector equipped with a 2-channel 5014B microdia-lysis cell, and a CoulArray for Windows data acquisition module (Version 1.00; ESA Biosciences Inc., Chelmsford, MA). The applied potentials were –175 mV (channel 1), +225 mV (channel 2), +350 mV (channel 3), and +450 mV (channel 4). Norepinephrine, EPI, DA, DOPAC, 5-HT, and 5-HIAA were detected on channel 2, and HVA was detected on channel 3. Injection volume was 10 µL.

The analyses were separated on a Zorbax SB-Aq reversed-phase column (2.1 x 100 mm, 3.5 µm; Agilent Technologies Inc., Wilmington, DE) with a Zorbax SB-Aq precolumn (2.1 x 12.5 mm, 5 µm; Agilent Technologies Inc.) in an isocratic run. The column was maintained at 35°C. The mobile phase was 100 mM monobasic Na3PO4 containing 4.75 mM C6H8O7, 7 mM 1-octanesulfonic acid, and 50 µM disodium EDTA-acetonitrile mixture (98:2, vol/vol). The range of the method was about 50 to 160,000 fmol/injection, and the lower limit of quantification for NE, EPI, DA, and DOPAC was about 50 fmol/injection and for 5-HT, 5-HIAA, and HVA was about 100 fmol/injection.

Statistical Analysis
Data were analyzed by ANOVA using the GLM procedure of SAS as a completely randomized design (Kuehl, 2000; SAS Institute, 2000). Multiple comparisons were made using Dunnett’s test to determine the nature of the response to control and contaminated diets. Statements of statistical significance were based on P ≤ 0.05.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Dietary Mycotoxin Concentrations
Dietary mycotoxin concentrations are given in Table 1Go. In the control diet of laying hens, DON and other mycotoxins were not detected. Deoxynivalenol concentrations in the contaminated diet and contaminated diet with GMA were 12.1 and 11.7 mg/kg, respectively. In the control diet of turkey poults, the DON concentration was 0.2 mg/kg, but other mycotoxins were not detected. Deoxynivalenol concentrations in the contaminated diet and contaminated diet + GMA were 6.8 and 7.1 mg/kg, respectively. In the control diet of broiler breeder hens, the DON concentration was 0.2 mg/kg, but other mycotoxins were not detected. Deoxynivalenol concentrations in the contaminated diet and the contaminated diet + GMA were 12.6 and 13.8 mg/kg, respectively. Zearalenone and 15-acetyl-DON were also detected in lesser quantities.


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  		Table 1. Mycotoxin concentrations in experimental diets (mg/kg)
 
Brain Neurotransmitter Concentrations
In the experiment of laying hens, the feeding of contaminated grains increased (P < 0.05) concentrations of 5-HT and decreased 5-HIAA:5-HT in the pons region in the brain stem, and dietary supplementation with GMA prevented these effects (Table 2Go). There was no effect of diet on other neurotransmitters or metabolites in the pons, hypothalamus, or cortex. In turkey poults, the only difference attributable to consumption of contaminated grains was a trend toward elevated concentrations of cortical 5-HT (P = 0.1). In broiler breeder hens, hypothalamic, pons, and cortex concentrations of neurotransmitters and metabolites were not affected by diet, although there was a trend toward an increase in 5-HT concentrations (P = 0.1) and a nonsignificant decrease in 5-HIAA:5-HT in the pons (P = 0.2). In Figures 1Go and 2Go, comparative effects of feeding grains naturally contaminated with Fusarium mycotoxins on 5-HT concentrations and 5-HIAA:5-HT in broiler breeders, laying hens, and turkey poults are illustrated.


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  		Table 2. Effects of Fusarium mycotoxins on the concentrations of biogenic amines in laying hens1
 

Figure 1
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  		Figure 1. Comparative effects of feeding grains naturally contaminated with Fusarium mycotoxins on 5-hydroxytryptamine (5-HT) concentrations (conc.) in different brain regions of broiler breeders, laying hens, and turkey poults. An asterisk (*) indicates a diet was significantly different from control.

 

Figure 2
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  		Figure 2. Comparative effects of feeding grains naturally contaminated with Fusarium mycotoxins on the ratio of 5-HIAA:5-HT (5-hydroxyindolacetic acid:5-hydroxytryptamine) in different brain regions of broiler breeders, laying hens, and turkey poults. An asterisk (*) indicates a diet was significantly different from control.

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
Dietary Mycotoxin Concentrations
Failure to achieve exactly the same concentrations of Fusarium mycotoxins in the contaminated diets with and without GMA may be the result of lack of uniformity in distribution of mycotoxins in contaminated grains (Hamilton, 1978) and sampling variability (Davis et al., 1980). In the current studies, the contaminated grains contained several Fusarium mycotoxins with DON as the major contaminant. This cocontamination is more representative of commercial conditions than the feeding of purified or semipurified DON. It has recently been shown that masked mycotoxins, in which the toxin is conjugated to glucose, can escape routine detection methods but can undergo hydrolysis, releasing free mycotoxins in the intestinal tract (Schneweis et al., 2002; Berthiller et al., 2005). This situation might have contributed to an underestimation of the total amount of Fusarium mycotoxins in the present studies.

Brain Neurotransmitter Concentrations
Although mechanisms responsible for feed refusal or reduced feed intake induced by Fusarium mycotoxins are not fully understood, it has been proposed that alterations in brain neurotransmitter concentrations are one of the possible mechanisms. There are species differences in the effects of these mycotoxins on brain regional neurochemistry (Boyd et al., 1988; Fitzpatrick et al., 1988a; Swamy et al., 2004b).

In the current study with laying hens, the feeding of contaminated grains decreased feed intake and egg production compared with controls after 4 wk of feeding (Chowdhury and Smith, 2004). This observation may well be related to the significant increase in 5-HT concentrations in the pons of these birds. This finding is in agreement with previous reports of a significant increase in the concentrations of 5-HT in the pons (Swamy et al., 2004b) and simultaneous reductions in feed intake of broiler chicks fed grains naturally contaminated with Fusarium mycotoxins for 8 wk (Swamy et al., 2004a). Elevated concentrations of 5-HT in the pons of laying hens may further support the concept that Fusarium mycotoxins alter serotonergic activity in the brain and cause subsequent reductions in feed intake (Smith and MacDonald, 1991; Prelusky et al., 1992; Prelusky, 1993; Swamy et al., 2002b; 2004b). It is difficult to interpret what the disturbed 5-HIAA:5-HT in the pons of laying hens actually signify in terms of the synthesis, storage, and release of 5-HT. It is apparent that consumption of a contaminated diet for 4 wk evoked prolonged disturbances in the turnover of neurotransmitters in the serotonergic nerves of the pons.

There are several reasons that might explain the pattern of these changes in the pons. The pons contains the area postrema, the region associated with vomiting (chemoreceptor trigger zone), and it is known that this region of the brain lies outside of the blood-brain barrier (Miller and Leslie, 1994). Blood-borne toxins or other mold toxin-induced changes in plasma constituents may affect this region more than other parts of the brain that are protected by the tight intercellular junctions of the endothelial cells lining the blood vessels. Another reason may be that the serotonergic neurons in the pons are more susceptible to the toxin-induced changes, although it has been shown that most drugs known to affect serotonergic nerves in rats tend to have greater effects on forebrain structures such as the cortex, hippocampus, and hypothalamus and lesser effect on the rear brain areas such as the pons and medulla (Muck-Seler et al., 1996; Datla and Curzon, 1997; Yamane et al., 1999). The pons region is also the site of the raphe nuclei, the cell bodies that innervate most regions of the brain. The raphe nuclei are known to be involved in appetite and feeding, and, thus, disturbances to 5-HT release in this region could reduce the feed intake (Cooper et al., 2003).

In the experiments with turkey poults and broiler breeder hens, feed intake was not affected by the feeding of contaminated grains (Chowdhury, 2005; Yegani et al., 2006), a finding paralleled by the lack of effect on the 5-HT concentrations in these species. Fitzpatrick et al. (1988a) demonstrated that feeding White Leghorn chicks 2.5 mg of DON/kg of BW did not influence whole brain concentrations of monoamine neurotransmitters or their metabolites. It was also shown that T-2 toxin orally dosed at 2.5 mg/kg of BW did not affect whole-brain neurotransmitter levels in White Leghorn chicks (Boyd et al., 1988).

Preventive Effects of GMA
The use of dietary adsorbents to prevent mycotoxicoses has recently been reviewed (Doll and Danicke, 2004). Mycotoxin adsorbents prevent mycotoxicoses by adsorbing mycotoxins in the intestinal lumen and preventing transfer through the blood to target tissues (Ramos et al., 1996). It has been shown that GMA is efficacious in preventing some of the adverse effects of Fusarium mycotoxins in broilers (Swamy et al., 2002a), layers (Chowdhury and Smith, 2004), ducklings (Chowdhury et al., 2005), and broiler breeders (Yegani et al., 2006).

In the current experiment with laying hens, GMA was effective in preventing Fusarium mycotoxin-induced changes in 5-HT concentrations and subsequent reductions in feed intake. Because there was no effect of diet on brain neurotransmitter concentrations in turkey poults and broiler breeder hens, the efficacy of GMA as a preventative substance could not be assessed.

The pattern of changes in brain neurotransmitter concentrations of laying hens, turkey poults, and broiler breeder hens might explain the greater sensitivity of laying hens to Fusarium mycotoxin-induced reductions in feed intake.


   ACKNOWLEDGMENTS
 
These studies were supported by the Ontario Ministry of Agriculture, Food and Rural Affairs (Guelph, Canada) and Alltech Inc. We thank the Arkell Poultry Research Station and Feed Mill staff for their continuous cooperation and Margaret Quinton and Ian McMillan for their statistical advice.

Received for publication April 5, 2006. Accepted for publication July 4, 2006.


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 DISCUSSION
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