Effects of foodborne Fusarium mycotoxins with and without a polymeric glucomannan mycotoxin adsorbent on food intake and nutrient digestibility, body weight, and physical and clinicopathologic variables of mature dogs

Maxwell C. K. Leung Department of Animal and Poultry Science, Ontario Agricultural College, University of Guelph, Guelph, ON N1G 2W1, Canada.

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Trevor K. Smith Department of Animal and Poultry Science, Ontario Agricultural College, University of Guelph, Guelph, ON N1G 2W1, Canada.

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Niel A. Karrow Department of Animal and Poultry Science, Ontario Agricultural College, University of Guelph, Guelph, ON N1G 2W1, Canada.

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Herman J. Boermans Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, ON N1G 2W1, Canada.

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Abstract

Objective—To investigate the effects of feeding cereal-based diets that are naturally contaminated with Fusarium mycotoxins to dogs and assess the efficacy of a polymeric glucomannan mycotoxin adsorbent (GMA) in prevention of Fusarium mycotoxicosis.

Animals—12 mature female Beagles.

Procedures—Dogs received each of 3 cereal-based diets for 14 days. One diet was uncontaminated (control diet), and the other 2 contained contaminated grains; one of the contaminated diets also contained 0.2% GMA. Contaminants included deoxynivalenol, 15-acetyl deoxynivalenol, zearalenone, and fusaric acid. Food intake and nutrient digestibility, body weight, blood pressure, heart rate, and clinicopathologic variables of the dogs were assessed at intervals during the feeding periods.

Results—Food intake and body weight of dogs fed the contaminated diet without GMA were significantly decreased, compared with effects of the control diet. Reductions in blood pressure; heart rate; serum concentrations of total protein, globulin, and fibrinogen; and serum activities of alkaline phosphatase and amylase as well as increases in blood monocyte count and mean corpuscular volume were detected. Consumption of GMA did not ameliorate the effects of the Fusarium mycotoxins. For the GMA-contaminated diet, digestibility of carbohydrate, protein, and lipid was significantly higher than that associated with the control diet, possibly because of physiologic adaptation of the recipient dogs to reduced food intake.

Conclusions and Clinical Relevance—Results indicated that consumption of grains naturally contaminated with Fusarium mycotoxins can adversely affect dogs' feeding behaviors and metabolism. As a food additive, GMA was not effective in prevention of Fusarium mycotoxicosis in dogs.

Abstract

Objective—To investigate the effects of feeding cereal-based diets that are naturally contaminated with Fusarium mycotoxins to dogs and assess the efficacy of a polymeric glucomannan mycotoxin adsorbent (GMA) in prevention of Fusarium mycotoxicosis.

Animals—12 mature female Beagles.

Procedures—Dogs received each of 3 cereal-based diets for 14 days. One diet was uncontaminated (control diet), and the other 2 contained contaminated grains; one of the contaminated diets also contained 0.2% GMA. Contaminants included deoxynivalenol, 15-acetyl deoxynivalenol, zearalenone, and fusaric acid. Food intake and nutrient digestibility, body weight, blood pressure, heart rate, and clinicopathologic variables of the dogs were assessed at intervals during the feeding periods.

Results—Food intake and body weight of dogs fed the contaminated diet without GMA were significantly decreased, compared with effects of the control diet. Reductions in blood pressure; heart rate; serum concentrations of total protein, globulin, and fibrinogen; and serum activities of alkaline phosphatase and amylase as well as increases in blood monocyte count and mean corpuscular volume were detected. Consumption of GMA did not ameliorate the effects of the Fusarium mycotoxins. For the GMA-contaminated diet, digestibility of carbohydrate, protein, and lipid was significantly higher than that associated with the control diet, possibly because of physiologic adaptation of the recipient dogs to reduced food intake.

Conclusions and Clinical Relevance—Results indicated that consumption of grains naturally contaminated with Fusarium mycotoxins can adversely affect dogs' feeding behaviors and metabolism. As a food additive, GMA was not effective in prevention of Fusarium mycotoxicosis in dogs.

On a global basis, Fusarium mycotoxins are the most economically important grain mycotoxins.1 These compounds are typically found in corn, wheat, and barley that grow in temperate regions and can affect the health and productivity of domestic animals worldwide.2 Fusarium mycotoxins have also been found in commercial cereal-based pet foods.3

Fusarium mycotoxins include zearalenone, fumonisins, and FA; these trichothecenes are diverse in their chemical structures and toxic effects. Trichothecenes, such as DON (vomitoxin), nivalenol, T-2 toxin, and DAS, cause vomiting, anorexia, gastrointestinal tract irritation, and immunosuppression in many mammalian species.4 Fusaric acid affects brain neurotransmitter concentrations and causes vomiting, lethargy, and hypotension.5-8 Although acute aflatoxicosis in dogs is frequently reported and studied,9,10 little research appears to have been devoted to Fusarium mycotoxicoses in dogs.

Polymeric mycotoxin absorbents have been reported11 to prevent mycotoxicosis in animals by reducing intestinal absorption of mycotoxins and their subsequent transport to target tissues. A yeast-derived polymeric GMA has been effective in preventing the development of mycotoxicoses in poultry, swine, and horses.12-14

The objective of the study reported here was to investigate the effects of feeding cereal-based diets that are naturally contaminated with Fusarium mycotoxins on food intake and nutrient digestibility, body weight, blood pressure, heart rate, selected clinicopathologic variables, and serum immunoglobulin concentrations of mature dogs. The efficacy of GMA consumption in prevention of Fusarium mycotoxicosis was also determined.

Materials and Methods

Animals and diets—Twelve mature female Beagles were included in the study. The mean ± SD body weight of the dogs was 10.1 ± 1.1 kg, and mean age was 2.8 ± 1.6 years. The dogs were assigned randomly into 3 groups (4 dogs/group). A 3 × 3 Latin square study design was used. Groups were assigned to receive 1 of 3 diets for a 14-day period followed by a 7-day recovery period; this was repeated until each group had received each diet. The duration of the recovery period was based on the findings of a pilot studya in which dogs recovered within 5 days from a 5% weight loss induced by an exposure to 4.4 mg of DON/kg of food.The uncontaminated (control) diet was fed during recovery periods.

The 3 diets were formulated to meet the nutritional requirements of a mature dog for maintenance.15 The control diet was prepared with corn, poultry by-product, and wheat as the main ingredients (Appendix). Two mycotoxin-contaminated diets were prepared by replacing corn and wheat in the control diet with naturally contaminated grains. One of the mycotoxin-contaminated diets was formulated to include 0.2% GMA.b Water was provided to the dogs ad libitum.

Dogs were housed in individual 2.5 × 1.5-m pens at the Central Animal Facility of the Ontario Veterinary College of the University of Guelph. All animals were examined daily for any adverse clinical signs, such as mucosal irritation, vomiting, abnormal rectal temperature, and diarrhea. For each dog, a 15-minute outdoor walk was provided daily.

Animal care—The experimental protocol was reviewed and approved by the University of Guelph Animal Care Committee. Animals were managed and cared for in accordance with the guidelines of the Canadian Council on Animal Care.

Mycotoxin analysis and exposure—The diets were analyzed for trichothecenes (ie, zearalenone, aflatoxins, and fumonisins) at the Veterinary Diagnostic Laboratory of North Dakota State University. Concentrations of DON, 3-acetyl DON, 15-acetyl DON, T-2 toxin, iso T-2 toxin, acetyl T-2 toxin, HT-2 toxin, T-2 triol, T-2 tetraol, fusarenon-X, DAS, scirpentriol, 15-acetyl scirpenol, neosolaniol, zearalenone, and zearalenol were analyzed by use of a combination of gas chromatography and mass spectrometry as described by Groves et al16 and modified by Raymond et al.14 The detection limit for these mycotoxin assays was 0.2 mg/kg.

Aflatoxin concentrations in the diets were determined by use of an HPLC system.c Twenty-five grams of ground food was extracted with an acetonitrile-water (84:16 ratio) mixture for 1 hour. The extract was purified through a C18-alumina (1:1) column, derivatized with trifluoroacetic acid, and analyzed by use of a 250 × 4 × 5-mm C18 column with a flow rate of 1.0 mL/min; fluorescence excitation was determined at 355 nm, and fluorescence emission was determined at 440 nm. Aflatoxin G2 was used as an internal marker, and the detection limit for the aflatoxin assays was 0.02 mg/kg.

Analysis of fumonisins was performed by use of an HPLC system.d Ten grams of ground food was extracted with 50 mL of an acetonitrile-water (1:1 ratio) mixture for 30 minutes. The extract was centrifuged and 2 mL of supernatant was evaporated to dryness at 65°C. The residue was added to potassium hydroxide and heated at 95°C for 2 hours to hydrolyze fumonisins. The hydrolyzed fumonisins were extracted with ethyl acetate (which was then evaporated) and redissolved in an acetonitrile-water (7:3 ratio) mixture. The solution was derivatized with ortho-phthalaldehyde and analyzed by use of a 250 × 4 × 5-mm RP-18 column with a flow rate at 1.2 mL/min. Fluorescence excitation was determined at 335 nm and fluorescence emission at 440 nm. The detection limit for the fumonisin assays was 2 mg/kg.

Fusaric acid concentrations in the diets were determined by use of an HPLC system with a photodiode array detector.e The sample preparation and detection method was described,17 modified,18 and confirmed19 previously. The detection limit for the FA assay was 0.77 mg/kg.

Foodborne mycotoxin exposure of each dog in each 14-day feeding period was estimated by use of an equation as follows:

article image

Assessments during each 14-day feeding period—For assessment purposes, the day before each 14day feeding trial was designated as day 0. The last day of the feeding period was designated as day 14.

Assessment of weight and food intake—Dogs were weighed at 9:30 AM on days 0, 5, 10, and 15 of each replicated 14-day feeding period. Each dog was given 600 g of diet daily, and leftovers were weighed at 8:30 AM on the following day.

Assessment of blood pressure, heart rate, and clinicopathologic variables—Systolic and diastolic arterial blood pressures and heart rate were measured from 9:30 AM to 12:30 PM on days 0 and 15 of each replicated 14-day feeding period.f Blood samples were then collected via jugular or saphenous venipuncture and analyzed immediately. Hematologic and serum biochemical analyses were performed at the Animal Health Laboratory of the University of Guelph.

For each blood sample, erythrocyte count, mean corpuscular volume, and Hct were determined and mean corpuscular hemoglobin concentration was calculated. Hemoglobin (cyanomethemoglobin) concentration was assessed by use of an autoanalyzerg after RBCs were lysed. A differential leukocyte count was performed manually to detect changes in absolute numbers of leukocytes, lymphocytes, neutrophils, band neutrophils, monocytes, eosinophils, and basophils. Prothrombin time, partial thromboplastin time, and serum fibrinogen concentration were also determined by use of a coagulometer.h

Serum concentrations of total protein, albumin, globulin, glucose, cholesterol, urea, creatinine, calcium, phosphorus, magnesium, sodium, potassium, chloride, carbon dioxide, bilirubin, and cortisol and activities of alkaline phosphatase, aspartate aminotransferase, G-glutamyltransferase, alanine aminotransferase, creatine kinase, amylase, and lipase were determined by use of an autoanalyzer.i,j Concentration of immunoglobulin A in serum samples obtained on days 0 and 15 was determined via a radial immunodiffusion technique.14,20

Blood samples were obtained with clients' consent from 86 clinically normal adult dogs at the Animal Health Laboratory to obtain the reference limits for hematologic and serum biochemical measurements. The reference limits were calculated in accordance with recommendations of Solberg21 by use of computer softwarek (parametric or nonparametric analyses were performed according to the type of data).

Nutrient digestibility—Each dog was given a 0.5-g capsule of Cr2O3, an indigestible dye marker, before feeding on days 10 and 14. Fecal output derived from food consumed on days 10 through 13 was identified, collected, weighed, and analyzed for nutrients at a commercial laboratoryl in Guelph. At collection, feces were assigned a score (5-point scale) to describe form and consistency (1 = hard, dry pellets; 2 = hard, formed, dry feces; 3 = soft, formed, moist feces; 4 = soft, unformed feces; and 5 = watery diarrhea).

Fecal contents of dry matter, ash, crude protein, and crude fat were determined via oven drying (method 4.1.06), furnace combustion (4.1.10), Dumas method (4.2.04), and ether extraction (4.5.01), respectively, as described by the Association of Official Analytical Chemists.22 The percentage content of carbohydrate was calculated as the percentage content of dry matter minus the combined percentage contents of crude protein, crude fat, and ash. Energy was calculated on the basis of the modified Atwater values of 3.5, 8.5, and 3.5 kcal/g for protein, fat, and carbohydrate, respectively.23 Apparent nutrient digestibility was calculated by use of an equation as follows:

article image

Statistical analysis—The experimental dogs were assigned to the various diets in a Latin square design. Computer softwarem was used to analyze data by use of an ANOVA. The statistical model included diet, dogs, periods, and, if applicable, pretreatment values as covariates. The effect of feeding the Fusarium mycotoxin– contaminated diet was determined by contrasting the characteristics of dogs fed the control diet with those of dogs fed the mycotoxin-contaminated diet (without GMA). The efficacy of GMA in preventing development of Fusarium mycotoxicosis was evaluated by contrasting the characteristics of dogs fed the control diet with those of dogs fed the contaminated diet with GMA. Changes in body weight and food intake were analyzed by use of a repeated-measures ANOVA to determine any significant changes over time. Differences were considered significant at a value of P < 0.05.

Results

Mycotoxin analysis and exposure—The concentrations of mycotoxins in the diets were analyzed (Table 1). In the uncontaminated control diet, DON and FA were detected at concentrations of 0.2 and 5.1 mg/kg, respectively. Compared with the control diet, higher concentrations of DON and FA as well as lower concentrations of zearalenone and 15-acetyl DON were detected in both the contaminated diets. The contaminated diet with GMA had higher concentrations of all 4 mycotoxins, compared with the contaminated diet without GMA.

Table 1—

Mycotoxin content (mg of mycotoxin/kg of feed) of an uncontaminated (control) diet and diets contaminated with grains containing Fusarium mycotoxins with and without GMA and mean ± SD estimated mycotoxin exposure* (μg of mycotoxin/kg of body weight) of 12 dogs fed each of those diets during separate 14-day feeding periods.

Table 1—

The estimated mycotoxin exposure in relation to the body weight of the dogs was assessed (Table 1). For dogs fed the contaminated diet with or without GMA, the degree of exposure to DON, 15-acetyl DON, and zearalenone was similar and each was higher than that for dogs fed the control diet. The feeding of the 3 experimental diets resulted in a similar degree of FA exposure.

Food intake and body weight—Among the study dogs, feeding the contaminated diets significantly reduced food intake and body weight, compared with effects of feeding the control diet (Table 2). Compared with the control diet, feeding of the mycotoxin-contaminated diet without GMA decreased the dogs' food intake by 35% and body weight by 5% within 14 days. Food intake was reduced by 25% on day 1, and no adaptation to the contaminated diet was evident during the 14-day feeding period (data not shown).

Table 2—

Mean daily feed intake and body weight in 12 dogs fed an uncontaminated (control) diet and diets contaminated with grains containing Fusarium mycotoxins with and without GMA during separate 14-day feeding periods.*

Table 2—

Dogs fed the contaminated diet with GMA had a significant (P = 0.001) weight loss by day 5 (Table 2). The repeated-measures ANOVA revealed significant linear and quadratic associations (P = 0.027 and P = 0.028, respectively) of weight loss with time in dogs fed the contaminated diet with GMA, compared with dogs fed the control diet. Such changes in weight loss over time were not significant, however, in dogs fed the mycotoxin-contaminated diet without GMA. During the study, only 2 instances of vomiting were recorded; both were in the same dog when the contaminated diets (with and without GMA) were fed.

Blood pressure and heart rate—After the 14-day feeding period, mean systolic and diastolic arterial blood pressure was 165 and 100 mm Hg, respectively, in the control dogs; heart rate was 119 beats/min. Compared with the effects of feeding the control diet, systolic and diastolic arterial blood pressures and heart rate were significantly decreased in dogs fed the contaminated diet with GMA (145 mm Hg, 78 mm Hg, and 103 beats/min [P = 0.008, P = 0.016, and P = 0.004], respectively). Feeding the dogs the mycotoxin-contaminated diet without GMA, however, did not significantly affect any of these variables, compared with control diet values; systolic and diastolic arterial blood pressure was 160 and 91 mm Hg, respectively, and heart rate was 112 beats/min. The overall SEM for mean systolic and diastolic arterial blood pressure and heart rate were 17 mm Hg, 22 mm Hg, and 9 beats/min, respectively.

Hematologic and serum biochemical variables—Among the study dogs, feeding the contaminated diet with GMA significantly decreased serum globulin concentration and serum amylase activity, compared with effects of feeding the control diet (Table 3). Feeding the dogs with the mycotoxin-contaminated diet without GMA, however, did not significantly affect either of those variables. Compared with dogs fed the control diet, serum concentrations of total protein and fibrinogen and serum activity of alkaline phosphatase were significantly decreased in dogs fed the contaminated diets with and without GMA.

Table 3—

Effects of feeding an uncontaminated (control) diet and diets contaminated with grains containing Fusarium mycotoxins with and without GMA on selected clinicopathologic variables in 12 dogs fed each of those diets during separate 14-day feeding periods.

Table 3—

Blood monocyte counts and mean corpuscular volume were significantly increased in dogs fed the contaminated diet without GMA, compared with effects in dogs fed the control diet (Table 3). In contrast, feeding of the contaminated diet with GMA had no significant effect on blood monocyte count and mean corpuscular volume, compared with the effects of feeding the control diet. Among the study dogs, other hematologic and serum biochemical variables were not significantly affected during feeding of either contaminated diet. These included Hct; mean corpuscular hemoglobin concentration; hemoglobin concentration; prothrombin and partial thromboplastin times; serum concentrations of cortisol, glucose, cholesterol, urea, creatinine, calcium, phosphorus, magnesium, sodium, potassium, chloride, carbon dioxide, bilirubin, and immunoglobulin A; serum activities of aspartate aminotransferase, G-glutamyltransferase, alanine aminotransferase, creatine kinase, and lipase; and counts of erythrocytes, leukocytes, neutrophils, band neutrophils, lymphocytes, eosinophils, and basophils (data not shown).

Nutrient digestibility—Among the study dogs, the apparent digestibility of crude protein, crude fat, carbohydrate, and energy was significantly higher for the contaminated diet with GMA than it was for the control diet (Table 4). However, the nutrient and energy digestibility of the contaminated diet without GMA was not significantly different from that of the control diet. Dogs fed either of the contaminated diets had firmer feces, compared with findings in dogs fed the control diet (P < 0.05).

Table 4—

Effects of feeding an uncontaminated (control) diet and diets contaminated with grains containing Fusarium mycotoxins with and without GMA on apparent nutrient digestibility (%) and fecal score in 12 dogs fed each of those diets during separate 14-day feeding periods.

Table 4—

Discussion

Deoxynivalenol, 15-acetyl DON, zearalenone, and FA were detected in all diets that were fed to dogs in the study reported here. To provide mycotoxin-contaminated diets for study purposes, corn and wheat in the control diet were replaced with grains naturally contaminated with Fusarium mycotoxins. Exposure to naturally contaminated grains more closely simulates field conditions in which dogs are usually exposed to combinations of mycotoxins, compared with exposure to a single purified mycotoxin that has been used in most investigations.6,7,24,25

The control diet contained a detectable amount of DON and FA (0.2 mg/kg and 5.1 mg/kg, respectively), thereby exemplifying the widespread nature of this Fusarium mycotoxin contamination in Ontario-grown cereal grains. However, the concentrations of DON and FA in the control diet were much lower than the concentrations reported to induce physiologic changes in other domestic animals.4 Contamination of feed with either DON (1 mg/kg of feed) or FA (200 mg/kg of feed) can significantly reduce feed intake in swine.4,8

In the present study, the contaminated diets contained differing amounts of mycotoxins, despite the inclusion of the same amount of mycotoxin-containing grains. This finding is similar to those of other clinical trials13,14,26,27 in which naturally contaminated grains were used as a source of Fusarium mycotoxins. This variation between diets may have been caused by uneven distribution of mycotoxins in the grains, despite attempts at thorough mixing.28 Infestation of grains by Fusarium fungi occurs heterogeneously, depending on the environmental conditions for fungal growth. Nevertheless, dogs received similar mycotoxin exposure during the periods of feeding each of the contaminated diets, despite the difference in analyzed mycotoxin concentrations. This was a result of decreased food intake in dogs fed the contaminated diet with GMA, compared with dogs fed the contaminated diet without GMA. Fusaric acid is not associated with any potent toxic effects when administered singly but is likely the most widespread Fusarium mycotoxin.8,29 Among the 3 experimental diets used in the present study, FA exposure was low and similar, but it is possible that FA may interact synergistically with the other mycotoxins.30

The concentration of zearalenone in the diets fed to the dogs in our study was not expected to have a physiologic effect. In another study,25 inhibition of humoral immunity and stimulation of hepatic detoxication were detected in dogs exposed to 25 to 50 μg of zearalenone/kg of body weight for 90 days. The amount and duration of exposure used in that study were much greater than those used in the present study (5 to 6 μg of zearalenone/kg of body weight administered during a 14-day feeding period). Zearalenone induces cytochrome P450 expression, which may enhance DON detoxication in animals.31 However, no toxicologic interaction between DON and zearalenone has been detected in swine or mice.32,33

Results of the present study have suggested that dogs are susceptible to the anorexic effect of Fusarium mycotoxins. Deoxynivalenol, the major mycotoxin contained in the contaminated diets, reduces food intake by inhibiting protein synthesis in the liver, increases serum concentration of tryptophan, and increases brain concentrations of serotonin and its metabolites, thereby influencing satiety mechanisms in the medial hypothalamus of swine.34 Deoxynivalenol also delays gastric emptying via peripheral action at serotonin-3 receptors in rodents.35

The concentration of DON at which food intake among dogs was reduced in the present study (3.0 mg of DON/kg of food) was lower than the concentration estimated by Hughes et al (4.5 mg of DON/kg of food).24 The difference may be attributable to the combined toxic effects of DON, 15-acetyl DON, and FA. In dogs, 15-acetyl DON has a similar mechanism of action to DON but has a less potent emetic effect.36 Although FA has a very low acute toxic effect, compared with the trichothecenes, it does potentiate DON-induced anorexia in swine.37 This is believed to be the result of competition with tryptophan for binding with serum albumin, which increases serum concentration of free tryptophan and brain concentrations of tryptophan and serotonin.8,30,38

The rapid onset of reduced food intake in the present study is in agreement with findings in swine intoxicated with DON.39 Species differences in susceptibility to trichothecenes may relate to varying sensitivity to changes in blood tryptophan concentration. In a comparative study40 with starter pigs and broiler chickens, differences in alterations in brain neurochemistry accounted for the species differences in the severity of DON-induced reductions in food intake. The more developed olfactory sense in pigs and dogs may also account for their rapid response to Fusarium-contaminated diets.

In the study of this report, the large range of individual food intakes and the fact that only 1 dog vomited after receiving the contaminated diets illustrated the differences in individual susceptibility to mycotoxins. Such differences were detected in another study24 in which food intake and body weight of some dogs fed a mycotoxin-contaminated diet remained unchanged and in which a high DON concentration (8 mg/kg) was needed to induce vomiting in dogs.

In our study, the weight loss of dogs fed the contaminated diets was likely caused by mycotoxin-induced reduction in food intake. In a feeding trial41 involving starter pigs, pigs that were fed a control diet ad libitum had a significantly higher weight gain than those fed a mycotoxin-contaminated diet ad libitum. No significant difference in weight gain, however, was found between pigs fed the control diet in the amounts equivalent to those consumed by the pigs fed the contaminated diets.

Compared with the dogs receiving the control diet in the present study, dogs fed the contaminated diet with GMA had lower systolic and diastolic arterial blood pressures as well as a lower heart rate. This result appeared to be associated with reduced food intake. Reduced food intake is known to have a hypotensive effect in rats.42 The FA exposure (128 to 144 μg/kg of body weight) of the dogs in the current study, however, was much lower than the effective dose reported in rats.42 In another study5 of dogs, a dose of 10 to 30 mg of FA/kg of body weight administered IV depressed cardiac function and reduced peripheral vascular resistance. Furthermore, the FA exposure of the dogs fed the control diet in the present study was similar to the exposures associated with the 2 contaminated diets.

Among the dogs of the present study, all clinicopathologic variables remained within reference limits. Although the results suggested that Fusarium mycotoxins affect serum protein concentrations and blood cell production, the effects did not appear to be pathologically important. Also, the hematologic and serum biochemical findings of our study have suggested that these clinical variables are not useful for the purpose of diagnosing Fusarium mycotoxicoses in dogs.

It is important that the mycotoxin challenge study of this report was conducted in an experimental environment in which exposure to pathogens was minimized. Pathogens in household environments, however, may compound the harmful effects of Fusarium mycotoxins in dogs.

Contamination of the control diet with Fusarium mycotoxins improved nutrient digestibility in the present study. The results of our study were consistent with the findings of Danicke et al43 who determined that mycotoxin-contaminated diets fed to broiler chickens had higher protein digestibility than an uncontaminated control diet. Those authors suggested that fungal metabolism may increase nutrient bioavailability in cereals. The increased nutrient digestibility associated with the mycotoxin-contaminated diets fed to the dogs of the present study was possibly attributable to a physiologic adaptation to decreased food intake. Mycotoxin exposure was minimized by the reduction in food intake. This resulted in lesser amounts of bulk passing through the gastrointestinal tract, thereby increasing nutrient digestibility and absorption. Dogs fed the contaminated diet with GMA not only had a significantly higher nutrient digestibility but also a 44% reduction in food intake and a 7% weight loss, compared with dogs fed the control diet. In rats, reduced food intake is associated with protein digestibility and absorption.44 The excretion of firmer feces by the dogs fed the contaminated diet with GMA also suggested that more water was absorbed from the ingested food in the large intestine.

The trichothecenes, especially T-2 toxin and DAS, can irritate intestinal epithelium and cause malabsorption and diarrhea.4,34 The experimental diets used in our study did not contain detectable amounts of T-2 toxin and DAS or sufficient amounts of trichothecenes to induce mucosal irritation. Inspection of the oral cavity of each dog after feeding revealed no signs of mucosal irritation. The higher fecal scores of dogs fed contaminated diets indicated that the feeding of contaminated diets had no diarrhetic effect.

The concentration of GMA included in one of the contaminated diets was based on the recommendation of the manufacturer as well as on reports13,14,26,27 regarding other domestic species. In immature swine, 0.2 g of GMA/kg of feed prevents the changes in neurochemistry and serum antibody concentrations caused by a foodborne combination of DON, 15-acetyl DON, FA, and zearalenone (5.5, 0.5, 26.8, and 0.4 mg/kg of feed, respectively).13 Inclusion of the same GMA concentration in feed has also been reported14,26,27 to prevent Fusarium mycotoxicosis in horses and poultry.

The Fusarium mycotoxins are known to have a potent anorectic effect in dogs. However, the inclusion of GMA in one of the contaminated diets did not ameliorate the anorectic effect of Fusarium mycotoxins in dogs even though the estimated mycotoxin exposure from each contaminated diet was similar. The polymeric GMA has a high adsorptive capacity for binding combinations of various mycotoxins, thereby preventing their intestinal absorption and transport to target tissues.45 The concentration of GMA included in the contaminated diet in the present study appeared to be insufficient to provide protective effects in dogs, particularly in light of the degree of reduced food intake, which subsequently reduced the effective dose of food additives. Future investigations should focus on the chronic effects of Fusarium mycotoxins in dogs as well as the efficacy of GMA in preventing the development of Fusarium mycotoxicosis when provided in the diet at higher concentrations.

ABBREVIATIONS

FA

Fusaric acid

DON

Deoxynivalenol

DAS

Diacetoxyscirpenol

GMA

Glucomannan mycotoxin adsorbent

HPLC

High-performance liquid chromatography

a.

Leung MCK. Physiological and proteomics effects of Fusarium mycotoxins in mature Beagles. MSc thesis, Department of Animal and Poultry Science, University of Guelph, Guelph, ON, Canada, 2007.

b.

Mycosorb, Alltech Inc, Nicholasville, Ky.

c.

Shimadzu VP system with a LC-10A pump, Shimadzu Corp, Tokyo, Japan.

d.

HPLC 1100 series, Agilent Technologies Inc, Palo Alto, Calif.

e.

Waters 2695 and 2996 series, Waters Corp, Milford, Mass.

f.

Cardell 9402, Benson Medical Instruments Co, Markham, ON, Canada.

g.

Advia 120 hematology system, Bayer Inc, Healthcare Division, Toronto, ON, Canada.

h.

Amelung KC4A coagulometer, Sigma Aldrich Inc, St Louis, Mo.

i.

Hitachi 911 autoanalyzer, Roche Diagnostics, Hoffman-La Roche Ltd, Montreal, QC, Canada.

j.

Immulite 1000 analyzer, Diagnostic Products Corp, Los Angeles, Calif.

k.

Analyse-it software, Analyse-It Software Ltd, Leeds, England.

l.

Agri-Food Laboratories, Guelph, ON, Canada.

m.

GLM procedure of SAS, version 9, SAS Institute Inc, Cary, NC.

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    • Export Citation
  • 12.

    Raju M, Devegowda G. Influence of esterified-glucomannan on performance and organ morphology, serum biochemistry and haematology in broilers exposed to individual and combined mycotoxicosis (aflatoxin, ochratoxin and T-2 toxin). Br Poult Sci 2000;41:640650.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13.

    Swamy HVLN, Smith TK, MacDonald EJ, et al. Effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on swine performance, brain regional neurochemistry, and serum chemistry and the efficacy of a polymeric glucomannan mycotoxin adsorbent. J Anim Sci 2002;80:32573267.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14.

    Raymond SL, Smith TK, Swamy HVLN. Effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on feed intake, serum chemistry, and hematology of horses, and the efficacy of a polymeric glucomannan mycotoxin adsorbent. J Anim Sci 2003;81:21232130.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15.

    National Research Council. Nutrient requirements of dogs and cats. Washington, DC: National Academy Press, 2006;354370.

  • 16.

    Groves FD, Zhang L, Chang YS, et al. Fusarium mycotoxins in corn and corn products in a high-risk area for gastric cancer in Shandong province, China. J AOAC Int 1999;82:657662.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 17.

    Matsui Y, Watanabe M. Quantitative analysis of fusaric acid in the cultural filtrate and soybean plants inoculated with Fusarium oxysporum var. redolens. J Rakuno Gakuen Univ Nat Sci 1988;13:159167.

    • Search Google Scholar
    • Export Citation
  • 18.

    Smith TK, Sousadias MG. Fusaric acid content of swine feedstuffs. J Agric Food Chem 1993;41:22962298.

  • 19.

    Porter JK, Bacon CW, Wray EM, et al. Fusaric acid in Fusarium moniliforme cultures, corn, and feeds toxic to livestock and the neurochemical effects in the brain and pineal gland of rats. Nat Toxins 1995;3:91100.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20.

    Mancini G, Carbonara AO, Heremans JF. Immunochemical quantification of antigens by single radial immunodiffusion. Immunochemistry 1965;2:235254.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 21.

    Solberg HE. IFCC and ICSH approved recommendation (1987) on the theory of reference values. Part 5. Statistical treatment of collected reference values. Determination of reference limits. J Clin Chem Clin Biochem 1987;25:645656.

    • Search Google Scholar
    • Export Citation
  • 22.

    Association of Official Analytical Chemists. Official methods of analysis. 16th ed. Washington, DC: Association of Official Analytical Chemists, 1996.

    • Search Google Scholar
    • Export Citation
  • 23.

    Case LP, Carey DP, Hirakawa DA, et al. Canine and feline nutrition: a resource for companion animal professionals. 2nd ed. St Louis: Mosby, 2000;314.

    • Search Google Scholar
    • Export Citation
  • 24.

    Hughes DM, Gahl MJ, Graham CH, et al. Overt signs of toxicity to dogs and cats of dietary deoxynivalenol. J Anim Sci 1999;77:693700.

  • 25.

    Gajecka M, Jakimiuk E, Skorska-Wyszynska E, et al. Influence of zearalenone mycotoxicosis on selected immunological, haematological and biochemical indexes of blood plasma in bitches. Pol J Vet Sci 2004;7:175180.

    • Search Google Scholar
    • Export Citation
  • 26.

    Davis ND, Dickens JW, Freie RL, et al. Protocols for surveys, sampling, post-collection handling, and analysis of grain samples involved in mycotoxin problems. J AOAC Int 1980;63:95102.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 27.

    Chowdhury SR, Smith TK, Boermans HJ, et al. Effects of feedborne Fusarium mycotoxins on hematology and immunology of laying hens. Poult Sci 2005;84:18411850.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28.

    Chowdhury SR, Smith TK, Boermans HJ, et al. Effects of feedborne Fusarium mycotoxins on hematology and immunology of turkeys. Poult Sci 2005;84:16981706.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29.

    Bacon CW, Porter JK, Norred WP, et al. Production of fusaric acid by Fusarium species. Appl Environ Microbiol 1996;62:40394043.

  • 30.

    Smith TK, McMillan EG, Castillo JB. Effect of feeding blends of Fusarium mycotoxin-contaminated grains containing deoxynivalenol and fusaric acid on growth and feed consumption of immature swine. J Anim Sci 1997;75:21842191.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 31.

    Sun JH, Zhu HJ, Zheng YF, et al. Study on the transcriptional modulation of cytochrome P450 3A4 expression by zearalenone [in Chinese]. Chin J Prev Med 2004;38:411414.

    • Search Google Scholar
    • Export Citation
  • 32.

    Cote LM, Beasley VR, Bratich PM, et al. Sex-related reduced weight gains in growing swine fed diets containing deoxynivalenol. J Anim Sci 1985;61:942950.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 33.

    Forsell JH, Witt MF, Tai JH, et al. Effects of 8-week exposure of the B6C3F1 mouse to dietary deoxynivalenol (vomitoxin) and zearalenone. Food Chem Toxicol 1986;24:213219.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 34.

    Rotter BA, Prelusky DB, Pestka JJ. Toxicology of deoxynivalenol (vomitoxin). J Toxicol Environ Health 1996;48:134.

  • 35.

    Fioramonti J, Dupuy C, Dupuy J, et al. The mycotoxin, deoxynivalenol, delays gastric emptying through serotonin-3 receptors in rodents. J Pharmacol Exp Ther 1993;266:12551260.

    • Search Google Scholar
    • Export Citation
  • 36.

    Yoshizawa T, Morooka N. Studies on the toxic substances in infected cereals; acute toxicities of new trichothecene mycotoxins: deoxynivalenol and its monoacetate. J Food Hyg Soc Jpn 1974;15:261269.

    • Search Google Scholar
    • Export Citation
  • 37.

    Hidaka HT, Nagatsu T, Takeya K, et al. Fusaric acid, a hypotensive agent produced by fungi. J Antibiot (Tokyo) 1969;22:228230.

  • 38.

    Prelusky DB. The effect of low-level deoxynivalenol on neurotransmitter levels measured in pig cerebral spinal fluid. J Environ Sci Health B 1993;28:731761.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 39.

    Young LG, McGirr L, Valli VE, et al. Vomitoxin in corn fed to young pigs. J Anim Sci 1983;57:655664.

  • 40.

    Swamy HVLN, Smith TK, MacDonald EJ. Effects of feeding blends of grains naturally contaminated with Fusarium mycotoxins on brain regional neurochemistry of starter pigs and broiler chickens. J Anim Sci 2004;82:21312139.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 41.

    Swamy HVLN, Smith TK, MacDonald EJ, et al. Effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on growth and immunological measurements of starter pigs, and the efficacy of a polymeric glucomannan mycotoxin adsorbent. J Anim Sci 2003;81:27922803.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 42.

    El Fazaa S, Somody L, Gharbi N, et al. Effects of acute and chronic starvation on central and peripheral noradrenaline turnover, blood pressure and heart rate in the rat. Exp Physiol 1999;84:357368.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 43.

    Danicke S, Matthes S, Halle I, et al. Effects of graded levels of Fusarium toxin-contaminated wheat and of a detoxifying agent in broiler diets on performance, nutrient digestibility and blood chemical parameters. Br Poult Sci 2003;44:113126.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 44.

    Williams VJ, Senior W. The effect of semi-starvation on the digestibility of food in young adult female rats. Aust J Biol Sci 1978;31:593599.

  • 45.

    Diaz DE, Smith TK. Mycotoxin sequestering agents: practical tools for the neutralisation of mycotoxins. In: Diaz D, ed. The mycotoxin blue book. Nottingham, England: Nottingham University Press, 2005;323339.

    • Search Google Scholar
    • Export Citation

Appendix

Composition (as-fed basis) of an uncontaminated (control) diet and diets contaminated with grains containing Fusarium mycotoxins with and without GMA for use in dogs.

table5
  • 1.

    Wood GE. Mycotoxins in foods and feeds in the United States. J Anim Sci 1992;70:39413949.

  • 2.

    Placinta CM, D'Mello JPF, MacDonald AMC. A review of worldwide contamination of cereal grains and animal feeds with Fusarium mycotoxins. Anim Feed Sci Technol 1999;78:2137.

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  • 3.

    Leung MCK, Diaz-Llano G, Smith TK. Mycotoxins in pet food: a review on worldwide prevalence and preventative strategies. J Agric Food Chem 2006;5:96239635.

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  • 4.

    Haschek WM, Voss KA, Beasley VR. Selected mycotoxins affecting animal and human health. In: Haschek WM, Roussex CG, Wallig MA, eds. Handbook of toxicological pathology. 2nd ed. New York: Academic Press Inc, 2002;645698.

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    • Export Citation
  • 5.

    Furuta Y, Washizaki M. Effects of fusaric acid and its derivative on the cardiovascular system. Nippon Yakurigaku Zasshi 1976;72:139144.

  • 6.

    Matsuzaki M, Yoshida A, Akutsu S, et al. Studies on toxicity of fusaric acid-Ca. IV. chronic toxicity in dogs. Jpn J Antibiot 1976;29:518542.

    • Search Google Scholar
    • Export Citation
  • 7.

    Matsuzaki M, Yoshida A, Tsuchida M, et al. Studies on toxicity of fusaric acid-Ca. III. subacute toxicity. Jpn J Antibiot 1976;29:491517.

    • Search Google Scholar
    • Export Citation
  • 8.

    Smith TK, MacDonald EJ. Effect of fusaric acid on brain regional neurochemistry and vomiting behavior in swine. J Anim Sci 1991;69:20442049.

  • 9.

    Garland T, Reagor J. Chronic canine aflatoxicosis and management of an epidemic. In: deKoe W, Samson R, van Egmond H, eds. et al. Mycotoxins and phycotoxins in perspective at the turn of the millennium. Wageningen, The Netherlands: Ponsen and Looven, 2001;231236.

    • Search Google Scholar
    • Export Citation
  • 10.

    Stenske KA, Smith JR, Newman SJ, et al. Aflatoxicosis in dogs and dealing with suspected contaminated commercial foods. J Am Vet Med Assoc 2006;228:16861691.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11.

    Ramos AJ, Fink-Gremmels J, Hernandez E. Prevention of toxic effects of mycotoxins by means of nonnutritive adsorbent compounds. J Food Protect 1996;59:631641.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12.

    Raju M, Devegowda G. Influence of esterified-glucomannan on performance and organ morphology, serum biochemistry and haematology in broilers exposed to individual and combined mycotoxicosis (aflatoxin, ochratoxin and T-2 toxin). Br Poult Sci 2000;41:640650.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13.

    Swamy HVLN, Smith TK, MacDonald EJ, et al. Effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on swine performance, brain regional neurochemistry, and serum chemistry and the efficacy of a polymeric glucomannan mycotoxin adsorbent. J Anim Sci 2002;80:32573267.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14.

    Raymond SL, Smith TK, Swamy HVLN. Effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on feed intake, serum chemistry, and hematology of horses, and the efficacy of a polymeric glucomannan mycotoxin adsorbent. J Anim Sci 2003;81:21232130.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15.

    National Research Council. Nutrient requirements of dogs and cats. Washington, DC: National Academy Press, 2006;354370.

  • 16.

    Groves FD, Zhang L, Chang YS, et al. Fusarium mycotoxins in corn and corn products in a high-risk area for gastric cancer in Shandong province, China. J AOAC Int 1999;82:657662.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 17.

    Matsui Y, Watanabe M. Quantitative analysis of fusaric acid in the cultural filtrate and soybean plants inoculated with Fusarium oxysporum var. redolens. J Rakuno Gakuen Univ Nat Sci 1988;13:159167.

    • Search Google Scholar
    • Export Citation
  • 18.

    Smith TK, Sousadias MG. Fusaric acid content of swine feedstuffs. J Agric Food Chem 1993;41:22962298.

  • 19.

    Porter JK, Bacon CW, Wray EM, et al. Fusaric acid in Fusarium moniliforme cultures, corn, and feeds toxic to livestock and the neurochemical effects in the brain and pineal gland of rats. Nat Toxins 1995;3:91100.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20.

    Mancini G, Carbonara AO, Heremans JF. Immunochemical quantification of antigens by single radial immunodiffusion. Immunochemistry 1965;2:235254.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 21.

    Solberg HE. IFCC and ICSH approved recommendation (1987) on the theory of reference values. Part 5. Statistical treatment of collected reference values. Determination of reference limits. J Clin Chem Clin Biochem 1987;25:645656.

    • Search Google Scholar
    • Export Citation
  • 22.

    Association of Official Analytical Chemists. Official methods of analysis. 16th ed. Washington, DC: Association of Official Analytical Chemists, 1996.

    • Search Google Scholar
    • Export Citation
  • 23.

    Case LP, Carey DP, Hirakawa DA, et al. Canine and feline nutrition: a resource for companion animal professionals. 2nd ed. St Louis: Mosby, 2000;314.

    • Search Google Scholar
    • Export Citation
  • 24.

    Hughes DM, Gahl MJ, Graham CH, et al. Overt signs of toxicity to dogs and cats of dietary deoxynivalenol. J Anim Sci 1999;77:693700.

  • 25.

    Gajecka M, Jakimiuk E, Skorska-Wyszynska E, et al. Influence of zearalenone mycotoxicosis on selected immunological, haematological and biochemical indexes of blood plasma in bitches. Pol J Vet Sci 2004;7:175180.

    • Search Google Scholar
    • Export Citation
  • 26.

    Davis ND, Dickens JW, Freie RL, et al. Protocols for surveys, sampling, post-collection handling, and analysis of grain samples involved in mycotoxin problems. J AOAC Int 1980;63:95102.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 27.

    Chowdhury SR, Smith TK, Boermans HJ, et al. Effects of feedborne Fusarium mycotoxins on hematology and immunology of laying hens. Poult Sci 2005;84:18411850.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28.

    Chowdhury SR, Smith TK, Boermans HJ, et al. Effects of feedborne Fusarium mycotoxins on hematology and immunology of turkeys. Poult Sci 2005;84:16981706.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29.

    Bacon CW, Porter JK, Norred WP, et al. Production of fusaric acid by Fusarium species. Appl Environ Microbiol 1996;62:40394043.

  • 30.

    Smith TK, McMillan EG, Castillo JB. Effect of feeding blends of Fusarium mycotoxin-contaminated grains containing deoxynivalenol and fusaric acid on growth and feed consumption of immature swine. J Anim Sci 1997;75:21842191.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 31.

    Sun JH, Zhu HJ, Zheng YF, et al. Study on the transcriptional modulation of cytochrome P450 3A4 expression by zearalenone [in Chinese]. Chin J Prev Med 2004;38:411414.

    • Search Google Scholar
    • Export Citation
  • 32.

    Cote LM, Beasley VR, Bratich PM, et al. Sex-related reduced weight gains in growing swine fed diets containing deoxynivalenol. J Anim Sci 1985;61:942950.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 33.

    Forsell JH, Witt MF, Tai JH, et al. Effects of 8-week exposure of the B6C3F1 mouse to dietary deoxynivalenol (vomitoxin) and zearalenone. Food Chem Toxicol 1986;24:213219.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 34.

    Rotter BA, Prelusky DB, Pestka JJ. Toxicology of deoxynivalenol (vomitoxin). J Toxicol Environ Health 1996;48:134.

  • 35.

    Fioramonti J, Dupuy C, Dupuy J, et al. The mycotoxin, deoxynivalenol, delays gastric emptying through serotonin-3 receptors in rodents. J Pharmacol Exp Ther 1993;266:12551260.

    • Search Google Scholar
    • Export Citation
  • 36.

    Yoshizawa T, Morooka N. Studies on the toxic substances in infected cereals; acute toxicities of new trichothecene mycotoxins: deoxynivalenol and its monoacetate. J Food Hyg Soc Jpn 1974;15:261269.

    • Search Google Scholar
    • Export Citation
  • 37.

    Hidaka HT, Nagatsu T, Takeya K, et al. Fusaric acid, a hypotensive agent produced by fungi. J Antibiot (Tokyo) 1969;22:228230.

  • 38.

    Prelusky DB. The effect of low-level deoxynivalenol on neurotransmitter levels measured in pig cerebral spinal fluid. J Environ Sci Health B 1993;28:731761.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 39.

    Young LG, McGirr L, Valli VE, et al. Vomitoxin in corn fed to young pigs. J Anim Sci 1983;57:655664.

  • 40.

    Swamy HVLN, Smith TK, MacDonald EJ. Effects of feeding blends of grains naturally contaminated with Fusarium mycotoxins on brain regional neurochemistry of starter pigs and broiler chickens. J Anim Sci 2004;82:21312139.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 41.

    Swamy HVLN, Smith TK, MacDonald EJ, et al. Effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on growth and immunological measurements of starter pigs, and the efficacy of a polymeric glucomannan mycotoxin adsorbent. J Anim Sci 2003;81:27922803.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 42.

    El Fazaa S, Somody L, Gharbi N, et al. Effects of acute and chronic starvation on central and peripheral noradrenaline turnover, blood pressure and heart rate in the rat. Exp Physiol 1999;84:357368.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 43.

    Danicke S, Matthes S, Halle I, et al. Effects of graded levels of Fusarium toxin-contaminated wheat and of a detoxifying agent in broiler diets on performance, nutrient digestibility and blood chemical parameters. Br Poult Sci 2003;44:113126.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 44.

    Williams VJ, Senior W. The effect of semi-starvation on the digestibility of food in young adult female rats. Aust J Biol Sci 1978;31:593599.

  • 45.

    Diaz DE, Smith TK. Mycotoxin sequestering agents: practical tools for the neutralisation of mycotoxins. In: Diaz D, ed. The mycotoxin blue book. Nottingham, England: Nottingham University Press, 2005;323339.

    • Search Google Scholar
    • Export Citation

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