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* Department of Animal and Poultry Science, University of Guelph, Guelph, ON N1G 2W1, Canada;
and
Department of Pharmacology and Toxicology, University of Kuopio, P.O. Box 1627, Fin-70211 Kuopio, Finland; and
and
Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, ON N1G 2W1, Canada
2 Correspondence:
phone: 519-824-4120, ext. 3746; fax: 519-822-7897; tsmith{at}uoguelph.ca.
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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Key Words: Fusaric Acid • Fusarium Mycotoxins • Immunoglobulins • Neurochemistry • Pigs • Vomitoxin
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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Mice fed a DON-containing diet had shown pronounced elevation in serum immunoglobulin (Ig)A and a concurrent depression in IgG and IgM concentrations (Forsell et al., 1986). Diets contaminated with DON, however, did not significantly affect serum IgA concentrations in pigs (Bergsjo et al., 1992).
Dietary mycotoxin adsorbent materials can only be effectively used to prevent mycotoxicoses if these materials possess the ability to adsorb a large number of chemically different mycotoxins. This has been demonstrated in the case of glucomannan polymer (GM polymer) extracted from the cell wall of yeast (Raju and Devegowda, 2000).
It was hypothesized, therefore, that the chronic exposure of pigs to a diet contaminated with a mixture of Fusarium mycotoxins might alter brain neurochemistry and serum Ig concentrations and that dietary supplementation of GM polymer may be beneficial in overcoming this toxicity. The objectives of the current experiment were, therefore, to investigate the effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on production parameters, brain regional neurochemistry, serum chemistry, hematology, and organ weights of starter pigs. Glucomannan polymer was also tested for efficacy in preventing Fusarium mycotoxicoses.
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Materials and Methods |
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A total of 175 Yorkshire starter pigs, with an average initial body weight of 10.0 ± 1.1 kg, were housed in floor pens at the Arkell Swine Research Station of the University of Guelph. Five pigs of mixed gilts and barrows were randomly allotted to each experimental unit (pen). Each treatment consisted of 15 gilts and 20 barrows. Ambient temperature was 23 to 25°C. Pens provided 2.25 m2 of floor space with one nipple drinker and one stainless steel three-hole feeder per pen. Animals had free access to feed and water and were observed daily for any adverse clinical signs. Lighting was provided for 16 to 18 h daily throughout the experiment. The experiment consisted of seven blocks with time as the basis for blocking. In each block, pigs in a pen were fed one of five diets for 21 d. The control diet was formulated to meet all nutritional requirements of 8 to 20 kg starter pigs (NRC, 1988). The mycotoxin-contaminated diet was formulated to the nutrient specifications similar to the control diet by replacing 18% of control diet corn and 10% of control diet wheat with corn and wheat naturally contaminated with Fusarium mycotoxins (Table 1
). To test the efficacy of GM polymer in preventing Fusarium mycotoxicoses, mycotoxin-contaminated diets were supplemented with 0, 0.05, 0.1, and 0.2% GM polymer. The GM polymer is a product of Alltech Inc. (MTB-100, Nicholasville, KY) and is extracted from the cell wall of Saccharomyces cerevisiae1026. Representative feed samples were taken at the beginning of the experiment and were analyzed for Fusarium mycotoxins and nutrient content. The animal care and use protocol was approved by the University of Guelph Animal Care Committee and met the guidelines of the Canadian Council on Animal Care.
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Dietary contents of DON, 3-acetyldeoxynivalenol, 15-acetyldeoxynivalenol, nivalenol, T-2 toxin, iso T-2 toxin, acetyl-T-2 toxin, HT-2 toxin, T-2 triol, T-2 tetraol, fusarenon-X, diacetoxyscirpenol, scirpentriol, 15-acetoxyscirpentriol, neosolaniol, zearalenone, and zearalenol were analyzed using GC-MS (North Dakota State University, Fargo, ND). The detection limit for these mycotoxins was 0.2 µg/g. Dietary fusaric acid content was determined in our laboratory using the HPLC method (0.77 µg/g detection limit) of Matsui and Watanabe (1988) as modified by Smith and Sousadias (1993) and confirmed by Porter et al. (1995).
Experimental Parameters Measured
Body Weight and Feed Consumption. Pigs were weighed individually and feed consumption for each pen was measured weekly. Cumulative weight gain and feed consumption were determined while weekly and cumulative gain:feed ratios were calculated. One pig fed the 0.2% GM polymer supplemented diet was culled on d 16 of the experiment because of leg weakness. Weight gain, feed intake, and gain:feed were adjusted for this pen. The removal of this pig from the pen did not affect other parameters.
Blood Collection. On d 21, blood was collected from the retro-orbital sinus of two pigs per pen (12 per treatment). Only the first six blocks were used for blood collection. One set of blood samples was collected in heparinized vials for hematology determinations, while another set was collected in vials without anticoagulant to collect sera for serum chemistry and Ig determinations. Aliquots of serum for measuring Ig were frozen at -80°C until analyzed.
Hematology and Serum Chemistry. Serum concentrations of total protein, albumin, globulin, glucose, beta-hydroxybutyrate, haptoglobin, urea, cholesterol, creatinine, bilirubin, calcium, phosphorus, magnesium, sodium, potassium, chloride, and activities of alkaline phosphatase, glutamate dehydrogenase (GLDH), aspartate aminotransferase, gamma glutamyltransferase (GGT), and creatine kinase were determined using a Hitachi 911 autoanalyzer (Roche Diagnostics, Division of Hoffman-La Roche Limited, Quebec, Canada). Red blood cell count, mean corpuscular volume (MCV), and hematocrit were determined, and mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin concentrations were calculated. Hemoglobin was measured as cyanomethemoglobin after lysing the red blood cells using an Advia 120 Hematology System (Bayer Inc., Healthcare Division, Toronto, ON, Canada). Complete blood cell counts (differential leukocyte count) were performed manually to test for changes in absolute numbers of leukocytes, lymphocytes, segmented neutrophils, banded neutrophils, monocytes, eosinophils, and basophils. Hematology and serum chemistry determinations were performed by Laboratory Services Division of the University of Guelph (Guelph, ON, Canada).
Analysis of Immunoglobulins in Serum
. Serum IgM, IgG, and IgA were analyzed by sandwich ELISA according to Bianchi et al. (1995) with some modifications. The assay was carried out at 23°C. All the antibodies and reference sera used in the assay were purchased from Bethyl Laboratories (Montgomery, TX). In this assay, 96-well Nunc Immunoplate microtiter plates (#446612, Invitrogen Canada Inc., Burlington, ON, Canada) were coated by a 60 min incubation with 100 µL of 1/100 affinity purified goat anti-pig IgM (µ-chain specific), goat antipig IgG (Fc-fragment specific), or goat antipig IgA (
-chain specific). Antibodies were diluted in 0.05 M sodium carbonate (pH 9.6, Sigma Chemical #C3041, St. Louis, MO). Coated plates were washed three times with 200 µL of 50 mM Tris buffered saline containing 0.05% Tween 20 (TBS-Tween, pH 8.0, Sigma Chemical #T9039) using Multiwash Plus automatic machine (Jencons Scientific, Inc., Bridgeville, PA). To reduce nonspecific protein binding, 200 µL of 1% BSA diluted in 50 mM TBS (Sigma Chemical #T6789) was added to each well. The plates were then incubated for 30 min and washed three times with TBS-Tween. For Ig determination, Ig (IgM, IgG, or IgA) reference sera or serum samples were diluted in sample/conjugate diluent (50 mM TBS with 1% BSA and 0.5% Tween 20) and 100 µL was added to appropriate wells. Concentrations of IgM, IgG, and IgA in the reference sera were 4.4, 18.2, and 3.0 mg/mL, respectively. Standard curves were constructed for IgM, IgG, and IgA by diluting the reference sera ranging from 0 to 1,000 ng/mL. The concentrations of Ig in the test serum sample were determined using these standard curves. Plates were sealed and incubated for 60 min and were then washed three times. This was followed by the addition of 100 µL of either 1/30,000 goat antpig IgM-horseradish peroxidase (HRP) (µ-chain specific), 1/100,000 goat antipig IgG-HRP (Fc-fragment specific), or 1/75,000 goat antipig IgA-HRP (-chain specific) diluted in sample/conjugate diluent to each well. Plates were then incubated for an additional 60 min. Plates were washed three times, and 100 µL of prewarmed TMB substrate (3,3',5,5'-tetramethyl benzidine, KPL #52-00-00, Gaithersburg, MD) was dispensed. Plates were incubated for 15 min, and the enzyme-substrate reaction was stopped by the addition of 100 µL of 2 M sulfuric acid to each well. The optical density readings of the wells were read at 450 nm using Microtiter Plate Reader (Model 550) and Microplate Manager/PC (Bio-Rad, Hercules, CA 94547).
Analysis of Neurotransmitters. On d 21, two pigs per pen (12 per treatment) were killed by injection of 5 mL Euthansol (pentobarbital sodium, 340 mg/mL, Schering Canada Inc., Pointe Claire, Canada) into the heart followed by decapitation. Brain sections (hypothalamus, pons, and cortex) were excised, immediately frozen in liquid nitrogen, and stored at -80°C until analyzed for neurotransmitters. Dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), norepinephrine (NE), tryptophan, 5-HT, and 5-HIAA were analyzed using HPLC with electrochemical detection as described by Mefford (1981) and modified by MacDonald et al. (1988).
Organ Weights. On d 21 of the experiment after the collection of brain sections, liver, kidney, and spleen were excised and weighed. Organ weights were expressed as percentage of body weight for statistical analysis.
Statistical Analyses
Data were subjected to Levene’s homogeneity of variances test before the analysis for treatment differences. Data were analyzed by analysis of covariance with initial body weight as the covariable (for production parameters) or by ANOVA (for other parameters) using the GLM procedure of SAS (SAS Inst. Inc., Cary, NC) as a completely randomized block design with subsamples. The pen with the group of five pigs was the experimental unit. The effect of feeding Fusarium mycotoxin-contaminated grains to pigs was determined by employing a simple contrast between mycotoxin-contaminated diet and control diet. Similarly, the ability of GM polymer to prevent Fusarium mycotoxin-induced effects was tested by employing simple contrasts between data from pigs fed mycotoxin-contaminated diet and those from pigs fed the three levels of GM polymer (Kuehl, 2000). Statements of statistical significance were based on P < 0.05.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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The concentrations of mycotoxins analyzed in the diets are given in Table 2. Deoxynivalenol and FA were found in the control diet. Zearalenone and 15-acetyl DON were also detected in the mycotoxin-contaminated diet and the diets supplemented with GM polymer.
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Feed intake and body weight gain of pigs fed contaminated diets were lower than those fed the control diet throughout the experiment (Table 3) (P < 0.001). Gain to feed ratios, however, were significantly reduced in pigs fed contaminated diets only during 0 to 7 d. The supplementation of GM polymer to contaminated diets did not influence the feed intake of pigs (P > 0.05). Weight gain of pigs fed contaminated diets supplemented with 0.1 and 0.2% GM ploymer were significantly lower than the pigs fed contaminated diet starting from wk 2 and 3, respectively (P < 0.05). Gain to feed ratios were significantly lower in pigs fed contaminated diet supplemented with 0.1% GM polymer than the pigs fed contaminated diet during 0 to 7, 0 to 14, and 0 to 21 d (P < 0.05).
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Hypothalamic DA concentrations were reduced in pigs fed contaminated diets compared with controls (Table 4) (P = 0.02). The hypothalamic 5-HIAA to 5-HT ratios, however, were elevated upon feeding contaminated diets (P = 0.012). The concentrations of NE, DA, and DOPAC in pons were lower in pigs fed contaminated diets, while the ratios of HVA to DA and 5-HIAA to 5-HT were higher (P < 0.05). Norepinephrine concentrations in cortex were decreased in pigs fed contaminated diets (P < 0.05). The supplementation of 0.2% GM polymer to the contaminated diet significantly decreased the 5-HIAA to 5-HT ratios in hypothalamus and significantly increased NE, DA, and DOPAC concentrations in pons as compared to the pigs fed contaminated diet (P < 0.05). The supplementation of 0.05% GM polymer, however, was able to prevent only the elevated DOPAC concentrations in pons. Supplementation with 0.1% GM ploymer was not able to prevent any of the neurochemical changes caused by the feeding of contaminated grains (P > 0.05).
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The feeding of contaminated diets to pigs increased serum IgM and IgA concentrations (Table 5) (P < 0.05). Serum IgG concentrations, however, were not affected by diets (P > 0.05). Supplementation with 0.05 or 0.1% GM polymer significantly prevented increased serum IgA concentrations, while only 0.1% GM polymer was effective in preventing elevated serum IgM concentrations (P < 0.05).
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Pigs fed contaminated diets had increased serum chlorine concentrations, but decreased calcium and phosphorous concentrations compared to controls (Table 6) (P < 0.05). Feeding contaminated diets also resulted in decreased MCV and MCH (Table 7). The supplementation of 0.2% GM polymer to the contaminated diets significantly increased MCH and activities of GLDH and GGT, whereas 0.1% GM polymer supplementation significantly reduced serum glucose concentrations (P < 0.05) (Tables 6 and 7). Other hematology and serum chemistry parameters were not affected by the dietary treatments (P > 0.05).
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The absolute weights of liver, kidney, and spleen were significantly lower in pigs fed contaminated grains compared with controls (P < 0.05, data not shown). The weights of liver and kidney, expressed as a percentage of body weight, were still reduced in the pigs fed contaminated diets (Table 7
) (P < 0.05), while the weight of spleen on a percent body weight basis was not altered. The supplementation of 0.05% GM polymer to contaminated diets significantly prevented decreased liver weights on a percent body weight basis (P < 0.05).
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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The variation in the level of DON (5.6 ± 0.6 ppm) in the four contaminated diets may be due to uneven distribution of mycotoxin in the grain and the limitations of mixing (Davis et al., 1980). It has been reported that the same level of inclusion of contaminated grains resulted in 1.9 ppm DON in one experiment and 4.4 ppm DON in another (Smith et al., 1997). Deoxynivalenol concentration of 0.8 ppm in the control diet is an illustration of the potential magnitude of mycotoxin contamination of Ontario-grown feedstuffs. Fusaric acid concentrations in the contaminated diets were reasonably constant, and its presence in the control diet may have arisen, in part, from contaminated soybean meal (Smith and Sousadias, 1993; Smith et al., 1997). Matsui and Watanabe (1988) had reported that soybean plants can be contaminated with FA. Bacon et al. (1996) have stressed that given the numerous common Fusarium species that produce FA, the natural occurrence of this compound as a contaminant in foods and feeds should be considered commonplace. The FA concentration in the contaminated diets is similar to that of the control diet, and it is possible, therefore, that contaminated corn and wheat might not have contributed to FA concentrations. Although DON, FA, and zearalenone are all Fusarium metabolites, they are not all produced in significant amounts by the same Fusarium strains (Smith and Sousadias, 1993).
The presence of FA in the test diets, whether contributed from contaminated grains or contaminated soybean meal, needs to be addressed in the context of possible synergistic interactions between FA and DON. Smith et al. (1997) reported a synergistic interaction between DON and FA on weight gains of pigs. Fusaric acid has a very low acute toxicity compared to trichothecene mycotoxins (Hidaka et al., 1969). Fusaric acid (Smith and MacDonald, 1991) and DON (Prelusky, 1993) have been shown to elevate pig brain concentrations of serotonin, albeit through different mechanisms, which can lead to loss of appetite, lethargy, and loss of muscle coordination (Leathwood et al., 1987). Trichothecenes (DON and T-2 toxin) can inhibit hepatic protein synthesis and cause aminoacidemia (Meloche and Smith, 1995). Elevated blood tryptophan concentrations can lead to tryptophan crossing the blood-brain barrier to elevate brain tryptophan, the precursor of serotonin (Leathwood, 1987). Trichothecene mycotoxins do not alter the ratio of free to protein-bound tryptophan (Cavan et al., 1988), although they do increase the total tryptophan concentration in blood. Fusaric acid, being a tryptophan analogue, competes with tryptophan for albumin binding sites and displaces tryptophan that would normally be in bound form (Chauloff et al., 1986). This elevates free blood tryptophan and promotes serotonin synthesis. There must be enough increase in the total tryptophan, caused by trichothecenes, for FA to displace tryphophan from significant amounts of albumin. This might explain why FA, when present alone, needs to be at high concentrations to cause changes in brain serotonin concentrations.
Reports of feeding zearalenone-contaminated diets to pigs have indicated that 1 ppm is the minimum concentration required to produce hyperestrogenism (James and Smith, 1982). The dietary zearalenone content of about 0.4 ppm in the current experiment, therefore, should not have caused metabolic effects in the test animals. It has been reported that dietary zearalenone as high as 10 ppm had no significant effects on swine growth rate, feed consumption, or feed efficiency (Young and King, 1986). Feeding of 2 ppm 15-acetyldeoxynivalenol along with 6 ppm DON did not enhance the toxicity of DON to pigs (Rotter et al., 1992). The adverse effects associated with the contaminated diet in the current experiment, therefore, were probably due to a combination of DON, FA, and any other unidentified Fusarium mycotoxins.
Growth Parameters
Growth and feed intake of pigs fed contaminated diets over 21 d were reduced by 34.6 and 32.6%, respectively, compared to controls. These findings are in reasonable agreement with literature reports on starter pigs fed Fusarium mycotoxin-contaminated grains (Smith et al., 1997). Overall feed efficiency, however, was affected only during 0 to 7 d, implying that the main effect of Fusarium mycotoxins was to reduce feed consumption (Rotter et al., 1994). This result is in contrast with reports from Smith et al. (1997) and Young et al. (1983) who reported a linear and a linear and quadratic response of gain to feed ratios to the inclusion of Fusarium mycotoxin-contaminated grains. These researchers, however, fed higher levels of DON than in the current study. Fusaric acid concentrations in the contaminated diets of Smith et al. (1997) were also twice as high as in the current experiment.
Brain Neurotransmitter Concentrations
To the best of our knowledge, no study to date has reported the effect of feeding blends of grains naturally contaminated with Fusarium mycotoxins on brain neurotransmitter concentrations of pigs. In the current study, the pigs were fed a combination of Fusarium mycotoxins and altered neurotransmitter concentrations were observed. Although hypothalamic and pons 5-HT and 5-HIAA concentrations were not altered in a statistically significant manner by the feeding of contaminated diets, 5-HIAA to 5-HT ratios were elevated. Leathwood (1987) suggested that the 5-HIAA to 5-HT ratio was a more sensitive index of changes in serotonergic neurotransmitter turnover than simple metabolite concentrations. The enhanced serotonergic response was earlier observed in pigs exposed to DON (Prelusky, 1993) and FA (Smith and MacDonald, 1991) and had been linked to decreased feed intake, vomition, behavioral changes, and delayed gastric emptying (Fioramonti, 1993; Leathwood, 1987).
The precise role of DA in mediating mycotoxin-induced altered feeding behavior is not well defined, except that dopaminergic activity comprises a necessary element of the interneuronal network regulating control of eating (Prelusky, 1993). Reduced DA and DOPAC concentrations in the pons of pigs fed contaminated diets suggests that the Fusarium mycotoxins decreased the release of dopamine from brain stores (MacDonald et al., 1988). Lowered NE concentrations in pons and cortex of pigs fed contaminated diets are in accordance with the findings of Hidaka (1971) and might reflect the inhibitory effect of FA on dopamine beta-hydroxylase. Since oral doses of T-2 toxin may act as an inhibitor of dopamine beta-hydroxylase in chick brain (Chi et al., 1981), DON might have similar effects in swine.
Serum Immunoglobulin Concentrations
Very limited information is available on the possible immunotoxicity of feeding Fusarium mycotoxin-contaminated grains to domestic animals. Bergsjo et al. (1992; 1993) fed up to 4.82 ppm DON from contaminated oats to pigs and found no significant effect of diet on the serum IgA concentrations. These researchers used radial immunodiffusion for measuring Ig concentrations. This technique has several limitations including the availability and quality of specific polyclonal antisera (Bianchi et al., 1995). In contrast, ELISA, the technique used in the current study, in combination with defined monoclonal antibodies offer conditions for reproducible assays with provision of reagents for many years. The higher sensitivity and accuracy of the ELISA might have aided in getting statistically different Ig concentrations in the current study.
Increased serum IgA concentrations in pigs fed Fusarium mycotoxin-contaminated grains in the current study are in accordance with a series of studies conducted with mice. Feeding of purified DON to mice caused a significant dose-dependent increase in serum IgA with a concurrent decrease in serum IgM and IgG concentrations (Forsell et al., 1986). The anorectic effect of DON, per se, is not the underlying cause for elevated serum IgA concentrations in mice (Rasooly and Pestka, 1992). These researchers also reported that DON could induce an increase in specific polyclonal serum IgA response to endogenous antigens and subsequent deposition of IgA immune complexes in kidney glomeruli. It is also reported that DON and zearalenone do not interact to alter serum Ig levels (Forsell et al., 1986). The increased serum IgM concentrations in the current study, unlike the studies in mice, might be due to species variation or due to the presence of FA (Chu et al., 1993) and other unidentified Fusarium mycotoxins in the diet.
It has been reported that a single oral exposure of mice to both 5 and 25 mg/kg body weight DON significantly induced the mRNA for the proinflammatory cytokines interleukin (IL)-1ß, IL-6, and tumor necrosis factor-; the T helper 1 cytokines interferon-
and IL-2; and the T helper 2 cytokines IL-4 and IL-10, whereas lower doses had no effect Zhou et al. (1997). Any of these cytokines could directly or indirectly enhance differentiation of IgA-secreting B cells. Zhou et al. (1998), however, fed subchronic levels of DON (0, 10, and 25 ppm) for 4 wk and observed increased mRNA expression only for IL-2, interferon-, IL-10 and tumor necrosis factor-. Domestic animals are exposed to mixtures of fungal toxins under the field conditions. The combined effects of several potential immunotoxins all with different mechanisms of toxicity are unknown. Research is needed to determine the etiology of elevated Ig concentrations in pigs exposed to combinations of mycotoxins.
Hematology and Serum Chemistry
The variability in hematology and serum chemistry of pigs fed DON-contaminated diets, reported by different researchers, might be the result of different doses of DON, different age group of pigs used, or the presence of other mycotoxins. Young et al. (1983) reported an inverse relationship between serum phosphorus concentration and level of DON (13.5 to 54 ppm) in the diet. In another study, Bergsjo et al. (1993) reported significant decreases in PCV and serum protein, albumin, calcium, and phosphorous concentrations in the pigs fed 3.5 ppm DON from contaminated oats. In contrast, Cote et al. (1985) reported no alterations in hematology and serum chemistry in starter pigs fed 0.7 to 5.8 ppm DON.
The differences in serum mineral concentrations in the current study indicated an influence of dietary Fusarium mycotoxins on mineral metabolism and are in agreement with Young et al. (1983). Deoxynivalenol can cause extensive necrosis in the gastrointestinal tract and thereby reduce intestinal absorption of essential nutrients such as D-glucose, 5-methyltetrahydrofolic acid, manganese, and molybdenum (Hunder et al., 1991). Reduced MCV and MCH upon exposure to Fusarium mycotoxins might explain early signs of alterations in red blood cell-related functions (Bergsjo et al., 1993). Given the current experimental design, it was not possible to separate the feed refusal effect of Fusarium mycotoxins from their systemic toxic effects on the aforementioned parameters.
Organ Weights
The significant reduction in the absolute weights of liver and kidney are in agreement with Pollman et al. (1985) who found a linear decline in these organ weights in starter pigs fed 0, 1.2, 2.4, and 3.6 ppm DON from contaminated wheat. These researchers, however, did not find significant differences in the absolute spleen weights. Forsell et al. (1986) commented that the organ weights in mice fed DON are directly related to the nutritional status of animals and organ mass changes in proportion to changes in body weight. Though the spleen weights in the current study follow the above association, the reduced liver and kidney weights are the combined result of feed refusal and systemic toxicity of Fusarium mycotoxins. The reduced liver and kidney weights related to body weight are contradictory to Trenholm et al. (1994), who observed a significant increase in these organ weights in pigs fed 3.9, 5.0, and 8.7 ppm DON from contaminated wheat for seven weeks. The effect of DON on relative organ weights seems to be dependent on the age of pigs, duration of exposure of pigs to mycotoxins, and dose of DON.
Effect of Glucomannan Polymer Supplementation
Glucomannan polymer derived from Saccharomyces cerevisiae1026 improved weight gain and feed intake and reduced organ weights in broiler chickens fed aflatoxins (Swamy and Devegowda, 1998) and aflatoxins and T-2 toxin (Raju and Devegowda, 2000). Previous studies in our laboratory indicated that the supplementation of Fusarium mycotoxin-contaminated diets with GM polymer prevented some of the mycotoxin-induced alterations in hematology, serum chemistry, and biliary IgA concentrations in broiler chickens (Swamy et al., 2002). Although the precise mode of action of GM polymer is not known, Raju and Devegowda (2000) hypothesized that GM polymer might trap the mycotoxin molecule in its glucomannan matrix preventing toxin absorption from the gastrointestinal tract and the subsequent toxin-induced tissue changes.
The uneven distribution of mycotoxins in contaminated grains made it difficult to interpret the effect of GM polymer supplementation (Davis et al., 1980). The depressing effect of DON on feed intake and weight gain was so profound that the GM polymer supplementation was unable to prevent these adverse effects. Instead, the supplementation of 0.1 and 0.2% GM polymer to the contaminated grains reduced weight gain and gain to feed ratios. It can be speculated that relatively higher concentrations of DON (6 µg/g) in 0.1 and 0.2% GM polymer supplemented diets as compared to the contamianted diet alone (4.6 µg/g) might be responsible for this effect. The supplementation of 0.2% GM polymer was very effective in preventing some of the neurochemical changes caused by the feeding of contaminated diets. It was apparent that 0.05 and 0.1% GM polymer supplementation might not be sufficient to prevent these neurochemical changes (except DOPAC concentrations in the pons). In contrast to the ability of GM ploymer to prevent some of the neurochemical changes, 0.1% GM ploymer supplementation was more effective in reversing the alterations in serum Ig concentrations. The reason for this discrepancy, however, is not known. The inability of 0.1 and 0.2% GM polymer supplementation in preventing reduced percentages of liver weights may be again attributed to high DON concentration in these diets.
Non-specific (unrelated to mycotoxins) increases in the serum GGT and GLDH activities, and glucose concentrations caused by the supplementation of GM polymer are difficult to explain. It can be speculated, however, that since GM polymer is nondigestible and nonfermentable and does not get translocated to the liver, the possibility of direct liver damage is precluded. In a turkey study conducted in our laboratory, 0.2% GM polymer supplementation to contaminated diets had been shown to significantly reduce serum cholesterol concentrations (unpublished data). Cholesterol is the precursor for hepatic bile salt synthesis. The GM polymer might have bound bile salts in the intestine thereby preventing enterohepatic recycling and forcing de novo hepatic synthesis from cholesterol. This might indirectly affect liver function causing seepage of GGT and GLDH into the circulation. Acetyl coenzyme A, an end product of mitochondrial oxidation of fatty acids or pyruvic acid, is the precursor for cholesterol synthesis. Glucose, in turn, is the precursor for pyruvic acid synthesis. This might also explain the decrease in serum glucose concentration when diet supplemented with 0.1% GM polymer was fed (Mathews and Van Holde, 1996).
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Footnotes |
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Received for publication May 16, 2002. Accepted for publication August 7, 2002.
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S. L. Raymond, T. K. Smith, and H. V. L. N. Swamy 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, September 1, 2003; 81(9): 2123 - 2130. [Abstract] [Full Text] [PDF]
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