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Effects of a Hydrated Sodium Calcium Aluminosilicate (T-Bind) on Mycotoxicosis in Young Broiler Chickens1 L. F., KUBENA,*,2 R. B. HARVEY,* R. H. BAILEY,* S. A. BUCKLEY,* and G. E. ROTTINGHAUS† *USDA, Agricultural Research Service, Food Animal Protection Research Laboratory, 2881 F&B Road, College Station, Texas 77845, and †University of Missouri, College of Veterinary Medicine, Veterinary Medical Diagnostic Laboratory, Columbia, Missouri 65211 ABSTRACT Experiments were conducted to determine the ability of a hydrated sodium calcium aluminosilicate (T-Bind) sorbent to reduce the toxicity of aflatoxins (AF) or T-2 toxin in male broiler chickens from day of hatch to 21 d of age. In Experiment 1, the sorbent was added at 0.250 or 0.375% to diets containing AF at 5 or T-2 toxin at 8 mg/kg of diet. When compared with controls, AF reduced BW gain by 27% and T-2 toxin reduced BW gain by 17%. The addition of the sorbent at 0.250 or 0.375%, in the absence of added mycotoxins, did not alter the performance of the chicks. The sorbent reduced the toxic effects of 5 mg AF/kg of diet on BW gain by 43% but did not significantly

diminish the toxic effects of 8 mg T-2 toxin/kg of diet. The decreased efficiency of feed utilization and the increased relative organ weights caused by AF were significantly diminished to differing degrees by the sorbent. Oral lesions caused by T-2 toxin were not affected by the sorbent. In Experiment 2, the sorbent was added at 0.80% to a diet containing 8 mg T-2 toxin/kg of diet. The sorbent did not diminish the toxic effects of T-2 toxin when added at 0.80% of the diet. These data demonstrate that this specific sorbent can provide protection against the toxicity of AF, but not T-2 toxin, in young broiler chicks.

(Key words: aflatoxin, T-2 toxin, sorbent, toxicity, broiler) 1998 Poultry Science 77:1502–1509

INTRODUCTION Aflatoxins (AF), a group of extremely toxic chemicals, are produced by certain species of fungi in the genus Aspergillus and have been detected as contaminants of crops before harvest, between harvest and drying, in storage, and after processing and manufacturing (Council for Agricultural Science and Technology, 1989). Aflatoxins cause severe economic losses in the poultry and livestock industries. In many cases, AF contamination may mean the difference between profit and loss to the poultry industry (Jones et al., 1982; Nichols, 1983; Hamilton, 1984). Experimentally induced toxicity in young growing chickens has been well documented, as indicated by Huff et al. (1988). The T-2 toxin is a naturally occurring mycotoxin produced by several species of fungi in the genus Fusarium (Bamburg et al., 1970) that are found in many cereals, feeds, and vegetables. The T-2 toxin causes

Received for publication October 14, 1997. Accepted for publication May 7, 1998. 1Mention of a trademark, proprietary product, or specific equipment does not constitute a warranty by the USDA and does not imply its approval to the exclusion of other products that may be suitable. 2To whom correspondence should be addressed: [email protected]

reductions in weight gain and feed consumption and severe oral lesions in chickens (Wyatt et al., 1972, 1973b; Chi et al., 1977; Chi and Mirocha, 1978; Hoerr et al., 1981a,b, 1982a,b; Huff et al., 1988; Kubena et al., 1989a,b, 1990a, 1994), abnormal behavior (Wyatt et al., 1973a), altered feathering (Wyatt et al., 1975), and a coagulopathy (Doerr et al., 1981). Methods to detoxify mycotoxin-containing feedstuffs on a large scale and in a cost-effective manner are not currently available. Numerous strategies, such as physical separation, thermal inactivation, irradiation, microbial degradation, and treatment with a variety of chemicals, have been used for the detoxification or inactivation of mycotoxin-contaminated feedstuffs (Goldblatt, 1971; Goldblatt and Dollear, 1979; Anderson, 1983). Many of the techniques are impractical, ineffective, or potentially unsafe. An additional approach to the detoxification of AF is the use of inorganic sorptive materials in the diet to reduce AF absorption from the gastrointestinal tract. Dalvi and Ademoyero (1984) and Dalvi and McGown (1984) reported a trend toward improvement in feed consumption and weight gain

Abbreviation Key: AF = aflatoxin; HSCAS = hydrated sodium calcium aluminosilicate.

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when activated charcoal was added to poultry diets containing AF. Kubena et al. (1990b) and Edrington et al. (1996) observed no improvement in performance from the dietary addition of charcoal when growing broilers or turkey poults were fed diets containing AF. Dietary additions of zeolite (Smith, 1980), bentonite (Carson, 1982), or spent bleaching clay from canola oil refining (Smith, 1984) have been reported to diminish the effects of T-2 toxin and zearalenone in rats. Clays and zeolitic materials are a complex and widely diverse family of aluminosilicates with a variety of functional properties. Some aluminosilicates bind aflatoxin B1 (AFB1) in vitro to varying degrees and form complexes of varying strengths with AFB1. One compound, a specific hydrated sodium calcium aluminosilicate (HSCAS) (NovaSil),3 formed a more stable complex with AFB1 than many of the other compounds evaluated in vitro (Phillips et al., 1988) and was selected for extensive in vivo experimental evaluation. The HSCAS at a concentration of 0.5 to 2.0% of the diet significantly diminished many of the adverse effects caused by AFB1 or AF in chickens (Kubena et al., 1987, 1990a,b, 1992, 1993; Phillips et al., 1988; Huff et al., 1992), in turkeys (Kubena et al., 1991), in swine (Colvin et al., 1989; Harvey et al., 1989), and in lambs (Harvey et al., 1991), and reduced the concentration of aflatoxin M1 in the milk of lactating dairy cows (Harvey et al., 1991) and lactating dairy goats (Smith et al., 1994). Several other adsorbent materials showed protection against the toxicity of AF ranging from 0 to 75% in chickens (Kubena et al., 1992, 1993; Harvey et al., 1993) and in swine (Harvey et al., 1994). None of the sorbents evaluated in vivo have shown protection against T-2 toxin, diacetoxyscirpenol, or ochratoxin A (Kubena et al., 1990a,b, 1993; Huff et al., 1992). The purpose of the present research was to evaluate the efficacy of an adsorbent (T-Bind)4 for reducing the toxicity of AF and T-2 toxin in young growing broiler chicks.

MATERIALS AND METHODS Day-old male broiler chicks were obtained from a commercial hatchery and individually weighed and wing-banded. The chicks were maintained in electrically heated batteries under continuous fluorescent lighting with feed and water provided for ad libitum consumption. The experimental design for Experiment 1 consisted of nine dietary treatments: 1) Control with 0 mg AF, 0 mg T-2 toxin, 0% adsorbent; 2) 0.250% adsorbent; 3) 0.375% adsorbent; 4) 5.0 mg AF/kg of diet; 5) 8.0 mg T-2 toxin/kg of diet; 6) 5.0 mg AF/kg of diet plus

3Engelhard Corp., Beachwood, OH 44122. 4Biotech Development Co., Atlanta, GA 30338. 5Kindly provided by G. H. Rottinghaus, Veterinary

Medical Diagnostic Laboratory, College of Veterinary Medicine, University of Missouri, Columbia, MO 65202. 6Coulter Electronics, Hialeah, FL 33012.

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0.250% adsorbent; 7) 5.0 mg AF/kg of diet plus 0.375% adsorbent; 8) 8.0 mg T-2 toxin/kg of diet plus 0.250% adsorbent; 9) 8.0 mg T-2 toxin/kg of diet plus 0.375% adsorbent. There were six replicates of six broilers per dietary treatment and the chicks were maintained on these treatments to 3 wk of age. The chicks were fed a basal commercial corn-soybean meal-based diet (without added antibiotics, coccidiostats, or growth promoters) that contained or exceeded the levels of nutrients recommended by the National Research Council (1994). The AF for the experiments was produced through the fermentation of rice by Aspergillus parasiticus NRRL 2999 by methods previously described by Kubena et al., (1990a). The AF content was measured by spectrophotometric analysis (Nabney and Nesbith, 1965), as modified by Wiseman et al. (1967). The AF within the rice powder consisted of approximately 79% AFB1, 16% AFG1, 4% AFB2, and 1% AFG2. The rice powder was incorporated into the basal diet to provide the desired level of 5.0 mg AF/kg of diet. Through nuclear magnetic resonance and mass spectrometry, the T-2 toxin5 was determined to be greater than 99% pure. The T-2 toxin was incorporated into the diet by dissolving the toxin in 95% ethanol and then mixing the appropriate quantities with 1 kg of the diet. After drying, the dissolved toxin was mixed with the basal diet to produce the treatments containing T-2 toxin. The basal diet was analyzed for mycotoxins and was found to be below detection limits for AF, deoxynivalenol, zearalenone, ochratoxin, and cyclopiazonic acid as established by the methods described by Clement and Phillips (1985). Broilers were weighed individually on a weekly basis, feed consumption was recorded weekly, and mortality was recorded as it occurred. When the chicks reached 3 wk of age, the feeding trial was terminated and 12 broilers (6 replicates of 2 chicks each) from each treatment were bled by cardiac puncture for serum biochemical analyses. Eight blood samples from these same chicks from each treatment were used for hematological determinations. Twelve broilers (two chicks from each replicate) were killed by cervical dislocation and the liver, kidney, heart, spleen, pancreas, proventriculus, gizzard, and bursa of Fabricius were removed and weighed. At the termination of the study, all chicks in the control group, 0.375% adsorbent group, and all groups fed diets containing T-2 toxin were visually scored for oral lesions (using a four-point scoring system ranging from 1 to 4) by the same individual without knowledge as to treatment groups. A lesion score of 1 indicated no visible lesions; a lesion score of 2 was seen as one or two mouth lesions clearly visible on either the lower or upper mandible; a lesion score of 4 was seen as large lesions occurring at several sites within the mouth, principally on the upper and lower mandibles, the corners of the mouth, and the back of the tongue; lesions scored as 3 were intermediate in appearance to lesions scored 2 or 4. Hemoglobin was measured as cyanmethemoglobin.6 Erythrocyte count, mean corpuscular volume, and

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TABLE 1. Effects of a hydrated sodium calcium aluminosilicate (T-Bind) on BW gains, efficiency of feed utilization, mortality, and oral lesions of broiler chicks fed diets containing no detectable mycotoxins, 5.0 mg aflatoxin (AF)/kg, or 8 mg T-2 toxin (T-2)/kg, Experiment 11 Treatment

BW gain

T-Bind

AF

(%) 0 0.25 0.375 0 0 0.25 0.375 0.25 0.375

(mg/kg) 0 0 0 0 0 0 5.0 0 0 8.0 5.0 0 5.0 0 0 8.0 0 8.0 LSD3

T-2

1 to 7 d

8 to 14 d

15 to 21 d

1 to 21 d

102a 97ab 102a 95ab 88b 96ab 99a 87b 88b 10

225ab 225ab 236a 167d 190c 195c 207bc 197c 195c 21

(g) 373a 365a 385a 249c 302b 293b 290b 307b 311b 37

699a 699a 723a 513c 580b 592b 593b 592b 594b 58

Change from control

Consumption Feed:gain per bird

Mortality

Oral lesion scores2

(%) 0 –2 +3 –26 –17 –15 –15 –15 –15

(g) 1,072a 1,005ab 1,055a 827d 956bc 902cd 905bcd 926bcd 921bcd 91

(%) 0b 0b 8ab 14a 0b 8ab 8ab 0b 0b 10

1.00b . . . 1.00b . . . 1.96a . . . . . . 1.92a 2.04a .2

(g:g) 1.53bc 1.44c 1.52bc 1.78a 1.68ab 1.55bc 1.49c 1.57bc 1.55bc 0.16

a–cMeans

within a column with no common superscript differ significantly (P < 0.05). represent the x of six groups of six broilers each per treatment minus mortality. 2Visually scored for oral lesions by the same individual (1 = no lesion; 4 = severe lesions). 3LSD = least significant difference as determined by Fisher’s Protected LSD procedure. 1Values

hematocrit were determined with a Coulter6 Model ZBI counter equipped with a mean corpuscular volume and hematocrit computer and channelyzer. The mean corpuscular hemoglobin and mean corpuscular hemoglobin concentrations were calculated. Serum concentrations of uric acid, creatinine, urea nitrogen, glucose, inorganic P, total protein, albumin, cholesterol, and triglycerides; and activities of alkaline phosphatase, cholinesterase, lactate dehydrogenase, aspartate aminotransferase, gamma glutamyltransferase, and creatine kinase were determined on a clinical chemistry analyzer7 according to the manufacturer’s recommended procedure. The experimental design for Experiment 2 consisted of four dietary treatments: 1) control with 0 mg T-2 toxin, 0% adsorbent; 2) 0.80% adsorbent; 3) 8.0 mg T-2 toxin/kg of diet; 4) 8.0 mg T-2 toxin/kg of diet plus 0.80% adsorbent. There were six replicates of six broilers per dietary treatment and the chicks were maintained on these treatments to 3 wk of age. The basal diet was of the same composition as in Experiment 1, and the adsorbent and T-2 toxin were added as in Experiment 1. The parameters measured were weekly individual body weights, pen feed consumption, and daily mortality. Data (pen means) for all response variables in each experiment were subjected to one-way ANOVA (Snedecor and Cochran, 1967) using the General Linear Models procedure in the PC-SAS Version 6.02 statistical software (SAS Institute, 1987). Variable means for treatments showing significant differences in the ANOVA were compared using the Fisher’s protected least significant difference procedure (Snedecor and Cochran, 1967). All statements of significance are based on the 0.05 level of probability.

7Gilford Impact 400E, Ciba Corning Diagnostics Corp., Gilford Systems, Oberlin, OH 44774.

RESULTS Data from Experiment 1 (Table 1) show that BW gains, feed consumption, efficiency of feed utilization, mortality, and lesion scores were not significantly influenced by the adsorbent in the absence of added toxins. When compared with controls, BW gains were reduced during the first time period (1 to 7 d) only for the chicks fed T-2 toxin with or without the adsorbent. During the second period, BW gains for the AF alone, AF plus 0.25% adsorbent, and all T-2 toxin treatments were reduced. There was no significant difference between the BW gains of the AF plus 0.375% adsorbent and controls during this time period. During the third period (15 to 21 d) and the overall experimental period (1 to 21 d) BW gains for all toxin treatments were reduced. The reduction in BW gain caused by 5.0 mg AF/kg of diet was diminished by the addition of 0.25 or 0.375% adsorbent. The addition of the adsorbent did not alter the effects caused by 8 mg T-2 toxin/kg of diet. When compared with controls, feed consumption per bird was reduced in all toxin treatments. The efficiency of feed utilization was significantly reduced in only the AF alone treatment. Mortality ranged from 0 to 14% with the chicks receiving the diet with AF alone having 14% mortality, which was significantly higher than the control treatment. All of the surviving chicks from the control, 0.375% adsorbent, and treatments containing T-2 toxin were examined for oral lesions at 3 wk of age; however, oral lesions were observed only in chicks receiving the diets containing T-2 toxin. There were no differences in lesion scores in chicks receiving T-2 toxin with or without the adsorbent. Data presented in Table 2 (Experiment 1) show the effects of dietary treatment on relative organ weights. Feeding AF alone caused significant increases in the relative weights of the liver, kidney, heart, spleen, pancreas, and proventriculus. Feeding T-2 toxin with or

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TABLE 2. Effects of a hydrated sodium calcium aluminosilicate (T-Bind) on relative organ weights of broiler chicks fed diets containing no detectable mycotoxins, 5.0 mg aflatoxin (AF)/kg, or 8 mg T-2 toxin (T-2)/kg, Experiment 1 at 21 d1 Treatment T-Bind (%) 0 0.25 0.375 0 0 0.25 0.375 0.25 0.375

AF

T-2

Liver

Kidney

Heart

0 0 0 0 8.0 0 0 8.0 8.0

3.28cd 3.39cd 3.06d 4.71a 3.52cd 4.41ab 3.85bc 3.30cd 3.46cd 0.58

0.48c 0.52c 0.48c 0.92a 0.52c 0.79ab 0.69b 0.48c 0.52c 0.14

0.76b 0.75b 0.75b 0.94a 0.76b 0.83ab 0.82ab 0.80b 0.76b 0.12

(mg/kg) 0 0 0 5.0 0 5.0 5.0 0 0 LSD2

Spleen (g/100 g BW) 0.112bcd 0.124abcd 0.106cd 0.155a 0.085d 0.149ab 0.133abc 0.092cd 0.088d 0.037

Pancreas

Proventriculus

0.37bc 0.37bc 0.33c 0.47a 0.34c 0.41b 0.37bc 0.38bc 0.35c 0.046

0.68b 0.66b 0.65b 0.87a 0.66b 0.74b 0.69b 0.68b 0.65b 0.10

a–dMeans

within a column with no common superscripts differ significantly (P < 0.05). represent the x of six groups of two broilers each per treatment. 2LSD = least significant difference as determined by Fisher’s Protected LSD procedure. 1Values

without the adsorbent did not alter relative organ weights. Addition of the adsorbent to the diet containing AF alleviated or significantly diminished the effects of AF on the relative weights of all organs (Table 2). None of the treatments altered the relative weights of the gizzard or bursa of Fabricius (data not shown). Data in Table 3 (Experiment 1) show that serum concentrations of total protein, albumin, cholesterol, and calcium were reduced and serum concentration of urea nitrogen and activity of creatine kinase were increased in chicks fed AF alone. Chicks fed the diet containing T2 toxin plus 0.25% adsorbent had a reduced serum concentration of total protein, when compared with controls. The adverse effects of AF on serum concentrations of albumin and cholesterol and the activity of creatine kinase were reduced by the addition of the adsorbent at 0.375% and also by 0.25% in the case of albumin.

The results of Experiment 2 are presented in Table 4. Beginning with the first period (1 to 7 d) and continuing for the remainder of the experiment, BW gain was significantly reduced in chicks fed the diets containing 8 mg T-2 toxin/kg of diet. The addition of the adsorbent at 0.80% did not protect against the toxicity of T-2 toxin. Feed consumption per bird was significantly reduced in the two T-2 toxin treatments. When compared with controls, efficiency of feed utilization was significantly decreased in those birds receiving T-2 toxin alone.

DISCUSSION Aflatoxin and T-2 toxin are important to the poultry industry because of their toxicity and frequency of occurrence in feedstuffs. The toxicity of AF in poultry has been well documented, as indicated by Huff et al. (1988). Although not as extensively studied as AF, the

TABLE 3. Effects of a hydrated sodium calcium aluminosilicate (T-Bind) on serum biochemical values and enzyme activities of broiler chicks fed diets containing no detectable mycotoxins, 5.0 mg aflatoxin (AF)/kg, or 8 mg T-2 toxin (T-2)/kg, Experiment 1 at 21 d1 Treatment T-Bind (%) 0 0.25 0.375 0 0 0.25 0.375 0.25 0.375 a–dMeans

AF

T-2

Total protein

(mg/kg) 0 0 0 5.0 0 5.0 5.0 0 0 LSD2

0 0 0 0 8.0 0 0 8.0 8.0

3.10a 2.47ab 2.38ab 1.90b 2.43ab 2.18b 1.83b 2.22b 2.38ab 0.74

Albumin (g/dL) 1.15ab 1.22a 1.27a 0.53d 1.02b 0.68c 0.78c 1.10ab 1.10ab 0.14

Urea nitrogen

Cholesterol

Calcium

Creatine kinase

0.86b 1.12ab 1.04ab 1.48a 0.83b 1.52a 1.28ab 1.19ab 0.98ab 0.53

(mg/dL) 161a 159a 160a 69c 146a 92bc 113b 152a 146a 29

10.00a 9.70a 10.14a 8.55c 9.46ab 8.90bc 8.79bc 9.98a 9.97a 0.69

(IU) 984c 944c 1,117c 3,102a 879c 2,493ab 1,547bc 785c 957c 1,262

within a column with no common superscript differ significantly (P < 0.05). represent the x of six groups of two broilers each per treatment. 2LSD = least significant difference as determined by Fisher’s Protected LSD procedure. 1Values

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KUBENA ET AL. TABLE 4. Effects of a hydrated sodium calcium aluminosilicate (T-Bind) on BW gain and efficiency of feed utilization of broiler chicks fed diets containing no detectable mycotoxins or 8.0 mg T-2 toxin (T-2)/kg, Experiment 21

Treatment

BW gain

T-Bind

T-2

(%) 0 0.80 0 0.80

(mg/kg) 0 0 8.0 8.0 LSD

1 to 7 d

7 to 20 d

96a 101a 86b 87b 10

502a 526a 401b 408b 42

1 to 20 d

(g) 598a 627a 487b 495b 50

Change from control

Consumption per bird

Feed:gain

(%) 0 +5 –19 –17

(g) 931a 945a 819b 836b 76

(kg:kg) 1.56b 1.54b 1.69a 1.65ab 0.13

a,bMeans

within a column with no common superscript differ significantly (P < 0.05). represent the x of six broilers each per treatment. 2LSD = least significant difference as determined by Fisher’s Protected LSD procedure. 1Values

toxicity of T-2 toxin in poultry has been well documented, as indicated by Kubena et al. (1997a). The addition of the adsorbent (T-Bind) at 0.25, 0.375, or 0.80%, in the absence of added mycotoxins, did not alter the performance of the chicks. In Experiment 1, the addition of 5.0 mg AF/kg or 8.0 mg T-2 toxin/kg of diet significantly reduced BW gain by 26 and 17%, respectively. The addition of 0.25 or 0.375% adsorbent resulted in a 15% reduction in BW gain in chicks fed the AF diet, representing a protective effect of approximately 43%. These data agree with previous results on the protective effects of an HSCAS compound (Nova Sil) on body weights in chickens (Kubena et al., 1987, 1990 a,b, 1993, 1994; Phillips et al., 1988; Huff et al., 1992; Abo-Norag et al., 1995) in turkeys (Kubena et al., 1992), in swine (Colvin et al., 1989; Harvey et al., 1989), and in lambs (Harvey et al., 1991). Previous studies in lactating dairy cows (Harvey et al., 1991) and lactating dairy goats (Smith et al., 1994) also mirror the effects reported here. Several other adsorbents showed protection against the toxicity of AF in chickens (Kubena et al., 1992, 1993; Harvey et al., 1993) and in swine (Harvey et al., 1994). The addition of the adsorbent at 0.25 or 0.375% resulted in no significant protection against the toxicity of T-2 toxin. The lack of protection against the toxicity of T-2 toxin agrees with previous work where no protection in vivo was observed against T-2 toxin, diacetoxyscirpenol, or ochratoxin A with several adsorbents (Kubena et al., 1990a,b, 1992, 1993; Huff et al., 1992). Feed consumption was reduced in all treatments receiving diets containing toxins; however, the efficiency of feed utilization was adversely affected in only the AF alone treatment. When compared with controls, mortality was significantly increased only in chicks receiving the diet with AF alone. Oral lesions were observed in only chicks receiving diets containing T-2 toxin and the incidence and severity did not differ with the addition of the adsorbent. The liver is considered to be the principal target organ for aflatoxicosis; and in poultry, the relative weight of the liver is increased more than that of any other organ by lower concentrations of AF (Smith and Hamilton, 1970; Huff et al., 1986). The present data

indicate that the relative weights of the liver were significantly increased in chicks fed diets containing AF alone and AF plus 0.25% adsorbent. There was significant protection against this adverse effect by 0.375% adsorbent. These data show the protective effects of 0.375% adsorbent with respect to liver damage, as indicated by less liver enlargement, when 0.375% adsorbent was added to the diet containing 5 mg AF/ kg. The relative weights of the kidney were significantly increased in chicks fed the diet containing AF; however, significant protection against these increases was provided for the kidney, pancreas, and proventriculus by 0.375% adsorbent, with values in between the control and AF alone treatment. The addition of T-2 toxin to the diet did not significantly affect any of the relative organ weights. The relative weights of the bursa and gizzard were not affected by any of the dietary treatments (data not shown). Reduced serum concentrations of total protein and albumin, indicators of protein synthesis (Tung et al., 1975) and aflatoxicosis Huff et al., 1986; Kubena et al., 1992), were observed in chicks fed the diets containing AF alone. The reduced serum concentration of cholesterol by AF is most likely due to the inhibition of cholesterol biosynthesis, with liver involvement, and perhaps a shift of concentration from the blood to the liver (Kubena et al., 1993). The increased serum activity of creatine kinase most likely reflects tissue damage and leakage into the blood (Tietz, 1976; Kubena et al., 1995a,b, 1997b). The reduction in serum concentration of calcium may be a reflection of reduced feed intake. The increased concentration of blood urea nitrogen, coupled with the kidney enlargement observed, may indicate some kidney damage due to AF. The protection against changes in serum biochemical values provided by the adsorbent varied, but noteworthy were the significant improvements in serum concentrations of albumin and cholesterol and the activity of the enzyme creatine kinase. The addition of the adsorbent at 0.80% did not protect against the toxicity of 8.0 mg T-2 toxin/kg of diet, as evidenced by the lack of significant differences between the T-2 toxin alone and the T-2 toxin plus adsorbent treatments for BW gains, feed consumption per bird, or


efficiency of feed utilization. These data agree with previous research using lower concentrations of adsorbents. The present data and previous data clearly demonstrate that specific adsorbents can greatly diminish the toxicity of AF in young growing chicks. To date, none of the adsorbents evaluated have provided protection against any mycotoxins except AF. The basic mechanism for protection against the toxicity of AF appears to involve sequestration of AF in the gastrointestinal tract and chemisorption (i.e., tight binding) to the adsorbent, which reduces the bioavailability of AF (Davidson et al., 1987; Phillips et al., 1990a). More specifically, a proposed mechanism of AF chemisorption by the adsorbent (HSCAS) is the formation of a complex by the Bcarbonyl system of the AF with uncoordinated “edge site” aluminum ions in HSCAS (Phillips et al., 1990b; Sarr et al., 1990). The research to date indicates that adsorbent compounds, when used in conjunction with other sound mycotoxin management practices, may prove to be another tool for the development of an integrated approach to the preventive management of AF-contaminated feedstuffs in poultry.

ACKNOWLEDGMENTS The authors gratefully acknowledge the excellent technical assistance of Maurice Connell, Laura Ripley, Albert Blanks, and Johel Bielke.

REFERENCES Abo-Norag, M., T. S. Edrington, L. F. Kubena, R. B. Harvey, and T. D. Phillips, 1995. Influence of a hydrated calcium aluminosilicate and virginiamycin on aflatoxicosis in broiler chicks. Poultry Sci. 74:626–632. Anderson, R. A., 1983. Detoxification of aflatoxin-contaminated corn. Pages 87–90 in: Aflatoxin and Aspergillus flavus in Corn. U. Diener, R. Asquith, and J. Dickens, ed. Southern Coop. Ser., Bull. 279, Auburn University, Auburn, AL. Bamburg, J. R., F. M. Strong, and E. B. Smalley, 1970. Toxins from moldy feed cereals. J. Agric. Food Chem. 17:443–450. Carson, M. S., 1982. The Effect of Dietary Fiber and Nonnutritive Mineral Additives on T-2 Toxicosis in Rats. M. S. thesis, University of Guelph, Guelph, ON, Canada. Chi, M. S., and C. J. Mirocha, 1978. Necrotic oral lesions in chickens fed diacetoxyscirpenol, T-2 toxin and crocotin. Poultry Sci. 57:807–808. Chi, M. S., C. J. Mirocha, H. J. Kurtz, G. Weaver, F. Bates, and W. Shimoda, 1977. Subacute toxicity of T-2 toxin in broiler chicks. Poultry Sci. 56:306–313. Clement, B. A., and T. D. Phillips, 1985. Advances in the detection and determination of mycotoxins via capillary GC/quadrupole mass spectrometry. Toxicologist 5(1):232. (Abstr.) Colvin, B. M., L. T. Sangster, K. D. Hayden, R. W. Bequer, and D. M. Wilson, 1989. Effect of high affinity aluminosilicate sorbent on prevention of aflatoxicosis in growing pigs. Vet. Hum. Toxicol. 31:46–48. Council for Agricultural Science and Technology, 1989. Pages 1–91 in: Mycotoxins: Economic and Health Risks. K. A.

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Nisi, ed. Council for Agricultural Science and Technology, Ames, IA. Dalvi, R. R., and A. A. Ademoyero, 1984. Toxic effects of aflatoxin B1 in chickens given feed contaminated with Aspergillus flavus and reduction of the toxicity by activated charcoal and some chemical agents. Avian Dis. 28:61–69. Dalvi, R. R., and C. McGowan, 1984. Experimental induction of chronic aflatoxicosis in chickens by purified aflatoxin B1 and its reversal by activated charcoal, phenobarbital, and reduced glutathione. Poultry Sci. 63:485–491. Davidson, J. N., J. G. Babish, K. A. Delaney, D. R. Taylor, and T. D. Phillips, 1987. Hydrated sodium calcium aluminosilicate decreases the bioavailability of aflatoxin in the chicken. Poultry Sci. 66(Suppl. 1):89.(Abstr.) Doerr, J. A., P. B. Hamilton, and H. R. Burmeister, 1981. T-2 toxicosis and blood coagulation in young chickens. Toxicol. Appl. Pharmacol. 60:157–162. Edrington, T. S., A. B. Sarr, L. F. Kubena, and T. D. Phillips, 1996. Hydrated sodium calcium aluminosilicate (HSCAS), acidic HSCAS, and activated charcoal reduce urinary excretion of Aflatoxin M1 in turkey poults. Lack of effect by hydrated charcoal on aflatoxicosis. Toxicol. Lett. 89: 15–122. Goldblatt, L. A., 1971. Control and removal of aflatoxin. J. Am. Oil Chem. Soc. 48:605–610. Goldblatt, L. A., and F. G. Dollear, 1979. Modifying mycotoxin contamination in feeds—Use of mold inhibitors, ammoniation, roasting. Pages 167–184 in: Interactions of Mycotoxins in Animal Production. National Academy of Sciences, Washington, DC. Hamilton, P. B., 1984. Determining safe levels of mycotoxins. J. Food Prot. 47(7):570–575. Harvey, R. B., L. F. Kubena, M. Y. Elissalde, D. E. Corrier, and T. D. Phillips, 1994. Comparison of two hydrated calcium aluminosilicate compounds to experimentally protect growing barrows from aflatoxicosis. J. Vet. Diagn. Invest. 6:88–92. Harvey, R. B., L. F. Kubena, T. D. Phillips, M. H. Elissalde, and W. E. Huff, 1991. Diminution of aflatoxin toxicity to growing lambs by dietary supplementation with hydrated sodium calcium aluminosilicate. Am. J. Vet. Res. 52: 152–156. Harvey, R. B., L. F. Kubena, M. H. Elissalde, and T. D. Phillips, 1993. Efficacy of zeolitic ore compounds on the toxicity of aflatoxin to growing broiler chickens. Avian Dis. 37:67–73. Harvey, R. B., L. F. Kubena, T. D. Phillips, W. E. Huff, and D. E. Corrier, 1989. Prevention of aflatoxicosis by addition of hydrated sodium calcium aluminosilicate to the diets of growing barrows. Am. J. Vet. Res. 50:416–420. Harvey, R. B., T. D. Phillips, J. A. Ellis, L. F. Kubena, W. E. Huff, and H. D. Petersen, 1991. Effects on aflatoxin M1 residues in milk by addition of hydrated sodium calcium aluminosilicate to aflatoxin-contaminated diets of dairy cows. Am. J. Vet. Res. 52:1556–1559. Hoerr, F. J., W. W. Carlton, and B. Yagen, 1981a. The toxicity of T-2 toxin and diacetoxyscirpenol in combination for broiler chickens. Food Cosmetics Toxicol. 19:185–188. Hoerr, F. J., W. W. Carlton, and B. Yagen, 1981b. Mycotoxicosis caused by single dose of T-2 toxin or diacetoxyscirpenol in broiler chickens. Vet. Pathol. 18:652–664. Hoerr, F. J., W. W. Carlton, B. Yagen, and A. Z. Joffe, 1982a. Mycotoxicosis produced in broiler chickens by multiple

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doses of either T-2 toxin or diacetoxyscirpenol. Avian Pathol. 11:269–383. Hoerr, F. J., W. W. Carlton, B. Yagen, and A. Z. Joffe, 1982b. Mycotoxicosis caused by either T-2 toxin or diacetoxyscirpenol in the diet of broiler chickens. Fundam. Appl. Toxicol. 2:121–124. Huff, W. E., R. B. Harvey, L. F. Kubena, and G. E. Rottinghaus, 1988. Toxic synergism between aflatoxin and T-2 toxin in broiler chickens. Poultry Sci. 67:1418–1423. Huff, W. E., L. F. Kubena, R. B. Harvey, D. E. Corrier, and H. H. Mollenhauer, 1986. Progression of aflatoxicosis in broiler chickens. Poultry Sci. 65:1891–1899. Huff, W. E., L. F. Kubena, R. B. Harvey, and T. D. Phillips, 1992. Efficacy of hydrated sodium calcium aluminosilicate to reduce the individual and combined toxicity of aflatoxin and ochratoxin A. Poultry Sci. 71:64–69. Jones, F. T., W. M. Hagler, and P. B. Hamilton, 1982. Association of low levels of aflatoxin in feed with productivity losses in commercial broiler operations. Poultry Sci. 61:861–868. Kubena, L. F., T. S. Edrington, R. B. Harvey, S. A. Buckley, T. D. Phillips, G. E. Rottinghaus, and H. H. Casper, 1997a. Individual and combined effects of fumonisin B1 present in Fusarium moniliforme culture material and T-2 toxin or deoxynivalenol in broiler chicks. Poultry Sci. 76:1239–1247. Kubena, L. F., T. S. Edrington, C. Kamps-Holtzapple, R. B. Harvey, M. H. Elissalde, and G. E. Rottinghaus, 1995a. Influence of fumonisin B1 present in Fusarium moniliforme culture material and T-2 toxin in turkey poults. Poultry Sci. 74:306–313. Kubena, L. F., T. S. Edrington, C. Kamps-Holtzapple, R. B. Harvey, M. H. Elissalde, and G. E. Rottinghaus, 1995b. Effects of feeding fumonisin B1 present in Fusarium moniliforme culture material and aflatoxin singly and in combination to turkey poults. Poultry Sci. 74:1295–1303. Kubena, L. F., R. B. Harvey, S. A. Buckley, T. S. Edrington, and G. E. Rottinghaus, 1997b. Individual and combined effects of moniliformin present in Fusarium fujikuroi culture material and aflatoxin in broiler chicks. Poultry Sci. 76: 265–270. Kubena, L. F., R. B. Harvey, T. D. Phillips, D. E. Corrier, and W. E. Huff, 1990b. Diminution of aflatoxicosis in growing chickens by dietary addition of a hydrated sodium calcium aluminosilicate. Poultry Sci. 69:727–735. Kubena, L. F., R. B. Harvey, T. D. Phillips, and N. D. Heidelbaugh, 1987. Novel approach to the preventive management of aflatoxins in poultry. Pages 302–304 in: Proceedings of the United States Animal Health Association, Richmond, VA. Kubena, L. F., R. B. Harvey, W. E. Huff, D. E. Corrier, T. D. Phillips, and G. E. Rottinghaus, 1989a. Influence of ochratoxin A and T-2 toxin singly and in combination on broiler chickens. Poultry Sci. 68:867–872. Kubena, L. F., R. B. Harvey, W. E. Huff, D. E. Corrier, T. D. Phillips, and G. E. Rottinghaus, 1990a. Efficacy of a hydrated sodium calcium aluminosilicate to reduce the toxicity of aflatoxin and T-2 toxin. Poultry Sci. 69: 1078–1086. Kubena, L. F., R. B. Harvey, W. E. Huff, M. H. Elissalde, A. G. Yersin, T. D. Phillips, and G. E. Rottinghaus, 1993. Efficacy of a hydrated sodium calcium aluminosilicate to reduce the toxicity of aflatoxin and diacetoxyscirpenol. Poultry Sci. 72:51–59.

Kubena, L. F., R. B. Harvey, T. D. Phillips, and B. A. Clement, 1992. The use of sorbent compounds to modify the toxic expression of mycotoxins in poultry. Pages 357–360 in: Proceedings XIX World’s Poultry Congress. Vol 1. Kubena, L. F., W. E. Huff, R. B. Harvey, T. D. Phillips, and G. E. Rottinghaus, 1989b. Individual and combined toxicity of deoxynivalenol and T-2 toxin in broiler chicks. Poultry Sci. 68:622–626. Kubena, L. F., W. E. Huff, R. B. Harvey, A. G. Yersin, M. H. Elissalde, D. A. Witzel, L. E. Giroir, T. D. Phillips, and H. D. Petersen, 1991. Effects of a hydrated sodium calcium aluminosilicate on growing turkey poults during aflatoxicosis. Poultry Sci. 70:1823–1830. Kubena, L. F., E. E. Smith, A. Gentles, R. B. Harvey, T. E. Edrington, T. D. Phillips, and G. E. Rottinghaus, 1994. Individual and combined toxicity of T-2 toxin and cyclopiazonic acid in broiler chicks. Poultry Sci. 73: 1390–1397. Nabney, J., and B. F. Nesbitt, 1965. A spectrophotometric method of determining the aflatoxins. Analyst 90:155–160. National Research Council, 1994. Nutrient Requirements of Poultry. 9th rev. ed. National Academy Press, Washington, DC. Nichols, T. E., 1983. Economic effects of aflatoxin in corn. Pages 67–71 in: Aflatoxin and Aspergillus flavus in Corn. U. Diener, R. Asquith, and J. Dickens, ed. Southern Coop. Ser. Bulletin 279. Auburn University, Auburn, AL. Phillips, T. D., B. A. Clement, L. F. Kubena, and R. B. Harvey, 1990a. Detection and detoxification of aflatoxins: Prevention of aflatoxicosis and aflatoxin residues with hydrated sodium calcium aluminosilicate. Vet. Human Toxicol. 32: 15–19. Phillips, T. D., L. F. Kubena, R. B. Harvey, D. S. Taylor, and N. D. Heidelbaugh, 1988. Hydrated sodium calcium aluminosilicate: a high affinity sorbent for aflatoxin. Poultry Sci. 67:243–247. Phillips, T. D., A. B. Sarr, B. A. Clement, L. F. Kubena, and R. B. Harvey, 1990b. Prevention of aflatoxicosis in farm animals via selective chemisorption of aflatoxin. Pages 223–237 in: Pennington Center Nutrition Series. Vol. 1, Mycotoxins, Cancer, and Health. G. A. Bray and D. H. Ryan, ed. Louisiana State University Press, Baton Rouge, LA. SAS Institute, 1987. SAS/STAT Guide for Personal Computers. 6th ed. SAS Institute, Inc., Cary, NC. Sarr, A. B., B. A. Clement, and T. D. Phillips, 1990. Effects of molecular structure on the chemisorption of aflatoxin B1 and related compounds by hydrated sodium calcium aluminosilicate. Toxicologist 10(1):163. (Abstr.) Smith, E. E., T. D. Phillips, J. A. Ellis, R. B. Harvey, L. F. Kubena, J. Thompson, and G. Newton, 1994. Hydrated sodium calcium aluminosilicate reduction of AFM1 residues in dairy goat milk. J. Anim. Sci. 72:677–682. Smith, J. W., and P. B. Hamilton, 1970. Aflatoxicosis in the broiler chicken. Poultry Sci. 49:207–215. Smith, T. K., 1980. Influence of dietary fiber, protein and zeolite on zearalenone toxicosis in rats and swine. J. Anim. Sci. 50:278–285. Smith, T. K., 1984. Spent canola oil bleaching clays: potential for treatment of T-2 toxicosis in rats and short-term inclusion in diets for immature swine. Can. J. Anim. Sci. 64:725–732.

ALUMINOSILICATE REDUCTION OF MYCOTOXIN TOXICITY Snedecor, G. W., and W. G. Cochran, 1967. Pages 258–380 in: Statistical Methods. 6th ed. The Iowa State University Press, Ames, IA. Tietz, N., 1976. Fundamentals of Clinical Chemistry. W. B. Saunders, Philadelphia, PA. Tung, H. T., R. D. Wyatt, P. Thaxton, and P. B. Hamilton, 1975. Concentrations of serum proteins during aflatoxicosis. Toxicol. Appl. Pharmacol. 34:320–326. Wiseman, H. G., W. C. Jacobson, and W. E. Harmeyer, 1967. Note on removal of pigments from chloroform extracts of aflatoxin cultures with copper carbonate. J. Assoc. Off. Agric. Chem. 50:982–983.

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Wyatt, R. D., W. M. Colwell, P. B. Hamilton, and H. R. Burmeister, 1973a. Neural disturbances in chickens caused by dietary T-2 toxin. Appl. Microbiol. 26:757–761. Wyatt, R. D., P. B. Hamilton, and H. R. Burmeister, 1973b. The effects of T-2 toxin in broiler chickens. Poultry. Sci. 52: 1853–1859. Wyatt, R. D., P. B. Hamilton, and H. R. Burmeister, 1975. Altered feathering of chicks caused by T-2 toxin. Poultry Sci. 54:1042–1045. Wyatt, R. D., B. A. Weeks, P. B. Hamilton, and H. R. Burmeister, 1972. Severe oral lesions in chickens caused by ingestion of dietary fusariotoxin T-2. Appl. Microbiol. 24: 251–257.