J. Dairy Sci. 2009. 92:3959-3963. doi:10.3168/jds.2009-2031
© 2009 American Dairy Science Association ®
Efficacy of Solis, NovasilPlus, and MTB-100 to reduce aflatoxin M1 levels in milk of early to mid lactation dairy cows fed aflatoxin B1
R. E. Kutz*,
J. D. Sampson*,
L. B. Pompeu*,
D. R. Ledoux*,1,
J. N. Spain*,
M. Vázquez-Añón
and
G. E. Rottinghaus*
* University of Missouri, Columbia 65211
Novus International, St. Charles, MO 63304
1 Corresponding author: ledouxd{at}missouri.edu
 |
ABSTRACT
|
|---|
An experiment was conducted to determine the efficacy of 3 adsorbents, Solis (SO; Novus International Inc.), NovasilPlus (NOV; Engelhard Corp.), and MTB-100 (MTB; Alltech), in reducing aflatoxin (AF) M1 concentrations in milk of dairy cows fed an AF-contaminated diet. Twelve early to mid lactation dairy cows averaging 163 d in milk were used in a 4 x 4 Latin square design with 3 replications. Cows were blocked by parity, body weight, and milk production and were provided ad libitum access to feed and water. Within each replicate, cows were randomly assigned to the 4 dietary treatments for 4 consecutive 7-d periods. Dietary treatments included AF [112 µg of AFB1/kg of diet dry matter (DM)]; AF + 0.56% SO; AF + 0.56% NOV; and AF + 0.56% MTB. Milk samples were collected on d 6 and 7 of each of the experimental periods. Feed intake, milk production, milk fat percentage, milk protein percentage, and linear somatic cell scores were not affected by dietary treatments and averaged 22.20 kg/d of DM, 33.87 kg/d, 3.78%, 2.95%, and 1.60, respectively, across all treatments. Transfer rates of AF from feed to milk averaged 2.65, 1.48, 1.42, and 2.52% for cows fed AF, AF + SO, AF + NOV, and AF + MTB, respectively. Daily AFM1 excretion in milk averaged 66, 37, 35, and 63 µg/d for cows fed AF, AF + SO, AF + NOV, and AF + MTB, respectively. The addition of SO and NOV to the AF diet resulted in a significant reduction in milk AFM1 concentrations (SO, 45%; NOV, 48%) and AFM1 excretion (SO, 44%; NOV, 46%). In contrast, MTB was not effective in reducing milk AFM1 concentrations (4%), AFM1 excretion (5%), or AF transfer from feed to milk (2.52%). Results indicated that SO and NOV at 0.56% of the diet were effective in reducing milk AFM1 concentrations in cows consuming a total mixed ration containing 112 µg of AFB1/kg of diet DM.
Key Words: aflatoxin B1 • aflatoxin M1 • lactating dairy cow • adsorbent
|
INTRODUCTION
|
|---|
Aflatoxins (AF), a class of mycotoxins produced by fungal species of the genus Aspergillus (flavus and parasiticus), are sometimes found in feed ingredients used in dairy rations. Major forms of aflatoxins include AFB1, AFB2, AFG1, and AFG2, with AFB1 being the most common and biologically active component (Busby and Wogan, 1981). In general, dietary concentrations of AF found in dairy rations are not usually high enough to cause reductions in feed intake and milk production. However, at these lower dietary AF concentrations AFM1, a metabolite of AFB1, is secreted into the milk. Aflatoxin M1 is toxic and carcinogenic, and is of great concern with respect to human health because of the high consumption of milk and milk products by humans, especially children. Because of this concern, the AFM1 level in milk is regulated by the US Food and Drug Administration at a maximum of 0.5 µg/L.
Measures used by the livestock industry to protect animals from the toxic effects of AF include grain testing (Stoloff and Scott, 1984), use of mold inhibitors (Hamilton, 1985), fermentation (Dam et al., 1977), microbial inactivation (Ciegler et al., 1966), physical separation (Huff, 1980), thermal inactivation (Conway et al., 1978), irradiation (Shantha and Sreenivasa, 1977), ammoniation (Brekke et al., 1977, 1979), ozonation (McKenzie et al., 1997, 1998), and the use of adsorbents (Masimanco et al., 1973; Phillips et al., 1990a,b). Unfortunately, most of these measures are costly, time consuming, and only partially effective. At present, one of the more effective and practical approaches is the use of adsorbents. Selected adsorbents added to AF-contaminated feeds can sequester AF during the digestive process, allowing AF to pass harmlessly through the animal (Davidson et al., 1987; Phillips et al., 1990a,b). Major advantages of these adsorbents are that they are relatively inexpensive, generally recognized as safe (GRAS), and can be easily added to animal feeds. However, not all adsorbents are equally effective at sequestering AF (Stroud, 2006). An experimental lactating dairy cow model has been developed (Diaz et al., 2004; Stroud, 2006) to evaluate the effectiveness of different adsorbents at reducing AFM1 levels in milk. Using this model, we hypothesized that different sources of adsorbents would differ in their effectiveness to sequester AF in feed and, consequently, to reduce AFM1 in milk. It should be noted that none of these products have been approved for commercial use by FDA. The objective of this study was to determine the efficacy of 3 adsorbents, Solis (Novus International Inc., St. Charles, MO), NovasilPlus (Engelhard Corp., Cleveland, OH), and MTB-100 (Alltech Inc., Nicholasville, KY), to reduce the levels of AFM1 in the milk of early to mid lactating dairy cows fed AF.
|
MATERIALS AND METHODS
|
|---|
Experimental Procedures
Twelve early to mid lactation dairy cows averaging 651 ± 62 kg of BW and 163 ± 54 DIM were transported from the University of Missouri Dairy Research Center and housed in Unit C of the Animal Sciences Research Center. Cows were provided ad libitum access to feed and water. During the study, all cows were treated with Posilac (recombinant bST, Elanco Animal Health, Indianapolis, IN) every 2 wk according to the manufacturer’s recommendations. The experimental design consisted of a 4 x 4 Latin square replicated 3 times. Cows were blocked by parity, BW, and milk production. Each block was housed in a separate environmentally controlled room. Cows were assigned to a randomized schedule to receive each of the 4 dietary treatments during 4 consecutive 7-d periods.
The dietary treatments were formulated to include: A) 100 µg of AFB1/kg of diet DM; B) 100 µg of AFB1/kg of diet DM + 0.5% Solis; C) 100 µg of AFB1/kg of diet DM + 0.5% NovasilPlus; and D) 100 µg of AFB1/kg of diet DM + 0.5% MTB-100. Both NovasilPlus and Solis are classified as hydrated sodium calcium aluminosilicates (HSCAS). By contrast, MTB-100 is a commercial modified yeast cell culture preparation based on a Saccharomyces cerevisiae strain 1026, with HSCAS as one of the stated ingredients on the label.
Each period of the Latin square lasted 7 d, with milk samples collected on d 6 and 7 for analysis of milk AFM1 concentrations. Dietary AFB1 was supplied by Aspergillus parasiticus (NRRL-2999) culture material containing 760 mg/kg of AFB1, 28 mg/kg of AFB2, 440 mg/kg of AFG1, and 13 mg/kg of AFG2. The TMR fed to all cows in the study consisted of corn silage, alfalfa silage, alfalfa hay, ground corn, soybean meal, whole cottonseed, wet brewers grain, roasted soybeans, brome hay, soyhulls, and mineral and vitamin premixes. The diet was formulated to meet the nutrient requirements of a second-lactation Holstein producing 41 kg/d of milk containing 3.8% milk fat, as defined by NRC (2001; Table 1).
It was estimated that cows would consume an average of 25 kg of DM each day, resulting in a daily intake of 2,500 µg of AFB1 (25 kg of DM x 100 µg of AFB1/kg) and a daily intake of 125 g (25 kg of DM x 0.5%) of adsorbent. Cows were fed the TMR in 3 equal aliquots daily (0700, 1200, and 1900 h). The daily dose of AFB1 was divided into 3 aliquots, and each aliquot was mixed with 99 g of grain containing molasses to encourage consumption. The daily dose of adsorbents was also divided into 3 aliquots and each aliquot was mixed with 258 g of TMR. At each feeding period, cows were first fed the aliquots of AFB1 in the grain mix, followed by the aliquots of adsorbent and TMR. After the cows consumed the AFB1 + grain mix and the adsorbents + TMR mix (10 to 15 min), they were then fed one-third of their daily aliquot of TMR. This feeding regimen ensured that each cow consumed the allotted amounts of AFB1 and adsorbent, and prevented AFB1 contamination of TMR mixing facilities.
Analytical Procedures
A bronopol preservative (Broad Spectrum Microtabs II, D and F Control Systems Inc., Dublin, CA) was added to each milk sample and samples were sent to the Missouri DHIA laboratory (Springfield, MO) for analysis of milk components. Milk samples were collected on d 6 and 7 of each of the 4 experimental periods. On each of the 2 d, milk samples from the a.m. and p.m. milking were composited and frozen until analyzed. Milk samples were thawed and centrifuged at 1,875 x g, and as much fat as possible was removed. The milk filtrates (25 mL) were then passed through AFLAPREP M immunoaffinity cleanup columns (R-Biopharm Rhone Ltd., Glasgow, Scotland). Columns were washed twice with 10 mL of PBS, and AFM1 was then eluted from the columns with 1.5 mL of acetonitrile, followed by 1.5 mL of water. These were combined, placed in autosample vials, and analyzed by HPLC with fluorescence detection. The HPLC system consisted of a Hitachi Model L-7100 pump with a Hitachi Model L-7485 fluorescence detector (365 nm excitation and 440 nm emission), a Hitachi Model L-7200 autosampler with Hitachi D-7000 data acquisition interface, and Concert Chrom software on a microcomputer. The HPLC column was a 150 x 4.6 mm reversed-phase HyperClone 3-µm C18 BDS column (Phenomenex) with a C18 SecurityGuard precolumn (Phenomenex). The mobile phase was acetonitrile:methanol:water (15:15:70) and run at 1 mL/min. The injection volume was 50 µL for all standards and samples. The detection limit was set at 40 ng/kg of AFM1.
Statistical Procedures
Data were analyzed by ANOVA using the MIXED procedure (SAS Institute, 2003) as a replicated Latin square split plot in time (repeated-measures ANOVA), with cow as the experimental unit (Littell et al., 1998). The linear statistical model contained the effects of cow, period, treatment, cow (period treatment), time, and time interaction of treatment x time. Cow (period treatment) was used as the denominator of F to test the main-plot effect. The residual mean was used as a denominator of F to test the day and the treatment x day interaction. Mean differences were tested using Fisher’s least significant difference. All statements of significance are based on the 0.05 level of probability.
|
RESULTS AND DISCUSSION
|
|---|
It was estimated that cows would consume an average of 25 kg of DM each day, resulting in a daily intake of 2,500 µg of AFB1 (25 kg of DM x 100 µg of AFB1/kg), and a daily intake of 125 g (25 kg of DM x 0.5%) of adsorbent. However, daily DM feed intake averaged only 22.29 kg/cow, which resulted in a daily intake of 2,500 µg of AFB1 but a dietary concentration of 112.2 µg of AFB1/kg of DM. Similarly, the dietary concentration of the adsorbents changed from 0.5 to 0.56%.
With the exception of 1 cow that developed mastitis, cows did not behave abnormally and had no clinical signs associated with aflatoxicosis. Feed intake and milk production were not affected by dietary treatments (P > 0.05) and averaged 22.29 kg and 33.87 kg/d (Tables 2 and 3), respectively, across all treatments. Milk composition (Table 2) was also not affected (P > 0.05) by dietary treatments, with fat percentage, protein percentage, and linear SCS averaging 3.78%, 2.95%, and 1.60, respectively, across all treatments.
View this table:
[in this window]
[in a new window]
|
Table 2. Effects of dietary treatments on milk production and composition of dairy cows fed 112 µg of aflatoxin B1 (AFB1)/kg of DM1
|
|
View this table:
[in this window]
[in a new window]
|
Table 3. Efficacy of adsorbents in reducing aflatoxin M1 (AFM1) residues in milk of dairy cows fed 112 µg of AFB1/kg of DMI1
|
|
Effects of dietary treatments on AFM1 residues in milk are summarized in Table 3. Aflatoxin M1 concentrations for the control (no adsorbent), Solis, NovasilPlus, and MTB-100 treatments averaged 1.92, 1.06, 1.00, and 1.84 µg/kg, respectively. Compared with the AF-only diet, AFM1 concentrations in milk were reduced (P < 0.0001) by the addition of Solis and NovasilPlus. The addition of MTB-100 to the AF diet was not effective in reducing milk AFM1 concentrations (P > 0.05).
Aflatoxin M1 excretion via milk, as calculated from milk AFMI concentration and total milk volume produced (concentration of AFM1 in milk x amount of milk produced), was 66.21, 36.99, 35.47, and 62.98 µg/d for the control (no adsorbent), Solis, NovasilPlus, and MTB-100 treatments, respectively (Table 3). Compared with the AF-only diet, AFM1 excretion in milk was reduced (P < 0.0001) by the addition of Solis and NovasilPlus. The addition of MTB-100 to the AF diet was not effective (P > 0.05) in reducing AFM1 excretion in milk.
Transfer of AF from feed to milk, as calculated from AF intake and total milk volume [(excretion of AFM1/AFB1 consumption) x 100] averaged 2.65, 1.48, 1.42, and 2.52% for the control (no adsorbent), Solis, NovasilPlus, and MTB-100 treatments, respectively (Table 3). Compared with the AF-only diet, AFM1 transfer from feed to milk was reduced (P < 0.0001) by the addition of Solis and NovasilPlus. The addition of MTB-100 to the AF diet was not effective (P > 0.05) in reducing AF transfer from feed into milk.
Milk AFM1 concentrations ranged from 1.00 to 1.92 µg/L, and transfer rates of AF from feed to milk ranged from 1.42 to 2.65%. Transfer rates observed in the current study are consistent with previous reports for dairy cows indicating AF transference rates ranging from 0.25 to 4.8% (Applebaum et al., 1982; Price et al., 1985; Frobish et al., 1986; Harvey et al., 1991; Veldman et al., 1992; Stroud, 2006).
The addition of NovasilPlus (0.56%) to the AF diet resulted in a 48% reduction in milk AFM1 concentrations, a 46% reduction in AF excretion, and a 47% reduction in AF transfer from feed to milk. Similar reductions in milk AFM1 concentrations, AF excretion, and AF transfer in response to supplemental NovasilPlus have been reported previously. Harvey et al. (1991) reported a 44% reduction in milk AFM1 concentrations of dairy cows fed 100 µg of AF/kg of feed and 1% NovasilPlus. More recently, Stroud (2006) reported a 40% reduction in milk AFM1 concentrations, a 43% reduction in AF excretion, and a 42% reduction in AF transfer from feed to milk in dairy cows fed 170 µg of AFB1/kg of feed and 0.5% NovasilPlus. Results of the current study with respect to NovasilPlus are consistent with previous reports on the efficacy of this product in reducing AFM1 levels in milk of cows fed AF.
Results of the current study indicate that Solis at 0.56% of the diet was just as effective as 0.56% NovasilPlus in reducing milk AFM1 concentrations (45 vs. 48%), AF excretion (44 vs. 46%), and AF transfer (44 vs. 47%) from feed to milk. The effectiveness of Solis has also been observed in growing broilers exposed to feed contaminated with AF (Shirley et al., 2008). However, this is the first report demonstrating the effectiveness of Solis in early to midlactating dairy cows. In contrast, MTB-100 (0.56%) was not effective in reducing AFM1 concentrations (4%), AF excretion (5%), or AF transfer (5%) from feed to milk. Stroud (2006) also reported that MTB-100 at 0.5% of a diet containing 170 µg of AFB1/kg of feed was not effective in reducing milk AFM1 concentrations (–8%), AF excretion (–7%), or AF transfer (–4%) from feed to milk. Results of these 2 studies with MTB-100 are in contrast to a previous study (Diaz et al., 2004) in which MTB-100 at 0.05% of a diet containing 55 µg of AFB1/kg was reported to reduce milk AFM1 concentrations by 59%. The lower dietary concentration of AFB1 (55 µg/kg of AFB1) used in the study by Diaz et al. (2004) compared with that used in the current study (112 µg/kg of AFB1) and in the study by Stroud (2006; 170 µg/kg of AFB1) may have contributed to the observed differences among the studies.
The differences in milk AFM1 reduction among the products tested might be due to their composition and mechanism of action of the active compounds. Solis and NovasilPlus are sources of HSCAS, whereas MTB-100 contains a modified yeast cell culture with some amount of HSCAS. Initially, Phillips et al. (1990a,b) proposed that AF was bound to HSCAS as a result of the β-carbonyl system of AF forming a complex with uncoordinated edge site aluminum ions of HSCAS. It is now postulated that the major site of chemisorption of AF to HSCAS is at the interlayer surfaces (Phillips, 1999). The dicarbonyl portion of the AF molecule was found to be essential for tight binding of the molecule by HSCAS. The interaction with HSCAS makes AF unavailable for absorption.
In contrast, the mechanism for the modified yeast product has not been well described. Yiannikouris et al. (2003, 2004) proposed it as a 2-level interaction between the glucan portion of the yeast cell wall and the mycotoxin molecule. However, Yiannikouris et al. (2003, 2004) did not evaluate binding of AF, but instead evaluated binding of zearolenone to the yeast cell wall, and only under in vitro conditions.
|
CONCLUSIONS
|
|---|
Solis and NovasilPlus at 0.56% of the diet were effective in reducing milk AFM1 concentrations in cows consuming a TMR containing 112 µg of AFB1/kg of diet DM. Under the current study conditions, MTB-100 at 0.56% was not effective in reducing milk AFM1 concentrations.
Received for publication January 13, 2009.
Accepted for publication April 25, 2009.
|
REFERENCES
|
|---|
Applebaum, R. S., Brackett, R. E., Wiseman, D. W. and Marth, E. H.. 1982. Responses of dairy cows to dietary aflatoxin: Feed intake and yield, toxin content, and quality of milk of cows treated with pure and impure aflatoxin. J. Dairy Sci. 65:1503–1508.[Abstract/Free Full Text]
Brekke, O. L., Peplinski, A. J., Nofsinger, G. W., Conway, H. F., Stringfellow, A. C., Montgomery, R. R., Silman, R. W., Sohns, V. E. and Bagley, E. B.. 1979. Aflatoxin inactivation in corn by ammonia gas: A field trial. Trans. Am. Soc. Ag. Engr. 22:425–432.
Brekke, O. L., Sinnhuber, R. O., Peplinski, A. J., Wales, J. H., Putnam, G. B., Lee, D. J. and Ciegler, A.. 1977. Aflatoxin in corn: Ammonia inactivation and bioassay with rainbow trout. Appl. Environ. Microbiol. 34:34–37.[Abstract/Free Full Text]
Busby, W. F., Jr., and G. N. Wogan. 1981. Aflatoxins. Pages 3–27 in Mycotoxins and N-nitrosocompounds: Environmental Risks. Vol. 2. R. C. Shank, ed. CRC Press Inc., Boca Raton, FL.
Ciegler, A., Lillehoj, E. B., Peterson, R. E. and Hall, H. H.. 1966. Microbial detoxification of aflatoxin. Appl. Microbiol. 14:934–939.[Medline]
Conway, H. F., Anderson, R. A. and Bagley, E. B.. 1978. Detoxification of aflatoxin-contaminated corn by roasting. Cereal Chem. 55:115–117.
Dam, R., Tam, S. W. and Satterlee, L. D.. 1977. Destruction of aflatoxins during fermentation and by-product isolation from artificially contaminated grain. Cereal Chem. 54:705–714.
Davidson, J. N., Babish, J. G., Delaney, K. A., Taylor, D. R. and Phillips, T. D.. 1987. Hydrated sodium calcium aluminosilicate decreases the bioavailability of aflatoxin in the chicken. Poult. Sci. 66:89. (Abstr.)
Diaz, D. E., Hagler, W. M., Jr., Blackwelder, J. T., Eve, J. A., Hopkins, B. A., Anderson, K. L., Jones, F. T. and Whitlow, L. W.. 2004. Aflatoxin binders II: Reduction of aflatoxin M1 in milk by sequestering agents of cows consuming aflatoxin in feed. Mycopathologia 157:233–241.[CrossRef][Medline]
Frobish, R. A., Bradley, B. D., Wagner, D. D., Long-Bradley, P. E. and Hairston, H.. 1986. Aflatoxin residues in milk of dairy cows after ingestion of naturally contaminated grain. J. Food Prot. 49:781–785.
Hamilton, P. B. 1985. Factors influencing activity of fungi and anti-fungal agents in poultry feed. Pages 207–218 in Tricothecenes and Other Mycotoxins. J. Lacey, ed. John Wiley and Sons Ltd., New York, NY.
Harvey, R. B., Phillips, T. D., Ellis, J. A., Kubena, L. F., Huff, W. E. and Petersen, H. D.. 1991. Effects of 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.[Medline]
Huff, W. E. 1980. A physical method for the segregation of aflatoxin contaminated corn. Cereal Chem. 57:236–238.
Littell, R. C., Henry, P. R. and Ammerman, C. B.. 1998. Statistical analysis of repeated measures data using SAS procedures. J. Anim. Sci. 76:1216–1231.[Abstract/Free Full Text]
Masimanco, N., Remacle, J. and Ramaut, J.. 1973. Elimination of aflatoxin B1 by absorbent clays in contaminated substrates. Ann. Nutr. Aliment. 23:137–147.
McKenzie, K. S., Kubena, L. F., Denvir, A. J., Rogers, T. D., Hitchens, G. D., Bailey, R. H., Harvey, R. B., Buckley, S. A. and Phillips, T. D.. 1998. Aflatoxicosis in turkey poults is prevented by treatment of naturally contaminated corn with ozone generated by electrolysis. Poult. Sci. 77:1094–1102.[Abstract/Free Full Text]
McKenzie, K. S., Sarr, A. B., Mayura, K., Bailey, R. H., Miller, D. R., Rogers, T. D., Norred, W. P., Voss, K. A., Plattner, R. D., Kubena, L. F. and Phillips, T. D.. 1997. Oxidative degradation and detoxification of mycotoxins using a novel source of ozone. Food Chem. Toxicol. 35:807–820.[CrossRef][Medline]
NRC. 2001. Nutrient Requirements of Dairy Cattle. 7th rev. ed. Natl. Acad. Press, Washington, DC.
Phillips, T. D. 1999. Dietary clay in the chemoprevention of aflatoxin-induced disease. Toxicol. Sci. 52(Suppl.):118–126.[Abstract]
Phillips, T. D., Clement, B. A., Kubena, L. F. and Harvey, R. B.. 1990a. Detection and detoxification of aflatoxins: Prevention of aflatoxicosis and aflatoxin residues with hydrated sodium calcium aluminosilicate. Vet. Hum. Toxicol. 32:15–19.[Medline]
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 Mycotoxins, Cancer, and Health. Pennington Center Nutrition Series. Vol. 1. G. A. Bray and D. H. Ryan, ed. Louisiana State Univ. Press, Baton Rouge.
Price, R. L., Paulson, J. H., Lough, O. G., Gingg, C. and Kurtz, A. G.. 1985. Aflatoxin conversion by dairy cattle consuming naturally-contaminated whole cottonseed. J. Food Prot. 48:11–15.
SAS Institute. 2003. SAS 9.1 for Windows. SAS Inst. Inc., Cary, NC.
Shantha, T. and Sreenivasa, M.. 1977. Photo-destruction of aflatoxin in groundnut oil. Ind. J. Technol. 15:453–454.
Shirley, R. B., F. A. Uraizee, and C. D. Knight, J. J. Dibner, D. R. Ledoux, G. E. Rottinghaus, and D. Joardar. 2008. Managing aflatoxin (AFB1) in broiler diets with dietary clay adsorbents. Page 221 in XXIII World Poult. Congr. World’s Poult. Sci. J. and World’s Poult. Sci. Assoc., Beekbergen, the Netherlands.
Stoloff, L., and P. M. Scott. 1984. Natural poisons. Pages 477–500 in Official Methods of Analysis of the Association of Official Analytical Chemists. 14th ed. S. Williams, ed. Assoc. Off. Anal. Chem., Arlington, VA.
Stroud, J. 2006. The effect of feed additives on aflatoxin in milk of dairy cows fed aflatoxin-contaminated diets. MS Thesis. North Carolina State Univ., Raleigh.
Veldman, A., Meijs, J. A. C., Borggreve, G. J. and Heeres-van der Tol, J. J.. 1992. Carry-over of aflatoxin from cows’ food to milk. Anim. Prod. 55:163–168.
Yiannikouris, A., Andre, G., Buleon, A., Jeminet, G., Canet, I., Francois, J., Bertin, G. and Jouany, J. P.. 2004. Comprehensive conformatinal study of key interactions involved in zearalenone complexation with β-D-glucan. Biomacromolecules 5:2176–2185.[CrossRef][Medline]
Yiannikouris, A., Poughon, L., Cameleyre, X., Dussap, C.-G., Francois, J., Berting, G. and Jouany, J. P.. 2003. A novel technique to evaluate interactions between Saccharomyces cerevisiae cell wall and mycotoxins: Application to zearalenone. Biotechnol. Lett. 25:783–788.[CrossRef][Medline]
TOP
ABSTRACT
INTRODUCTION
