**4. Decontamination of Aflatoxins by Yeasts**

Yeasts are non-photosynthetic organisms with a separate nucleus and complex life cycle. They are larger than bacteria, normally spherical, non-motile, and reproduce by budding. Although their main function is alcoholic fermentation, these organisms are also capable of producing enzymes and vitamins. The primary substrates for yeasts are fermentable sugars, which are mainly transformed in ethanol, carbon dioxide, and biomass under oxygen-limit‐ ed conditions. Under adequate oxygen supply, yeast produces carbon dioxide, water, and biomass [65]. *Saccharomyces cerevisiae* (SC) is the most well-known and commercially impor‐ tant species of yeast, and SC strains are widely used in the production of alcoholic drinks and in the baking industry.

As it occurs with LAB, SC cells have been studied to evaluate their ability to remove aflatox‐ ins from contaminated media. The most important results obtained until now are summar‐ ized in Table 2. Products based on SC (cell wall from baker and brewer yeasts, inactivated baker yeast, or alcohol yeast) was studied, and it was observed that in pH 3, 37 °C and 15 minutes of contact, AFB1 removal ranged from 2.5% to 49.3%, depending on the concentra‐ tion of the toxin in the medium, and on the yeast-based products used [66]. These authors also observed a decrease in toxin adsorption as the initial concentration increased, and con‐ cluded that adsorption is not a linear phenomenon. Similar results with a SC strain and AFB1 concentration ranging from 1 to 20 µg/mL was also reported [56]. At the 1 µg/mL con‐ centration, 69.1% AFB1 was removed; at 5 g/mL, removal rate was 41%; and at 20 µg/mL, 34%. *S. cerevisiae* strains were isolated from animal feed, feces and intestines, and tested for their ability to tolerate gastrointestinal conditions and remove AFB1 from a contaminated medium [67]. These researchers observed that all strains isolated were able to survive in gas‐ trointestinal conditions, and that the percentage of toxin removed ranged among SC strains (107 CFU/mL), and with AFB1 concentration used (16.4% to 82% of adsorption for 50 ng/mL AFB1; 21.3% to 48.7% for 100 ng/mL AFB1; and 20.2% to 65.5% for 500 ng/mL AFB1).

The ability of SC (0.1%, 0.2%, and 0.3%) to adsorb AFB1 in contaminated corn (150, 300, 450 and 800 µg/kg corn was analyzed [68]. The adsorption process showed an inversely propor‐ tional relationship with the concentration, that is, the greater the AFB1 concentration in the medium, the lower the efficiency of AFB1 removal by SC (16% to 66% for 800 µg/kg AFB1 vs. 40% to 93% for 150 µg/kg AFB1). The authors concluded, using densitogram analysis, that the adsorption process did not change the molecular structure of the mycotoxin, and that the decreased AFB1 adsorption rates observed as the toxin concentration increased may pos‐ sibly be caused by saturation of the adsorption sites on the SC cell. Other factors, such as length of incubation, pH, method of biomass purification, and methods of analysis, may also influence this process.

**Microorganism AF Bound**

**4. Decontamination of Aflatoxins by Yeasts**

"In vivo"

78 Aflatoxins - Recent Advances and Future Prospects

"In vitro"

"In vitro"

and in the baking industry.

formingunit.

(107

*shermanii* JS "In vivo"

*P. freudenreichii* subsp.

**(%)**

36 71 77

37 82 22

**Table 1.** Aflatoxin binding / absorption by microorganisms. Note: PBS, Phosphate-Buffered Saline; cfu, colony

Yeasts are non-photosynthetic organisms with a separate nucleus and complex life cycle. They are larger than bacteria, normally spherical, non-motile, and reproduce by budding. Although their main function is alcoholic fermentation, these organisms are also capable of producing enzymes and vitamins. The primary substrates for yeasts are fermentable sugars, which are mainly transformed in ethanol, carbon dioxide, and biomass under oxygen-limit‐ ed conditions. Under adequate oxygen supply, yeast produces carbon dioxide, water, and biomass [65]. *Saccharomyces cerevisiae* (SC) is the most well-known and commercially impor‐ tant species of yeast, and SC strains are widely used in the production of alcoholic drinks

As it occurs with LAB, SC cells have been studied to evaluate their ability to remove aflatox‐ ins from contaminated media. The most important results obtained until now are summar‐ ized in Table 2. Products based on SC (cell wall from baker and brewer yeasts, inactivated baker yeast, or alcohol yeast) was studied, and it was observed that in pH 3, 37 °C and 15 minutes of contact, AFB1 removal ranged from 2.5% to 49.3%, depending on the concentra‐ tion of the toxin in the medium, and on the yeast-based products used [66]. These authors also observed a decrease in toxin adsorption as the initial concentration increased, and con‐ cluded that adsorption is not a linear phenomenon. Similar results with a SC strain and AFB1 concentration ranging from 1 to 20 µg/mL was also reported [56]. At the 1 µg/mL con‐ centration, 69.1% AFB1 was removed; at 5 g/mL, removal rate was 41%; and at 20 µg/mL, 34%. *S. cerevisiae* strains were isolated from animal feed, feces and intestines, and tested for their ability to tolerate gastrointestinal conditions and remove AFB1 from a contaminated medium [67]. These researchers observed that all strains isolated were able to survive in gas‐ trointestinal conditions, and that the percentage of toxin removed ranged among SC strains

CFU/mL), and with AFB1 concentration used (16.4% to 82% of adsorption for 50 ng/mL

AFB1; 21.3% to 48.7% for 100 ng/mL AFB1; and 20.2% to 65.5% for 500 ng/mL AFB1).

**Conditions Ref.**

1 min, duodenum of chicks 1 h, duodenum of chicks 37 °C, 1h , pH 7.3

1 min, duodenum of chicks 1 h, duodenum of chicks 37 °C, 1h , pH 7.3

> Immobilized SC cells (ATTC 9763) was investigated for their ability to remove AFB1 from pistachio seeds, and it was observed that the amount of toxin removed was dependent on its concentration in the medium (40% and 70% of removal for concentrations of 10 ng/mL and 20 ng/mL AFB1, respectively) [69]. The authors also concluded that this ability to remove the toxin was greater in SC exponential growth phase, and that the process was a quick one, be‐ ing saturated after 3 hours of contact. Besides, the ability of SC cells to remove toxin was increased after treatment with acid (60% and 73% for 10 ng/mL and 20 ng/mL AFB1, respec‐ tively) and heat (55% and 75%, respectively). In another study, authors also concluded that the treatment of SC cells with heat at 60 °C and 120 °C, and with chloric acid (2 mol/L) in‐ creased their ability to remove AFB1 from the medium to 68.8%, 79.3%, and 72.1%, respec‐ tively, against 38.7% when viable yeast cells were used [56].

> Heat treatment may increase the permeability of the external layer of the cell wall due to the suspension of some mannanes on the cell surface, leading to increased availability of previ‐ ously hidden binding sites. Besides, countless physical-chemical changes take place on the cell wall during heat treatment, leading to more exposed binding sites. On the other hand, acid conditions may affect polysaccharides by releasing monomers, which are further frag‐ mented in aldehydes after glycosidic bonds are broken. Continuous removal of aflatoxin, even after use of acid and heat treatments, confirms that yeast cell viability is not a signifi‐ cant factor for the removal of aflatoxin from the medium [69].

> During the fermentation of broiler feed using LAB (3 strains of *Lactobacillus*) and SC strains resistant to gastric juices and bile, 55% AFB1 was removed when AFB1 concentration in the medium was 1 mg/kg, and 39% when concentration was 5 mg/kg AFB1, after 6 hours [70]. This tendency for removal was maintained as incubation continued, and after 24 hours, the amount of AFB1 removed was 73% and 53%, respectively, for the two concentrations of the toxin. The authors considered that, from a practical point of view, the most important factor was the 6-hour fermentation period, once the passage of feed through the gastrointestinal tract of broilers lasts from 4 to 8 hours. In reference [71], authors analyzed the ability of SC to remove AFB1 from a contaminated medium at different pH values (3.0, 6.0, and 8.0), and observed that the three strains analyzed showed great ability to remove the toxin (41.6% to 94.5%), and that after washing, only a small amount of AFB1 was released back into the me‐ dium. *In vitro* studies are not always good indications of the *in vivo* responses, as *in vivo*

studies are affected by physiological parameters, such as pH, peristaltic movements, and gastric and intestinal secretions.

SC cell wall is mainly made up of polysaccharides (80-90%), and its mechanical resistance is due to an inside layer composed of β-D-glucans, which are formed by a complex network of highly polymerized β-(1,3)-D-glucans, branched off as β-(1,6)-D-glucans, that have a low level of polymerization. This inside layer is firmly bound to the plasmatic membrane by lin‐ ear chains of chitin, which have a significant role in the insolubility of the overall structure and packing of the branched β-D-glucans. Both chitin chains and β-D-glucans affect the plasticity of the cell wall. The external layer of the yeast cell wall is formed by mannopro‐ teins, which have an important role in the exchanges with the external environment. This whole structure is highly dynamic and may vary according to the yeast strain, phase of the cell cycle, and culture conditions, such as pH, temperature, oxygenation rate, nature of the medium, concentration and nature of the carbon source. Thus, these differences in the com‐ position of the cell wall among yeast strains are related with their ability to bind to the my‐

Recent Trends in Microbiological Decontamination of Aflatoxins in Foodstuffs

http://dx.doi.org/10.5772/51120

81

Studies have shown that the components of SC cell wall, called oligomannanes, after esterifi‐ cation, are able to bind more than 95% AFB1 [78]. Addition of 0.05% glucomannanes in the

The possible binding mechanisms between yeast cell wall and mycotoxins were studied, and authors suggested that β-D-glucans are the components of the cell wall that are respon‐ sible for forming the complex with the toxin, and that the reticular organization of β-D-glu‐ cans and their distribution in β-(1,3)-D-glucans and β-(1,6)-D-glucans have an important role in the efficiency of the bond [77]. Besides, studies have shown that weak hydrogen and van der Waals bonds are involved in the complex chemical connection between the myco‐ toxins and β-D-glucans, a chemical interaction that is much more "adsorption" than "bond". As for AFB1, they observed that the aromatic ring, the lactone and ketone groups of the po‐ lar form of AFB1, or chemical bonds with glucose units in the single helix of the β-D-glucans,

It was demonstrated that yeast strains isolated from environments were animals are raised are able to bind to AFB1 in saline solution (PBS, pH 7) [67]. These strains presented other properties that were beneficial to the host, such as the inhibition of pathogenic bacteria. Therefore, SC strains acted both as probiotics (co-aggregation and inhibition of pathogenic

In reference [72], SC was able to reduce the deleterious effects of AFB1 in the diet of broilers and in [68] authors replicated these findings in rats. Protective effect against aflatoxins pro‐ duced by yeasts was confirmed in rats. However, when yeast cells were inactivated by heat, they were inefficient [80] but when glucomannanes extracted from the cell wall of yeasts were used, there was an increase in the efficiency of the bond with AFB1, OTA and T-2 toxin [81-84], individually or in combination [75, 79, 85, 86]. The addition of SC in the diet reduced AFB1 toxic effects in chickens [72, 87]. The ability of SC to reduce AFB1 toxic effects in quails was demonstrated, and this effect was apparently more efficient with the increase in inclu‐

cotoxin [77].

basal diet improved broiler performance [79].

are what keep the toxin bound to the glucans.

bacteria), and as mycotoxin adsorbents.

sion rates [88].

*In vivo* studies using SC are not as rare as those with LAB, mainly in poultry science. Gener‐ ally, SC is added to the feed as a growth promoter. However, the addition of yeasts has also presented beneficial effects against the exposure to AFB1. It was observed that the addition of 1% SC to feed contaminated with 5 g/g of AFB1 prevented loss of weight; liver and heart hyperplasia; and decreased serum albumin and total protein concentrations in broilers [72]. The addition of SC in feed containing aflatoxin decreased the deleterious effects on feed in‐ take, weight gain, and feed conversion in Japanese quails [73]. Compared with control ani‐ mals, weight gain was 37% lower in birds fed a diet added only of aflatoxin, and was 15% greater than the control in the group that received feed containing aflatoxin and SC. The au‐ thors concluded that the diet containing with only SC significantly improved all growth pa‐ rameters investigated (about 40%), compared with the control group.

In a study with mice, it was observed that the addition of AFB1 to the diet (0.4 and 0.8 mg/kg) caused a significant reduction in weight gain, and an increase of 85% (0.8 mg/kg) in the rate of micronucleated normochromatic erythrocytes (MNE) after 3 weeks of ingestion, compared with the control group [68]. When diets containing AFB1 and SC (0.3%) were ad‐ ministered, weight gain was twice greater than in diets that contained only the toxin, and the rate of MNE increased only 46% (0.8 mg/kg) The authors stated that reduced body weight is one of the most common consequences of AFB1 ingestion, because the toxin alters the activity of several digestive enzymes, giving rise to a malabsorption syndrome charac‐ terized by steatorrhea, hypovitaminosis A and a decrease in the levels of bile, pancreatic li‐ pase, trypsin, and amylase. Besides, biotransformation of AFB1 gives rise to several metabolites, particularly AFB1-8,9-epoxide, which may bind covalently to DNA and pro‐ teins, changing enzymatic processes such as gluconeogenesis, Krebs cycle, and fatty acid synthesis [74]. MNE rate is used to determine the genotoxicity of AFB1, because it quantifies broken chromosomes and whole chromosomes that are abnormally distributed to daughter cells, showing thus, that AFB1 is a potent mutagenic agent.

A diet containing 5 g/g of aflatoxin (82.06% AFB1, 12.98% AFB2, 2.84% AFG1, and 1.12% AFG2) by female quails (49 to 84 days of age) led to decreased egg production, feed intake, and feed conversion (31%, 28%, and 47%, respectively) [75]. However, addition of SC (2 g/kg) significantly increased these parameters (16%, 4%, and 14%, respectively). They also observed that the diet with aflatoxins caused a marked decrease in weight gain and egg weight, besides increasing animal mortality (39%, 7%, and 50%, respectively), whereas addi‐ tion of SC reverted the negative effect on these parameters (65%, 8%, and 50%, respectively). The authors stated that these negative effects of aflatoxins in egg production, feed intake, and feed conversion may have been caused by anorexia, apathy, and inhibition of protein synthesis and lipogenesis. Besides, affected liver function and mechanisms of use of protein and lipids may have affected performance criteria and the general health of the animals. In reference [76] authors reported that the components of the cells wall of SC are able to adsorb mycotoxins, stimulate the immune system, and compete for binding sites in the enterocytes, inhibiting intestinal colonization by pathogens.

SC cell wall is mainly made up of polysaccharides (80-90%), and its mechanical resistance is due to an inside layer composed of β-D-glucans, which are formed by a complex network of highly polymerized β-(1,3)-D-glucans, branched off as β-(1,6)-D-glucans, that have a low level of polymerization. This inside layer is firmly bound to the plasmatic membrane by lin‐ ear chains of chitin, which have a significant role in the insolubility of the overall structure and packing of the branched β-D-glucans. Both chitin chains and β-D-glucans affect the plasticity of the cell wall. The external layer of the yeast cell wall is formed by mannopro‐ teins, which have an important role in the exchanges with the external environment. This whole structure is highly dynamic and may vary according to the yeast strain, phase of the cell cycle, and culture conditions, such as pH, temperature, oxygenation rate, nature of the medium, concentration and nature of the carbon source. Thus, these differences in the com‐ position of the cell wall among yeast strains are related with their ability to bind to the my‐ cotoxin [77].

studies are affected by physiological parameters, such as pH, peristaltic movements, and

*In vivo* studies using SC are not as rare as those with LAB, mainly in poultry science. Gener‐ ally, SC is added to the feed as a growth promoter. However, the addition of yeasts has also presented beneficial effects against the exposure to AFB1. It was observed that the addition of 1% SC to feed contaminated with 5 g/g of AFB1 prevented loss of weight; liver and heart hyperplasia; and decreased serum albumin and total protein concentrations in broilers [72]. The addition of SC in feed containing aflatoxin decreased the deleterious effects on feed in‐ take, weight gain, and feed conversion in Japanese quails [73]. Compared with control ani‐ mals, weight gain was 37% lower in birds fed a diet added only of aflatoxin, and was 15% greater than the control in the group that received feed containing aflatoxin and SC. The au‐ thors concluded that the diet containing with only SC significantly improved all growth pa‐

In a study with mice, it was observed that the addition of AFB1 to the diet (0.4 and 0.8 mg/kg) caused a significant reduction in weight gain, and an increase of 85% (0.8 mg/kg) in the rate of micronucleated normochromatic erythrocytes (MNE) after 3 weeks of ingestion, compared with the control group [68]. When diets containing AFB1 and SC (0.3%) were ad‐ ministered, weight gain was twice greater than in diets that contained only the toxin, and the rate of MNE increased only 46% (0.8 mg/kg) The authors stated that reduced body weight is one of the most common consequences of AFB1 ingestion, because the toxin alters the activity of several digestive enzymes, giving rise to a malabsorption syndrome charac‐ terized by steatorrhea, hypovitaminosis A and a decrease in the levels of bile, pancreatic li‐ pase, trypsin, and amylase. Besides, biotransformation of AFB1 gives rise to several metabolites, particularly AFB1-8,9-epoxide, which may bind covalently to DNA and pro‐ teins, changing enzymatic processes such as gluconeogenesis, Krebs cycle, and fatty acid synthesis [74]. MNE rate is used to determine the genotoxicity of AFB1, because it quantifies broken chromosomes and whole chromosomes that are abnormally distributed to daughter

A diet containing 5 g/g of aflatoxin (82.06% AFB1, 12.98% AFB2, 2.84% AFG1, and 1.12% AFG2) by female quails (49 to 84 days of age) led to decreased egg production, feed intake, and feed conversion (31%, 28%, and 47%, respectively) [75]. However, addition of SC (2 g/kg) significantly increased these parameters (16%, 4%, and 14%, respectively). They also observed that the diet with aflatoxins caused a marked decrease in weight gain and egg weight, besides increasing animal mortality (39%, 7%, and 50%, respectively), whereas addi‐ tion of SC reverted the negative effect on these parameters (65%, 8%, and 50%, respectively). The authors stated that these negative effects of aflatoxins in egg production, feed intake, and feed conversion may have been caused by anorexia, apathy, and inhibition of protein synthesis and lipogenesis. Besides, affected liver function and mechanisms of use of protein and lipids may have affected performance criteria and the general health of the animals. In reference [76] authors reported that the components of the cells wall of SC are able to adsorb mycotoxins, stimulate the immune system, and compete for binding sites in the enterocytes,

rameters investigated (about 40%), compared with the control group.

cells, showing thus, that AFB1 is a potent mutagenic agent.

inhibiting intestinal colonization by pathogens.

gastric and intestinal secretions.

80 Aflatoxins - Recent Advances and Future Prospects

Studies have shown that the components of SC cell wall, called oligomannanes, after esterifi‐ cation, are able to bind more than 95% AFB1 [78]. Addition of 0.05% glucomannanes in the basal diet improved broiler performance [79].

The possible binding mechanisms between yeast cell wall and mycotoxins were studied, and authors suggested that β-D-glucans are the components of the cell wall that are respon‐ sible for forming the complex with the toxin, and that the reticular organization of β-D-glu‐ cans and their distribution in β-(1,3)-D-glucans and β-(1,6)-D-glucans have an important role in the efficiency of the bond [77]. Besides, studies have shown that weak hydrogen and van der Waals bonds are involved in the complex chemical connection between the myco‐ toxins and β-D-glucans, a chemical interaction that is much more "adsorption" than "bond". As for AFB1, they observed that the aromatic ring, the lactone and ketone groups of the po‐ lar form of AFB1, or chemical bonds with glucose units in the single helix of the β-D-glucans, are what keep the toxin bound to the glucans.

It was demonstrated that yeast strains isolated from environments were animals are raised are able to bind to AFB1 in saline solution (PBS, pH 7) [67]. These strains presented other properties that were beneficial to the host, such as the inhibition of pathogenic bacteria. Therefore, SC strains acted both as probiotics (co-aggregation and inhibition of pathogenic bacteria), and as mycotoxin adsorbents.

In reference [72], SC was able to reduce the deleterious effects of AFB1 in the diet of broilers and in [68] authors replicated these findings in rats. Protective effect against aflatoxins pro‐ duced by yeasts was confirmed in rats. However, when yeast cells were inactivated by heat, they were inefficient [80] but when glucomannanes extracted from the cell wall of yeasts were used, there was an increase in the efficiency of the bond with AFB1, OTA and T-2 toxin [81-84], individually or in combination [75, 79, 85, 86]. The addition of SC in the diet reduced AFB1 toxic effects in chickens [72, 87]. The ability of SC to reduce AFB1 toxic effects in quails was demonstrated, and this effect was apparently more efficient with the increase in inclu‐ sion rates [88].

In [89] authors obtained a significant reduction in AFB1 concentration during beer produc‐ tion, probably due to the bond between mycotoxins and SC cell. This hypothesis was sup‐ ported by other studies [39, 90]. A 19% reduction in AFB1 during dough fermentation in bread production was observed [91].

**Microorganism AF Bound**

B1 1 mg/kg 5 mg/kg

Strain RC008

Strain RC009

Strain RC012

Strain RC016

*S. cerevisiae* Yeast concentration:

0.1 %

0.2 %

0.3 %

None

0140

*S. cerevisiae* ATTC 9763 Pre-treatment:

Acid treated cells (2 mol/L / 90 min) Heat-treated cells (120 °C / 20 min)

*L. paracasei* LOCK 0920, *L. brevis* LOCK 0944, *L. plantarum* LOCK 0945, and *S. cerevisiae* LOCK

**(%)**

67.6 43.5 38.2 16.4 21.3 31.8 29.6 20.6 20.2 82.0 48.7 65.5

> 55 39

feed

**Conditions Ref.**

http://dx.doi.org/10.5772/51120

83

[68]

[69]

[70]

107 cells/mL, 1h, 37 °C, PBS

Recent Trends in Microbiological Decontamination of Aflatoxins in Foodstuffs

37 °C, 24 h, corn

37 °C, 24 h, corn

37 °C, 24 h, corn

3 h, 25 °C, pistachio nuts

37 °C, 6h fermentation in broiler


Recent Trends in Microbiological Decontamination of Aflatoxins in Foodstuffs http://dx.doi.org/10.5772/51120 83


In [89] authors obtained a significant reduction in AFB1 concentration during beer produc‐ tion, probably due to the bond between mycotoxins and SC cell. This hypothesis was sup‐ ported by other studies [39, 90]. A 19% reduction in AFB1 during dough fermentation in

**(%)**

15 min, 37 °C:

Alcohol yeast

3h, 25 C, PBS

3h, 25 C, PBS

3h, 25 C, PBS

YCW from brewer's yeast YCW from brewer's yeast Inactivated baker's yeast YCW from baker's yeast Inactivated baker's yeast YCW from baker's yeast YCW from baker's yeast

7.6-49.3 7.6-29 10-24 4-29 17-44 3-44 23-35 27-44

69.1 41 33 34.2 65.1 37.2 31 32.6

58.8 56.5

64.5 64

68.8 67

79.3 77.7

72.1 69.3

*S. cerevisiae* B1 (ng/mL) [67]

**Conditions Ref.**

[66]

[56]

bread production was observed [91].

82 Aflatoxins - Recent Advances and Future Prospects

*S. cerevisiae* Strain A18

Strain 26.1.11

Pre-treatment: Heated cells 52°C Strain A18 Strain 26.1.11 Heated cells 55 °C Strain A18 Strain 26.1.11 Heated cells at 60 °C

Strain A18 Strain 26.1.11 Heat cells at 120 °C Strain A18 Strain 26.1.11 2 mol/L HCl / 1h Strain A18 Strain 26.1.11

*S. cerevisiae* B1

**Microorganism AF Bound**

0.0058- 6.35 μg/mL

B1 1 μg/mL 5 μg/mL 10 μg/mL 20 μg/mL 1 μg/mL 5 μg/mL 10 μg/mL 20 μg/mL

5 μg/mL


\*Address all correspondence to: carlosaf@usp.br

**References**

*Technology*, 69-155.

ton, CRC Press.

47-984.

Boca Raton: CRC Press , 457-472.

on humans and animals. *Toxicology*, 167-101.

*tional Journal of Food Microbiology*, 109-121.

animal feed. *Trends in Food Science & Technology*, 41-334.

tial and preventive measures. *Mutation Research*, 259-291.

[10] Abbas, H. K. (2005). Aflatoxin and food safety. Boca Raton, CRC Press.

1 Faculty of Animal Science and Food Engineering, University of São Paulo, Brazil

feed by microorganisms. *Trends in Food Science & Technology*, 10-223.

Biológico de 1989 a 1999. *Biológico*, 63(1/2), 15-19.

[1] Bata, A., & Lasztity, R. (1999). Detoxification of mycotoxin-contaminated food and

Recent Trends in Microbiological Decontamination of Aflatoxins in Foodstuffs

http://dx.doi.org/10.5772/51120

85

[2] Gonçalez, E., Pinto, M. M., & Felicio, J. D. (2001). Análise de micotoxinas no Instituto

[3] D'Mello, J. P. F., & Mac, Donald. A. M. C. (1997). Mycotoxins. *Animal Feed Science and*

[4] Nierman, W. C., Cleveland, T. E., Payne, G. A., Keller, N. P., Campbell, B. C., Ben‐ nett, J. W., Guo, B., Yu, J., & Robens, J. F. (2008). Mycotoxin Production and Preven‐ tion of Aflatoxin Contamination in Food and Feed. In: Goldman GH, Osmani SA. The Aspergilli: Genomics, Medical Aspects, Biotechnology, and Research Methods.

[5] Hussein, H. S., & Brasel, J. M. (2001). Toxicity, metabolism, and impact of mycotoxins

[6] Bhat, R., Rai, R. V., & Karim, A. A. (2010). Mycotoxins in Food and Feed: Present Sta‐ tus and Future Concerns. *Comprensive Reviews in Food Science and Food Safety*, 9-57.

[7] Alberts, J. F., Engelbrecht, Y., Steyn, P. S., Holzapfel, W. H., & Van Zyl, W. H. (2006). Biological degradation of aflatoxin B1 by Rhodococcus erythropolis cultures. *Interna‐*

[8] Park, D. L., & Liang, B. (1993). Perspectives on aflatoxin control for human food and

[9] Chu, F. S. (1991). Mycotoxins: food contamination, mechanism, carcinogenic poten‐

[11] Magan, N., & Olsen, M. (2006). Mycotoxins in food: Detection and Control. Boca Ra‐

[12] Prandini, A., Tansini, G., Sigolo, S., Filippi, L., Laporta, M., & Piva, G. (2009). On the occurrence of aflatoxin M1 in milk and dairy products. *Food and Chemical Toxicology*,

2 Research and Development Department, SRI Biotech Laboratories Ltd, India

**Table 2.** Aflatoxin binding by yeasts. YCW, Yeast Cell Wall
