Research in Veterinary Science 89 (2010) 391–395

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Research in Veterinary Science

journal homepage: www.elsevier.com/locate/rvsc

Probiotic preparation reduces the faecal water genotoxicity in chickens fed

with aflatoxin B1 contaminated fodder
Katarzyna Slizewska a,1, Adriana Nowak a,*,1, Zdzislawa Libudzisz a, Janusz Blasiak b
a
Institute of Fermentation Technology and Microbiology, Department of Biotechnology and Food Sciences, Technical University of Lodz, ul. Wolczanska 171/173, 90-924 Lodz, Poland
b
Department of Molecular Genetics, University of Lodz, Banacha 12/16, 90-237 Lodz, Poland

a r t i c l e i n f o a b s t r a c t

Article history: The aim of the study was to evaluate the influence of a probiotic preparation on the genotoxicity of faecal
Accepted 5 April 2010 water of broiler chickens fed with a fodder contaminated with aflatoxin B1 (AFB1) at 1 or 5 mg per kg.
Human blood lymphocytes were exposed to chicken’s faecal water samples and DNA damage was mea-
sured using the comet assay. Genotoxicity of faecal water did not depend on the AFB1 concentration in
Keywords: the fodder. The mean DNA damage, measured as the percentage of DNA in the tail of the comets, for
Aflatoxin B1 chickens fed with fodder with AFB1 at 1 mg/kg was 16.80 ± 0.66, at 5 mg/kg – 16.73 ± 1.51 and in the con-
Probiotics
trols – 12.79 ± 0.66. The supplementation of fodder with the probiotic preparation decreased the extent
Chicken
Contamination
of DNA damage to 10.02 ± 0.39 for 1 mg/kg AFB1 and to 11.89 ± 0.72 for 5 mg/kg.
Fodder Ó 2010 Elsevier Ltd. All rights reserved.

1. Introduction Protection against mycotoxin contamination of a raw plant

Mycotoxins are secondary metabolites of some filamentous
fungi, mainly those belonging to Aspergillus, Penicillium and
Fusarium and they are toxic. They can be found in raw materials
and products of food industry as well as in feedstuffs. Mycotoxin
can be present in an organism as a result of food intake producing
mycotoxicosis (Mishra and Chitrangada, 2003). The transmission
via food may have primary or secondary character. The former
occurs when a toxin invades a human organism along with the
food containing toxinogenic moulds or produced from plant raw
materials contaminated with toxins. The secondary transmission
is related to the intake of animal products contaminated with
toxins, mainly due to feeding animals with mycotoxin-containing
feed.
The adverse effect of mycotoxins involves their mutagenic, car-
cinogenic (especially to kidneys and liver), teratogenic and oestro-
gen immunosuppressive effects. AFB1 is one of the strongest
carcinogens and it was included by WHO and the International
Agency for Research on Cancer in the list of carcinogenic sub-
stances Group I; i.e. substances with confirmed carcinogenic effect
in humans (IARC, 1993; JECFA, 1998).
* Corresponding author. Tel.: +48 42 631 34 70; fax: +48 42 636 59 76.
E-mail addresses: adriana.nowak@p.lodz.pl, adriana_nowak13@wp.pl (A. Nowak).
1
These authors contributed equally to the work.
material, processed during biotechnological course and used as
an animal feed focuses on its growth requirements, harvest and
storage (Park, 1993; Fraga et al., 2007). However, sometimes it is
very difficult to minimise the production of toxins by moulds,
especially if a crop is exposed to changeable weather conditions
favourable for contamination of cereals with moulds and their
products, mycotoxins. When a plant material is contaminated with
mycotoxins, it should be subject to detoxification (Akande et al.,
2006). In case of feed FAO accepts the methods of eliminating
toxins by means of chemical compounds and physical processes
that fulfil several requirements, e.g. those related to preservation
of nutritive and sensory value and physical properties of product,
as well as economic justification of decontamination process
(Allameh et al., 2005).
Biological detoxication of mycotoxins in food, raw material and
concentrated feed as well as in human and animal organisms is a
new and very promising method. Microorganisms used for elimi-
nation of mycotoxins include lactic acid bacteria – Lactobacillus
sp. and yeast Saccharomyces sp. (El-Nezami et al., 2000; Styriak
et al., 2001; Madrigal-Santillán et al., 2006; Shetty and Jespersen,
2006). Particular attention is paid to lactic acid bacteria (LAB),
because they can contribute to the inhibition of moulds develop-
ment and production of mycotoxins (Wiseman and Marth, 1981;
Haskard et al., 2001; Tavan et al., 2002; Byun and Yoon, 2003;
Lahtinen et al., 2004; Niderkorn et al., 2006). The aim of the present
study was to assess the influence of a probiotic preparation on
genotoxicity of faecal water of chickens fed with AFB1 contami-
nated fodder and potential.

0034-5288/$ - see front matter Ó 2010 Elsevier Ltd. All rights reserved.
doi:10.1016/j.rvsc.2010.04.004
392 K. Slizewska et al. / Research in Veterinary Science 89 (2010) 391–395
2. Materials and methods
2.1. Probiotic preparation
The probiotic preparation consisted of (per 1 kg): 1010 of Lacto-
bacillus cells (L. paracasei LOCK 0920, L. brevis LOCK 0944 and L.
plantarum LOCK 0945), 106 of yeast Saccharomyces cerevisiae LOCK
0140 and 50 g of Yucca schidigera extract. The strains derived from
Centre of Industrial Microorganisms (LOCK), Institute of Fermen-
tation Technology and Microbiology, Technical University of Lodz
in Poland. The strains used in the studies as the preparation pos-
sess full probiotic documentation (Smulikowska et al., 2005) and
they were licensed (Michalowski et al., 2004; Slizewska et al.,
2008).
2.2. Animals treatment
The study was performed on 30 healthy female Ross broiler
chickens divided into six groups, five animals each, kept separately
at Institute of Animal Physiology and Nutrition, Polish Academy of
Sciences, Jablonna, Poland. The groups were: control chickens – fed
with non-supplemented fodder; PP chickens – fed with fodder sup-
plemented with the probiotic preparation (2 g/kg of fodder be-
tween 1st and 14th day of life and 1 g/kg until the end of the
experiment); 1AFB1 chickens – fed with fodder contaminated with
1 mg per kg of AFB1; 1AFB1 + PP chickens – fed with fodder con-
taminated with 1 mg per kg of AFB1 and supplemented with the
probiotic preparation; 5AFB1 chickens – fed with fodder contami-
nated with 5 mg per kg of AFB1; 5AFB1 + PP chickens – fed with
fodder contaminated with 5 mg per kg of AFB1 and supplemented
with the probiotic preparation.
2.3. Faecal water preparation
Faecal water samples were extracted from faecal samples col-
lected on 35 day of life. Samples were homogenized for 2 min
and then centrifuged (7100g for 30 min). Aliquots of the superna-
tants (aqueous faecal extracts) were distributed to 1.5 ml Eppen-
dorf tubes and stored at 20 °C prior to analysis.
2.4. Lymphocyte isolation and cell treatment
Blood was obtained from young, healthy, non-smoking donors.
Peripheral blood lymphocytes were isolated by centrifugation in a
density gradient of Histopaque-1077 (15 min, 1100g). The pellet
containing peripheral blood lymphocytes was suspended in RPMI
1640 medium. The final concentration of the lymphocytes in each
sample was adjusted to 1  105 cells/ml. Lymphocytes were incu-
bated with 100 ll of faecal water for 1 h at 37 °C. The control cells
received only RPMI 1640 medium. The experiment included a po-
sitive control, which was hydrogen peroxide at 20 lM applied for
10 min at 4 °C.
2.5. Comet assay
After incubation the lymphocytes were centrifuged (1100g,
15 min, 4 °C) and the comet assay was performed in alkaline con-
ditions according to the procedure of Singh et al. (1988) with some
modifications. The cells were suspended in 0.75% LMP agarose and
layered onto slides precoated with 0.5% agarose and lysed for 1 h at
4 °C in buffer consisting of 2.5 M NaCl, 1% Triton X-100, 100 mM
EDTA and 10 mM Tris. After lysis the slides were placed in an elec-
trophoresis unit and DNA was allowed to unwind for 20 min in an
electrophoretic solution containing 300 mM NaOH and 1 mM
EDTA. Electrophoresis was conducted at 4 °C for 20 min at an elec-
tric field strength 0.73 V/cm (30 mA). Then, the slides were neu-
tralized with 0.4 mol/l Tris and stained with 1 lg/ml DAPI (40 ,6-
diamidino-2-phenylindole) and covered with cover slips. Comets
were observed at 200 magnification in a fluorescence microscope
(Nikon, Japan) attached to a video camera and connected to a per-
sonal computer-based image analysis system Lucia-Comet v. 4.51
(Laboratory Imaging, Prague, The Czech Republic). Fifty images
were selected from each sample and DNA damage measured as
percentage of DNA in the tail of the comets was determined. Two
parallel tests with aliquots of the same sample were performed
for a total of 100 cells and the mean of DNA damage was calcu-
lated. Each experiment was repeated three times. Comet results
were analysed using two-way analysis of variance (ANOVA) and
a particular mode of interaction  time was used to compare ef-
fects evoked by chemicals at this mode of interaction and suitable
control. No statistically significant interaction was found, so one-
way analysis of variance was applied. The differences between
means were compared using Scheffe’s multiple comparison test.
Results were presented as mean ± SEM.
3. Results
3.1. DNA damage
Non-exposed samples (lymphocytes in RPMI 1640, a negative
control) displayed DNA damage of 1.68 ± 0.13. Treatment of cells
with 20 lM hydrogen peroxide (positive control samples) resulted
in the damage of 26.36 ± 1.62 (results from three independent
experiments).
3.2. Chickens fed with fodder supplemented with probiotic preparation
Supplementation of fodder with probiotic preparation only (PP –
probiotic group of chickens) decreased genotoxicity of faecal water
comparing to the control group of chickens (with no supplementa-
tion) (Fig. 1 and Table 1). In the control group DNA damage was in
the range from 10.46 ± 0.89 to 14.94 ± 1.17, while in the probiotic
preparation group of chickens (PP group) it was from 8.07 ± 0.69
to 13.36 ± 1.06 (Fig. 2A and B). Probiotic effect in reducing genotox-
icity was appreciable (p < 0.05) as shown in Fig. 1.
3.3. Chickens fed with fodder contaminated with AFB1
Incubation of human lymphocytes with faecal water of the
chickens induced considerable DNA damage, yielding comet tail
from 12.83 ± 1.02 to 22.02 ± 1.24 for chickens fed with fodder con-
taminated with 1 mg/kg of AFB1 (1AFB1 group) and from
Fig. 1. The effect of probiotic preparation on chicken faecal water-induced DNA
damage expressed as percentage of DNA in the tail of comets in alkaline comet
assay. Asterisks indicate significant differences (P < 0.05). The results displayed are
means (±SEM) of three independent experiments.
 K. Slizewska et al. / Research in Veterinary Science 89 (2010) 391–395 393

Table 1
DNA damage measured as percentage of DNA in the comet tail in alkaline comet assay in human peripheral blood lymphocytes induced by faecal water of broiler chickens.

Chicken number Control PP 1AFB1 1AFB1 + PP 5AFB1 5AFB1 + PP

DNA (%) in comet tail ± S.E.M.
1 12.30 ± 1.08 12.80 ± 0.86 15.67 ± 1.15 7.30 ± 0.59 16.52 ± 1.42 16.74 ± 1.69
2 14.94 ± 1.17 13.02 ± 1.08 22.02 ± 1.24 11.06 ± 0.65 17.98 ± 1.15 9.91 ± 0.85
3 10.46 ± 0.89 9.54 ± 0.70 12.83 ± 1.02 10.94 ± 0.98 22.18 ± 1.02 9.10 ± 0.84
4 12.34 ± 0.82 8.07 ± 0030.69 14.02 ± 1.03 8.04 ± 0.85 14.40 ± 0.94 9.51 ± 1.01
5 13.88 ± 0.95 13.36 ± 1.06 19.48 ± 1.38 12.98 ± 1.29 13.68 ± 0.78 15.25 ± 1.04
Meana ± S.E.M. 12.79 ± 0.66 11.26x ± 0.52 16.80 ± 0.66 10.02y ± 0.39 16.73 ± 0.62 11.89z ± 0.72

The number of cells analysed in each treatment was 100. Data are mean values (±S.E.M.) from all chickens of each group for which faecal samples were available.
a
the results displayed are the mean of three independent experiments; x,y,zstatistically different from: xcontrol, yAFB1 (1 mg/kg), zAFB1 (5 mg/kg), ANOVA (P < 0.05).

Fig. 2. Representative comets of DAPI stained human blood lymphocytes incubated for 1 h at 37 °C with faecal water of broiler chickens: (A) control groups of chickens; (B)
chickens fed with fodder supplemented with probiotic preparation; (C) chickens fed with fodder contaminated with 5 mg/kg of AFB1; (D) chickens fed with fodder
contaminated with 5 mg/kg of AFB1 and supplemented with probiotic preparation.

13.68 ± 0.78 to 22.18 ± 1.02 for chickens fed with fodder contami-
nated with 5 mg/kg of AFB1 (5AFB1 group) (Fig. 2C). Therefore, the
genotoxicity of faecal water of chickens was independent of AFB1
concentration in the fodder in the range of 1 and 5 mg/kg (Fig. 1
and Table 1).
3.4. Chickens fed with fodder contaminated with AFB1
and supplemented with probiotic preparation
After supplementation of fodder with probiotic preparation, we
observed a statistically significant decrease in the level of DNA
damage, which was in the range from 7.3 ± 0.59 to 12.98 ± 1.29
for chickens fed with fodder contaminated with 1 mg/kg of AFB1
(1AFB1 + PP group) and from 9.10 ± 0.84 to 16.74 ± 1.69 for chick-
ens fed with fodder contaminated with 5 mg/kg of AFB1
(5AFB1 + PP group). Therefore, the protective effect of the probiotic
preparation seems to depend on the concentration of AFB1
(Fig. 2D). Supplementation with the probiotic preparation reduced
the genotoxicity of faecal water in chickens fed with fodder con-
taminated with 1 or 5 mg/kg of AFB1 (Fig. 1 and Table 1).
4. Discussion
There are reports on massive poisonings of poultry and cattle
due to the presence of aflatoxins in feed (Rodricks et al., 1977;
Galvano et al., 1996; Akande et al., 2006). The major reason for this
was feeding animals with contaminated bruised peanut grain or
corn. Chickens are relatively resistant, however longer application
of feed contaminated with AFB1 may lead to adverse effects. The
symptoms of poisoning may include: loss of weight, depression,
muscle paralysis and cyanosis of combs and wattles. In addition
fast breathing, chronic inflammation of mucous membrane of the
digestive tract, sporadic focal congestion, and particularly local
ecchymosis on the surface of liver, kidneys and heart may be ob-
served (Rodricks et al., 1977; Akande et al., 2006).
Biological detoxification of mycotoxins in food, raw products,
mixed protein feeds and also in human and animal organisms is
relatively new and promising method. Several microorganisms
have been used to eliminate mycotoxins: Acinetobacter calcoaceti-
cus, Aspergillus niger, Lactobacillus sp. strains and Saccharomyces
sp. (Styriak et al., 2001). Special attention should be paid to lactic
acid bacteria because of their favourable influence on human
394 K. Slizewska et al. / Research in Veterinary Science 89 (2010) 391–395
organisms (probiotic bacteria) and the widespread use in the pro-
duction of fermented foods. These bacteria inhibit the growth of
moulds as well as mycotoxins production (Wiseman and Marth,
1981).
The aim of our study was to check if the probiotic preparation
(composed of lactic acid bacteria, yeasts and Yucca schidigera ex-
tract) influenced the genotoxicity of faecal water of chickens fed
with AFB1 contaminated fodder. We observed that genotoxicity
of faecal water did not depend on the AFB1 concentration in the
fodder. After supplementation of the fodder with probiotic prepa-
ration observed genotoxicity was decreased and it was statistically
significant. The decrease was more pronounced for the group of
chickens fed with the fodder contaminated with lower concentra-
tion of AFB1 (1AFB1 + PP). Therefore, supplementation with the
probiotic preparation contributes to reduction of genotoxicity of
faecal water of chickens fed with AFB1 contaminated fodder. The
mechanism underlying this effect may be associated with the abil-
ity of probiotic preparation to bind AFB1, resulting in its decreased
concentration in chicken colon, although supplementation of fod-
der with probiotic preparation only (PP) also decreased DNA dam-
age of the control group.
Several mechanisms underlay anti-carcinogenic and anti-geno-
toxic action of probiotics in the colon and these may include bind-
ing or degradation of carcinogens and toxins (Burns and Rowland,
2000; Commane et al., 2005). The mechanism determined the abil-
ity of probiotics to bind or metabolise different colon carcinogens
is not completely known and is a challenge for scientists. Although
Lactobacillus species are only a small part of intestinal microbiota
(about 2%) their anti-cancer and anti-genotoxic action against hu-
man colon carcinogens was proved either in vitro or in vivo exper-
iments (Zhang and Ohta, 1993; Lankaputhra and Shah, 1998; Burns
and Rowland, 2000; Hirayama et al., 2000; Tavan et al., 2002)
Lactobacillus casei Shirota was reported to decrease DNA damage in
rat colon after exposure to MNNG (N-methyl-N-nitro-N-nitrosogua-
nidyne) and genotoxicity induced by DMH (dimethylhydrazine)
(Commane et al., 2005). Lactobacillus delbrueckii ssp. bulgaricus
inhibited progression and promotion of colon adenocarcinoma in
mice after exposure to DMH (Santosa and Farnworth, 2006).
Many microorganisms including bacteria, yeasts, moulds, acti-
nomycetes and algae are able to remove or degrade small amounts
of aflatoxin in food or feeds, but their use in biological detoxifica-
tion has not been established yet (Styriak et al., 2001). Results of
several studies suggest that the binding is the main mechanism
of detoxification of aflatoxins (El-Nezami et al., 1998; Oatley
et al., 2000; Peltonen et al., 2000, 2001; Byun and Yoon, 2003;
Niderkorn et al., 2006; Gratz, 2007). Strains Lactobacillus rhamnosus
GG and LC-705 seem to be the most effective in such mechanism of
detoxification of aflatoxins (El-Nezami et al., 2000; Haskard et al.,
2001; Lahtinen et al., 2004). However, the binding mechanism
has not been thoroughly understood. It was suggested that carbo-
hydrate-rich mannoproteins or glucans might be involved in the
binding, which can be strain-specific (Shetty and Jespersen,
2006). Raju and Devegowda (2000) attributed the aflatoxin binding
by yeast cell walls to mannan oligosaccharides, but zearalenone
binding has been attributed to glucan components (Yiannikouris
et al., 2004). Haskard et al. (2001) suggested that AFB1 binds pre-
dominantly to carbohydrate and protein components of viable
cells. However, systematic studies are still needed to understand
the mechanisms of binding (Shetty and Jespersen, 2006).
Metabolism of aflatoxins can be considered as the second mech-
anism of their detoxification. Few studies addressed the role and
importance of the gastrointestinal tract in AFB1 metabolism. Stud-
ies in rats identified free hydroxylated metabolites of AFB1: AFM1
and AFL (Gratz, 2007). In the presence of probiotics an increased
excretion of AFM1 was observed in the presence of probiotics, sug-
gesting a reduced AFB1 uptake and hepatic metabolism. Some of
the metabolites diffuse back into the lumen and probiotics bind
it and excrete via the faeces – L. rhamnosus GG is known to bind
AFM1 equally efficiently as AFB1 (Kabak and Var, 2004; Gratz,
2007). AFM1 and AFM2 are excreted with milk of cows fed with
aflatoxin contaminated feed what implies on gastrointestinal
metabolism of the mycotoxins. Microorganisms reduce tissue up-
take of AFB1 from duodenum of chickens what may point out on
the reduction of aflatoxins absorption in the human gastrointesti-
nal tract (El-Nezami et al., 2000). These data imply that intestinal
metabolism of AFB1 is an important process and that probiotic bac-
teria impact upon these processes.
5. Conclusion
In summary our results show that probiotic preparation de-
creases genotoxicity of faecal water of chickens fed with aflatoxin
B1 contaminated fodder within the range of 1 and 5 mg/kg and can
be considered as a preventive agents in poultry breeding.
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