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Vol.2, No.7, 789-795 (2010)
doi:10.4236/health.2010.27119
Co
pyright © 2010 SciRes. Openly accessible at http://www.scirp.org/journal/HEALTH/
Health
Taxol as chemical detoxificant of aflatoxin produced by
aspergillus flavus isolated from sunflower seed
Narasimhan Banu
1
*, Johnpaul Muthumary
2
1
Department of Biotehnology, Vels University, Pallavaram, Chennai, India; *Corresponding Author: banunkl@yahoo.com
2
Centre for Advanced Studies in Botany, University of Madras, Chennai, India
Received 24 November 2009; revised 10 March 2010; accepted 12 March 2010.
ABSTRACT
Aflatoxins are the potent toxic, mutagenic, het-
erogenic and carcinogenic metabolites produc-
ed by species of A. flavus and A. parasiticus. In
the present study, an attempt has been made to
prevent aflatoxin production using an antican-
cerous drug taxol. Taxol (Paclitaxel) is a well
known drug for its anticancerous property mainly
to treat breast and ovarian cancers. It was ob-
tained from Taxus brevifolia and it was also ob-
tained from the endophytic fungi present in
Taxus brefivolia [1]. Therefore, this drug is spe-
cifically selected to screen its activity on the
control of A. flavus and AFB1 production at va-
rious concentrations. Among the 6 concentra-
tions used, 3 μg of taxol was found to be suitable
to control the growth and AFB1 production. The
content of AFB1 found at this concentration was
6 ppm by TLC and 6.3 ppm by HPTLC. The
complete elimination of AFB1 might require
higher concentrations of taxol.
Keywords:
Aflatoxins; Taxol; Anticancerous Drug;
Liver Cancer
1. INTRODUCTION
Aflatoxins are the potent toxic, mutagenic, heterogenic
and carcinogenic metabolites produced by species of A.
flavus and A. parasiticus in food and feed, especially the
oil seeds and their products, both at pre and post harvest
conditions. Their occurrence in food and feed materials
has caused not only health hazards in animals and hu-
mans but also economic losses especially to the export-
ing countries. They are initially classified as human car-
cinogens by the International Agency on Research in
Cancer in 1993 and further epidemiological experimen-
tal research continues to show a strong link between
aflatoxin exposure and hepato cellular carcinoma (HCC).
Although the prevention of mycotoxin contamination
in the field is the main goal of agricultural and food in-
dustries, under certain environmental conditions the con-
tamination of various commodities with fungi like Fusa-
rium, Aspergillus, Alternaria and Penicillium and their
mycotoxins are unavoidable for producers. Decontami-
nation/detoxification procedure is useful in order to re-
cuperate mycotoxin contaminated commodities. The
ideal decontamination procedure should be easy to use,
inexpensive and should not lead to the formation of
compound that are still toxic, or may reverse to reform
the parent mycotoxin or alter the nutritional and palat-
ability properties of the grain or grain products. The
frequent occurrence of aflatoxins in food materials poses
a serious threat to the consumers. Therefore, a consider-
able concern has been shown for prevention of the my-
cotoxins [2]. Hepatocellular carcinoma (HCC) is one of
the most prevalent cancers worldwide with incidence
rates highest in geographical regions of Africa and Asia
exhibiting climatic similarities of high heat, humidity
and poor food storage conditions. Reports have shown
that aflatoxins causes primary liver cancer in humans on
a worldwide basis [3-5]. The International Agency for
Research on Cancer [6] has declared AFB1 to be class I
carcinogen, on the basis of animal assays. Hence ap-
proaches involving physical [7-9] chemical and biologi-
cal [10-15] methods have been made to detoxify afla-
toxins in food and feedstuffs in the recent past. In India,
mycotoxin contamination in food and its control were
extensively studied by Bilgrami and his associates [16].
Examination of physico-chemical and biochemical
characteristics of AFB1 molecule reveals two important
sites for toxicological activity [17]. The first site is the
double bond in position c-8, 9, of furo-furan ring. The
aflatoxin-DNA and protein interactions, which occur at
this site, alter the normal biochemical functions of these
macromolecules leading to deleterious effects at the cel-
lular level. The second reactive group is the lactone-ring
in the coumarin moiety. The lactone ring is easily hy-
N. Banu et al. / HEALTH 2 (2010) 789-795
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790
drolyzed; it is therefore a vulnerable site for degradation.
Hence the degradation treatments should be aimed at
removing the double bond of the terminal furan ring or
in opening the lactone ring. Once the lactone ring is
opened, further reactions could occur to alter the binding
properties of the terminal furan ring to DNA and pro-
teins.
Structural degradation or inactivation of aflatoxins has
been found to be possible by the use of chemicals such
as chlorinating agents (sodium hypochlorite, chlorine
dioxide and gaseous chlorine), oxidizing agents (H
2
O
2
,
ozone, sodium bisulfite) and hydrolytic agents-acids
(organic and inorganic) and alkalies (sodium hydroxide,
ammonium hydroxide, potassium hydroxide, etc.). Some
of these chemicals are already being used in food indus-
try and are less prone to consumer resistance [18]. How-
ever, according to Park and Liang [8], most of these
chemicals are impractical and are particularly unsafe be-
cause they form toxic residues or damage nutrient content,
flavour, odour, color, texture or functional properties of
the product.
Among different processes, ammoniation process has
been extensively worked out and largely accepted in
spite of certain resulting nutritional losses. Liquor am-
monia, gaseous ammonia, in situ liberation of ammonia
by reaction of urea and urease as well as reacting amino
methylamine with lime has been used.
The noteworthy losses affecting the nutritional quality
of ammoniated animal feeds include 10% reduction of
protein quality [19], an irreversible reduction in the de-
gree of unsaturation in lipids [20], a significant drip in
lysine and methionine content [21,22]. The presence of
residual toxicity arising from hydrolyzed products [23]
along with the potential for covalent bonding of AFB1 to
proteins [24] and the loss in nutritional quality, make the
ammoniation treatment processes seem less acceptable.
However, under defined conditions the treatment of
grains (peanuts, cotton seed, corn) and their meals with
ammonia appears to be a commercially viable approach
to detoxification of aflatoxins to the extent of 99% [8]
particularly for feed purposes.
Ammonia degradation proceeds through hydrolysis of
lactone ring, and is followed by decarboxylation to pro-
duce non-toxic compounds. Due to severity of aflatoxins
contamination in selected agricultural commodities, in
various locales, specific decontamination processes have
been approved and put into use [8,25]. Ammoniation of
feeds is authorized by Food and Drug Administration of
the U.S.A. In the U.S.A., Arizona, California and Texas
permit the ammoniation of cotton seed products, and
Texas, North Carolina, Georgia and Alabama have ap-
proved the use in aflatoxin-contaminated corn. Mexico
and South Africa have approved the procedure for use on
corn. Treated peanut meal is widely used in animal feeds
in Europe and elsewhere; consequently the process is
routinely used in France, Senegal, Sudan and Brazil.
Several member countries of the European Community
import ammonia treated peanut meal on a regular basis.
Ammonia treatment processes for feed mill and at farm
level have been worked out intensively by Park et al.
[25]. Low ammonia concentration (0.2 to 2.0%) at high
pressure (35-50 psi) and high temperature (80-120ºC
would require less time (20-60 minutes) as compared to
high ammonia concentration (1-5%) at atmospheric
pressure, ambient conditions needed more time (14-21
days) for treating feed materials containing 12-16%
moisture [25] at feed mill level and form level, respec-
tively. Shannaz and Ghaffar [26] studied the use of am-
monia gas in the reduction of aflatoxin and aflatoxin
producing fungi in sunflower seeds. Use of ammonia gas
reduced the seed germination but infection of A. flavus
decreased with consequent reduction in aflatoxin pro-
duction. Feeding lactating cows with ammoniated peanut
meal can result in reduced levels of AFM1 in milk of
cows [27]. Namazi et al. [28] demonstrated that 0.9-
1.0% ammonia inhibited fungal growth together with
aflatoxin production.
Pathological and histo-pathological examinations made
with experimental and farm animals fed with ammoni-
ated meals did not show any signs of aflatoxicosis. Also
there were no differences in egg production and immu-
nological responses in poultry. Sodium bisulfite can re-
act with aflatoxin B1, G1, M1 and aflatoxicol at various
temperatures and concentrations at various times to form
water-soluble products [29]. Potassium bisulphite is a
common food preservative and does not pose any con-
sumer resistance problem [30]. Aflatoxin containing
copra at moisture contents of 24% and 7% was effec-
tively detoxified by ammonium hydroxide (> 97% and
89% reduction, respectively) [31]. Sharma et al. [32]
prevented aflatoxin formation in the commodities like
peanut and corn samples by the treatment with an aque-
ous solution of 2-chloroethylphosphoric acids. Buller-
man [33] studied the effects of cinnamon on growth and
aflatoxin production by known toxigenic strains of A.
parasiticus. It was observed that the cinnamon is an ef-
fective inhibitor of aflatoxin production even though
mycelium growth may be permitted.
Aflatoxin production by Aspergillus parasiticus was
markedly checked by O-vanillin on the cereals and oil
seeds by Bilgrami et al. [34]. Maximum inhibition was
recorded on rice (85.6%) followed by groundnut (76.25%),
wheat (54.2%), maize (52.3%) and mustard (51.1%).
O-vanillin did not have any pronounced effect on seed
germination.
The prevention of aflatoxin producing fungi and afla-
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791
toxin through some known anticarcinogenic compounds
viz., Redoxon (Ascorbic acid 0.1 g/ml) [35] and Serpasil
(Reserpine 2.5 mg/ml) [36] at different concentrations
[37]. It is evident that both these drugs had shown in-
hibitory effects on aflatoxin production at all concentra-
tions though in varying degrees.
Ozone effectively degraded AFB1 and AFG1 in 4%
dimethyl sulfoxide at room temperature within a few
minutes. The treated products were confirmed to be
non-toxic by various methods. It is reported to reduce
AFB1 levels by 91% in cottonseed meal containing 22%
moisture after treatment at 100ºC for 2 h; however, with
peanut meal (30% moisture) the reduction was only 78%
after exposure to ozone for 1 h. [38]. The destruction and
detoxification of aflatoxin B1, B2, G1 and G2 (50 µg/ml
in 4% dimethyl sulfoxide) with ozone were confirmed
by Maeba et al. [39].
2. MATERIALS AND METHODS
2.1. Chemical Method
2.1.1. Decontamination/Detoxification by Taxol
Taxol is an anti cancerous drug obtained from Taxus
brevifolia. Authentic sample of taxol (paclitaxel) was
obtained from Sigma chemicals. A sample of 0.02 mg
was dissolved in 1ml of 100% methanol. From this stock
different concentration of taxol viz., 0.5, 1.0, 1.5, 2.0,
2.5 and 3.0 µg was taken and added to 100 ml of Yeast
Extract Sucrose medium (2% yeast, 20% sucrose) [40]
separately. Then the medium was inoculated with a disc
of Aspergillus flavus isolate from the surface sterilized
sundried sunflower seed used for oil crushing and incu-
bated for 8 days at 30ºC as a stationary culture.
After 8 days, the cultures were killed and the culture
filtrate was filtered through Whatman’s No.1 filter paper.
One hundred milliliter of culture filtrate was extracted
thrice with equal volume of chloroform. The chloroform
extract was dried over rotary evaporator. The final resi-
due was dissolved in 0.2 ml of chloroform. The same
procedure was followed for control without adding taxol.
2.1.2. Quantification of Aflatoxin B1 by TLC
Five, 10, 20 and 40 µl of the above extracts were applied
to pre-coated TLC plates (Merck) along with the stan-
dard aflatoxin B1. The plates were developed in a tank
containing chloroform: acetone in the ratio of 88:12.
After the development, the plates were viewed under
long UV light at 365 nm. Blue-fluorescence similar to
standard aflatoxin B1 indicated the presence of aflatoxin
B1. Quantification of aflatoxin B1 was made by evalu-
ating on the plate itself using long UV light. The role of
taxol on detoxification was determined by quantifying
the intensity of blue fluorescence of aflatoxin B1.
2.1.3. High Performance Thin Layer
Chromatography
Twenty micro liter of the above sample extracts were
loaded onto pre-coated silica gel plate. The plate was
developed in a saturated tank containing tertiary butyl
methyl ether: methanol: water in a ratio of 9.6: 0.3: 0.1.
The developing distance of the plate was up to 80mm.
The developed plates were scanned in a Camag TLC
Scanner 3 at 366 nm. The presence of blue-fluorescence
indicated the presence of aflatoxin and confirmed with
authentic sample.
3. RESULTS AND DISCUSSION
An attempt has been made in the present investigation to
prevent aflatoxin production using an anticancerous drug
taxol. Taxol (Paclitaxel) is a well known drug for it anti-
cancerous property. It was obtained from Taxus brevifo-
lia and it was also obtained from the endophytic fungi
present in Taxus brefivolia [1], Pestalotiopsis termina-
liae, an endophyte of Terminalia arjuna [41], and Pesta-
lotiopsis versicolor and Phyllosticta murrayicola, a
pathogenic fungi [42]. It is mainly used to treat breast
and ovarian cancers. Therefore, this drug is specifically
selected to screen its activity on the control of A. flavus
and AFB1 production at various concentrations.
From authentic taxol (0.02 mg) (Sigma chemicals),
0.5, 1.0, 1.5, 2.0, 2.5 and 3.0 µg concentrations were
selected and amended with YES medium containing A.
flavus isolate. This isolate was used as control, its dry
weight was 3.9 g and its AFB1 content was 36 ppm
(Figure 2, Table 1). Except 2.5 µg concentration of
taxol, all the other concentrations showed marked reduc-
tion in the mycelial dry weight and AFB1 production.
But there was no correlation between the mycelial dry
weight and the AFB1 production. The dry weight of the
mycelium ranged from 2.6-4.6 g (Table 1).
Among the 6 concentrations used, 3 µg of taxol was
found to be suitable to control the growth and AFB1
production (Tabl e 1, Figure 8). The content of AFB1
found at this concentration was 6 ppm by TLC and 6.3
ppm by HPTLC. The complete elimination of AFB1
might require higher concentrations of taxol (Figures
1-8). This study indicate that the chemical taxol was a
effective inhibitor of aflatoxin production even though
mycelial growth may be permitted. Taxol is quite expen-
sive drug and we could not take this drug as food addi-
tives but the availability of Sargassum wightii is inex-
pensive and safe [15].
The U.S. FDA has currently established action levels
(max) of aflatoxin to be 20 ppb for human foods (except
milk), 0.5 ppb for milk, 20 ppb for animal feeds, except
some cases of feeds meant for maturing and finishing
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Table 1. Quantification by TLC and HPTLC.
Level of Aflatoxin B1 (ppm)
S.No.
Concentration
of Taxol (μg)
Mycelial dry
weight (g)
Quantifica-
tion by TLC
Quantification
by HPTLC
1 0.5 2.9 8 9.2
2 1.0 2.7 12 11
3 1.5 2.6 16 15
4 2.0 3.6 12 12
5 2.5 4.6 12 11
6 3.0 2.9 6 6.3
Control - 3.9 30 36
Figure 1. Authentic Aflatoxin B1.
Figure 2. Control.
Figure 3. Aspergillus flavus with 0.5 µg of Taxol.
Figure 4. Aspergillus flavus with 1µg of Taxol.
Figure 5. Aspergillus flavus with 1.5µg of Taxol.
Figure 6. Aspergillus flavus with 2.0µg of Taxol.
Figure 7. Aspergillus flavus with 2.5 µg of Taxol.
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Figure 8. Asper.gillus flavus with 3.0 µg of Taxol.
of meat animals, which varied from 100 to 300 ppb [8].
From the viewpoint of health and economics, it is im-
perative that such low levels of aflatoxin are prescribed
to follow up. To achieve such low levels, decontamina-
tion/ detoxification procedures are useful in order to re-
cuperate mycotoxin contaminated commodities. The ideal
decontamination procedure should be easy to use, inex-
pensive and should not lead to the formation of com-
pounds that are still toxic or may reverse to reform the
parent mycotoxin or alter the nutritional and palatability
properties of the product. Hence approaches involving
physical and biological methods have been made to de-
toxify aflatoxin in food and feedstuffs by many workers.
It was reported by Dollear [38] that in the case of
groundnut oil, the oils were alkali refined, the soap stock
removed and the oils subjected to two washing. No afla-
toxin could be detected in 100 ml of the refined, washed
oils. It is evident that conventional processing practices
remove completely any aflatoxin that may be found in
crude oils. Banu and Muthumary [43] were also found
the absence of fungal spores and aflatoxin in refined oil
collected from Tamil Nadu Agro Industries Corporation.
Chlorophyllin (CHL) has been found to be a safe and
effective agent for chemoprevention in humans exposed
to aflatoxin [44]. Substitution of antifungal and aflatoxin
inhibitory chemicals by natural compounds such as
thyme oils is recommended [45]. Examination of various
concentrations of thyme essential oils on the growth of A.
parasiticus showed promising prospectus on the utiliza-
tion of natural plant oils and extracts.
Prevention of aflatoxin elaboration has received con-
siderable attention. Various fungicides, fumigants and
chemicals [46,47], plant extracts [48], antibiotics [49]
have been suggested for controlling the growth of afla-
toxin producing fungi as well as aflatoxin production.
Ranjan and Sinha [37] used two anticarcinogenic com-
pound viz., Redoxon [35] and Serpasil [36] on AFB1
production and A. flavus control. Complete inhibition of
AFB1 was noticed at higher concentration of redoxon.
Combination of serpaisl and redoxon also significantly
inhibited aflatoxin production as well as mycelial growth.
4. CONCLUSIONS
By this study, it is evident that the taxol had inhibitory
effects on aflatoxin production at all the concentrations
mentioned though in varying degrees. It is apparent from
this study that the anticarcinogenic drug taxol can also
be exploited for the prevention of aflatoxin production
by A. flavus.
5. ACKNOWLEDGEMENTS
We greatly acknowledge the Department of Science and Technology,
Govt. of India for providing the financial support to carryout the re-
search work.
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