Comp Clin Pathol (2011) 20:121125

DOI 10.1007/s00580-010-0964-y

ORIGINAL ARTICLE

The effect of allicin on blood and tissue lead content in mice

Mohammad Reza Aslani & V. Najarnezhad & M. Mohri &
M. Azad

Received: 14 September 2009 / Accepted: 7 January 2010 / Published online: 9 February 2010
# Springer-Verlag London Limited 2010

Abstract Previous experimental results have revealed that

garlic (Alium sativum) can reduce lead toxicity and tissue
lead content in lead-exposed rodents. In the present study,
the effects of different doses of allicin, the main active
constituent of garlic, in reducing of organ and blood lead
levels were evaluated in mice exposed to 1,000 ppm of lead
acetate in drinking water. Three groups of mice received
allicin at doses of 12, 24, and 48 g/kg orally (twice daily)
during ongoing 14-day lead exposure. Mice were killed on
experimental day 15. Allicin treatment reduced lead retention
in blood and tissues. Reduction of lead concentration in
blood and tissues was dose dependent. With the highest dose
of allicin, the greatest rate of reduction of lead concentrations
were observed in liver (73.7%), kidney (45%), brain (45%),
and bone (44.4%), respectively. Liver zinc concentration was
significantly reduced in all treated groups. It was concluded
that allicin administered during lead exposure in mice can
reduce tissue lead retention and, therefore, might have some
therapeutic effect on lead poisoning.
Keywords Lead poisoning . Chelation . Allicin . Mice .
Garlic

Introduction
Lead, one of the oldest known metals, is also one of the
most common environmental and industrial pollutants that
has been found in almost all biological systems. Lead is a
highly toxic agent and has been shown to produce a wide
M. R. Aslani (*) : V. Najarnezhad : M. Mohri : M. Azad
Department of Clinical Sciences and Center of Excellence
Research in Ruminant Abortion and Neonatal Mortality,
School of Veterinary Medicine, Ferdowsi University of Mashhad,
P.O. Box 91775-1793, Mashhad, Iran
e-mail: mraslani@ferdowsi.um.ac.ir

range of biochemical and physiological dysfunctions

(Denver et al. 2000; Knight and Kent 2001; Casteel 2006;
Patrick 2006a, b; Degernes et al. 2006; Radostits et al.
2007). It adversely affects many cells, organs, and systems,
particularly the kidneys, liver, red blood cells, and skeletal,
reproductive, and nervous systems (Campbell et al. 2004;
Patrick 2006a; Radostits et al. 2007).
The major sources of lead are lead-containing paints,
lead-glazed ceramics, discarded batteries, used crankcase oil,
drinking water, and dusts (Casteel 2006; Patrick 2006b).
A threshold blood level below which lead has no adverse
effect has not been determined (Patrick 2006a, b; Gilbert
and Weiss 2006). At lower lead levels, there may be no
apparent clinical signs of toxicosis, but still there may be
adverse effects on the central nervous, renal, hematopoietic,
and skeletal systems (Campbell et al. 2004; Chiado et al.
2004; Gilbert and Weiss 2006).
Several metal chelators such as calcium disodium EDTA
(CaNa2EDTA) and meso-2,3-dimercaptosuccinic acid have
been used to manage lead toxicity in humans and some
domestic animals, but none are suitable in reducing lead
burden in chronic lead exposure (Osweiler 1999). On the
other hand, these chelators have various toxic potential in
themselves (Meldrum and Ko 2003; Kalia and Flora 2005)
and often fail to remove lead from all body tissues (Kostial
et al. 1999; Kalia and Flora 2005). Therefore, alternatives
for the treatment of lead poisoning are required. Recently,
there have been many studies on the use of natural agents
such as vitamins, minerals, and herbal drugs to prevent lead
absorption and reduce lead toxicity (Kim et al. 1992;
Tendon and Singh 2000; Aga et al. 2001; Kalia and Flora
2005; Xu et al. 2005; Rahman and Sultana 2006; Massadeh
et al. 2007; Wang et al. 2007).
It has been shown that garlic (Allium sativum) antagonizes lead toxicity. Thus, it may contain chelators which
can eliminate lead from the body (Senapati et al. 2001;

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Comp Clin Pathol (2011) 20:121125

Yassin 2005; Massadeh et al. 2007). Allicin (diallylthiosulfinate) is the most abundant thiosulfinate in garlic, which
is generated when the enzyme alliinase reacts with its
substrate alliin (Miron et al. 2004). Allicin has a variety of
biological effects including antimicrobial, hypolipidemic,
antithrombotic, anticancer, and antioxidant activities
(Chung 2006; Coppi et al. 2006).
In this study, the effects of different doses of allicin on
blood lead level and lead content of different tissues were
evaluated in mice at the time of lead exposure.

Analysis of lead concentrations

Blood and tissue lead concentrations were determined by
atomic absorption spectrophotometry (Perkin-Elmer 3030)
at 283.3 nm wavelength by use of a graphite furnace. Limit
of detection for this analysis was 5 ng/g and recovery for
spiked samples was >90%. Liver zinc was also analyzed by
flame atomic absorption spectrophotometry.
Statistical analysis
The statistical analyses were carried out using SPSS
software (version 13). KruskalWallis test was used to
compare the lead content in different groups. Adjusted Pvalue was used for pairwise comparison and P<0.008 was
considered as significant.

Materials and methods

Animals
Thirty two female Swiss albino mice, weighing 2935 g
and 78 weeks of age, were randomly divided into four
groups of eight animals each and kept in cages. Animals
were maintained on a standard pellet diet (Javaneh
Khorasan, Iran) and water provided ad libitum.
Four groups of mice were exposed to 1,000 ppm lead
acetate (Fluka, Germany) in drinking water for 14 days.
Group I received no treatment and served as control.
Groups II, III, and IV were treated with allicin (Allimed,
containing stabilized allicin; Nopex, UK) by doses of 12,
24, and 48 g/kg body weight (b.w.), respectively, by oral
gavages twice daily at the time of lead exposure.
Sampling
Blood samples were taken from the heart under ether
anesthesia on the day after the last dose of allicin (day 15)
in heparinized vials for measurement of lead. Liver,
kidneys, brain, and long bones were collected for lead
measurement. Samples of liver were also used for zinc
analysis.

Results
The blood and tissue lead concentrations of exposed mice and
the effect of different doses of allicin on tissues are presented
in Table 1. Among tissues, the bone showed the highest
concentration of lead followed by kidney, liver, and brain.
Administration of different doses of allicin reduced blood and
tissue lead content. The effect of allicin on blood and tissue
lead content appeared to be in a dose-dependent manner. The
highest dose of allicin (48 g/kg) led to a greatest reduction
of tissue lead content. From the magnitude of the lead levels
following allicin treatment, the greatest decrease in lead
concentrations was in liver, kidney, brain, and bone,
respectively. The least amount of lead reduction was found
in blood. Reduction of lead concentrations in liver, brain,
kidney, and bone in mice treated with 48 g/kg of allicin was
73.7%, 45%, 45%, and 44.4%, respectively. Zinc concentration of liver was significantly reduced in a dose-dependent
manner by different doses of allicin (Table 2).

Table 1 The effect of different doses of allicin on blood (g/dl) and tissue (g/g) lead content in mice (percentiles)
Parameters
Group

Lead in blood
Q1 Q2 Q3

Lead in liver
Q1 Q2 Q3

Control (I)

74.6 77.8 9.25

1.8 2.7 3.3

3.7 4.0 4.5

0.43 0.49 0.63

7.3 7.9 8.0

12 g/kg allicin (II)

24 g/kg allicin (III)
48 g/kg allicin (IV)
P-value

55.6 63.2 70.1

37.2 39.7a,b 47.3
35.1 44.2a,b 54.0
0.001*

0.91 1.1a 1.4

0.55 0.92a 1.2
0.55 0.71a 0.95
0.004*

1.8 2.4a 2.9

1.7 2.0a 2.2
1.44 2.2a 3.4
0.005*

0.30 0.35 0.45

0.22 0.31 0.42
0.07 0.27a 0.34
0.136*

4.2 6.15 6.8

4.9 5.1a 6.5
3.2 4.0a 5.1
0.005*

Q1 quartile 1, Q2 quartile 2 (median), Q3 quartile 3

*Significant differences at P<0.05
a

Differ significantly compared to control

Differ significantly compared to group II

Lead in kidney
Q1 Q2 Q3

Lead in brain
Q1 Q2 Q3

Lead in bone
Q1 Q2 Q3

Comp Clin Pathol (2011) 20:121125

123

Table 2 The effect of different doses of allicin on liver zinc (g/g)

(percentiles)
Parameters
Group

Zinc in liver
Q1 Q2 Q3

Control (I)
12 g/kg allicin (II)
24 g/kg allicin (III)
48 g/kg allicin (IV)
P-value

104.1 107.1 126.7

92.7 97.7a 98.9
78.4 88.1a 93.2
74.4 84.2a,b 85.2
0.001

Q1 quartile 1, Q2 quartile 2 (median), Q3 Quartile 3

a

Differ significantly compared to control

Differ significantly compared to group II

Discussion
The concomitant use of different doses of allicin prevented
the accumulation of lead in soft and hard tissues. Allicin
effectively lowered tissue lead content of lead-exposed
mice, and this effect was in a dose-dependent manner.
Allicin was capable of producing a significant reduction of
liver and kidney lead concentration in all treated groups of
mice. The effect of allicin on brain and bone lead content
was less than the effect on liver and kidney lead content.
Liver and kidneys, particularly in subacute cases, are the
target organs in lead intoxication, and accumulation of lead
in those organs results in structural damage and histochemical and histoenzymatical changes (Casteel 2006; Mudipali
2007). Therefore, removing lead from these organs will
ameliorate the toxic effects of lead.
The highest concentration of lead in the control group
was determined in bone. Bone is known as a lead pool in
the body with very slow turnover. Bone lead half-life is
estimated to be 2030 years (Pounds et al. 1991; Patrick
2006b). The conventional lead chelators are unable to
effectively chelate and remove lead from bones (Jones et al.
1994; Kalia and Flora 2005). Bone lead can contribute to
elevated blood lead levels long after the exposure no longer
exists (Patrick 2006b). Situations that increase bone
turnover, including pregnancy, lactation, osteoporosis,
hyperthyroidism, and cisplatin chemotherapy, have been
shown to increase blood lead levels as a result of the
mobilization of bone stores (Rabinowitz 1991; Silbergeld
1991; Kessler et al. 1999; Tellez-Rojo et al. 2002; Patrick
2006b) and can result in lead poisoning (Kessler et al.
1999; Riess and Halm 2007). Bone lead is also readily
transferred to the fetus during pregnancy (Gulson et al.
2003).
Allicin with doses of 48 g/kg b.w. significantly
decreased brain lead concentration. It produced a reduction
of about 45% of the brain lead concentration, and this is
comparable with the effect of the known conventional lead

chelators (Xu and Jones 1988; Flora et al. 1995; Pappas et

al. 1995; Kostial et al. 1999). Lead concentration in brain is
generally quite low (Jones et al. 1994; Kostial et al. 1999;
Varnai et al. 2004), and data from this study supports this
finding. Given this low tissue burden, it is usually difficult
to document that chelating agents have much effect on lead
concentrations in brain tissue. Because the deposition of
lead in brain tissue causes severe clinical disease and
permanent defects, decreasing of lead in that organ before
irreversible changes has been a primary goal of chelation
therapy in humans (Jones et al. 1994; Kostial et al. 1999)
and other animals (Smith et al. 1998; Jones et al. 1997).
The efficacy of allicin on the retention of lead by the
tissues has not been reported in laboratory animals.
However, therapeutic effects of garlic or its crude extract
on lead poisoning has been reported in chickens, mice, rats,
and goats (Hanafy et al. 1994; Senapati et al. 2001; Badiei
et al. 2005; Massadeh et al. 2007). It was postulated that
biologically active compounds of garlic may chelate lead
and enhance its excretion from the body, resulting in
reduced lead accumulation in tissues and blood (Senapati et
al. 2001).
Allicin represents about 70% of the overall thiosulfinate
present in the cloves of garlic upon mechanical crushing. It
is chemically an unstable and highly reactive molecule and,
therefore, its bioavailability is poor (Amagase et al. 2001;
Miron et al. 2004).
However, it has been suggested that once allicin ingested,
it is rapidly metabolized to sulfur-containing compounds in
stomach acid, blood cells, and liver (Rosen et al. 2001;
Amagase et al. 2001; Germain et al. 2002). The beneficial
effects of allicin may relate to its active metabolites.
Lead, as a divalent cation, has a strong binding capacity
for various nucleophilic functional groups (e.g., COOH,
NH2, SH) and attains maximum stability with sulfhydryl
groups. Lead, in fact, creates interference with enzymes and
structural proteins by binding to exposed sulfhydryl groups
(Casteel 2006; Patrick 2006a).
In general, sulfhydryl-containing compounds are used
for treating lead intoxication based on their chelation
activity. Many of those compounds also have an antioxidant
property. Recent studies suggest oxidative stress as one of
the important mechanisms of the toxic effects of lead.
Oxidative stress has been seen to contribute to leadassociated pathologies in the liver, kidneys, and brain
(Soltaninejad et al. 2003; Aykin-Burns et al. 2003; Patrick
2006a; Adegbesan and Adenuga 2007). A number of
compounds and elements including N-acetylcystein, methionine, taurine, melatonin, vitamins B1, B6, C, and E,
selenium, copper, calcium, zinc, and alpha-lipoic acid have
been shown, in animal studies, to interrupt or minimize the
damaging effects of lead and improve the effects of
pharmaceutical chelating agents (Patrick 2006a; Kalia and

124

Flora 2005). It has been shown that the combination of

agents such as thiamine and/or other antioxidants with
CaEDTA or succimer is more effective than the respective
individual treatments alone (Pande et al. 2001; Varnai et al.
2004; Kalia and Flora 2005; Wang et al. 2007). Our study
showed that the lowering effect of allicin on lead concentrations of different tissues of mice is superior to those that
have been reported for other antioxidants (Tendon and
Singh 2000; Varnai et al. 2003; Kalia and Flora 2005).
Allicin as a natural product has several advantages as a lead
chelator; it is administered orally and is a safe product with
high permeability through cell membranes (Miron et al.
2000). There is no report for any side effect of allicin;
however, zinc depletion of liver associated with allicin
administration was shown in the present study. On the other
hand, several adverse effects have been reported for
conventional lead chelators (Denver et al. 2000; Casteel
2006; Kalia and Flora 2005). Furthermore, allicin with
antioxidant activity (Prasad et al. 1995; Okada et al. 2006;
Chung 2006) may also depress pathogenesis of lead
intoxication.
Our findings revealed that allicin, a natural compound
derived from garlic, has the ability to reduce lead
accumulation in soft tissues (liver, kidney, and brain) and
bone. This effect is dose dependent. Therefore, allicin may
ameliorate the toxic effects of lead in various body organs.
Allicin is a safe compound and may be given to subjects
which are at risk of lead exposure even when it is not
possible to remove them from exposure to lead. However,
further studies are required to determine the molecular basis
of the anti-toxic mechanism of allicin.
Acknowledgments The authors wish to express their appreciation to
the research council of the Ferdowsi University of Mashhad for
financial support. We also wish to thank Mr. Mohsen Namei Ghasemi,
Medical Toxicology Research Center Laboratory, for his assistance in
toxicological analysis of the samples.

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