Hepatoprotective Effects of Camel Milk against CCl4-induced Hepatotoxicity in Rats
Amjad Ali Khan
Mohammad A. Alzohairy
Camel milk has been widely used in a number of countries as a food additive and for curing some commonly occurring diseases. Recently, camel milk has been deeply studied for its special properties because of higher hepatoprotective, insulin like and antibacterial activities. These properties distinguish camel milk from milk of other animals. The present study was carried out to investigate the protective effects of camel milk against CCl4-induced hepatotoxicity which lead to biochemical alterations in liver function of male albino wister rats. White albino male rats (200-250 g) were divided into 5 groups, a normal control water group, a control camel milk group and three CCl4-intoxicated groups treated with or without camel milk. Protective roles of camel milk were analyzed by assaying the liver function parameters as serum aminotransferases, alkaline phosphatase, serum proteins and cholesterol levels. Histopathological examinations were also studied in all groups of rats by microscopy. Data showed that intraperitoneal administration of CCl4 (1 mL kg-1 b.wt.) resulted in statistically significant increase in the serum levels of aminotransferases and change in serum protein, albumin and cholesterol levels which approach to normal levels after the treatment with raw camel milk. Furthermore, histopathological studies reveal that camel milk treatments significantly reduce the incidence of liver lesions induced by CCl4. Our findings demonstrate that CCl4 exposure alters liver function biochemical parameters, which shift towards normal values after treatment with camel milk. So camel milk has a good potent for curing some liver diseases.
Received: October 13, 2010;
Accepted: November 19, 2010;
Published: February 09, 2011
The liver is the organ for metabolism and detoxification of various components
that enter into the body. It is involved in wide range of functions and hence
it is exposed to toxic substances and drugs absorbed from the intestine. Apart
from the toxins and drugs, viral infections (hepatitis A, B, C, D, etc.) and
microbial infections also cause damage to the hepatocytes (Nunez,
Carbon tetrachloride (CCl4) is a highly toxic chemical agent, widely
used to elicit experimental liver damage. The effects of CCl4 on
hepatocytes are manifested histologically as hepatic steatosis, fibrosis, hepatocellular
death and carcinogenicity (Junnila et al., 2000).
Its toxic effect is believed to be due to trichloromethyl radical which is formed
by an unstable metabolic intermediate under the presence of oxidative stress
(Stoyanovsky and Cederbaum, 1999; Recknagel
et al., 1989).
However, few approaches which delineate the comprehensive metabolic disorders and metabolic syndromes of CCl4 induced hepatotoxicity have been investigated in literature.
Acute and chronic liver diseases constitute a global concern and medical treatments
for these diseases are often difficult to handle and have limited efficiency
(Lee et al., 2007). Therefore, there has been
considerable interest in role of complementary and alternative medicines for
the treatment of liver disease. Developing therapeutically effective agents
from natural products may reduce the risk of toxicity when the drug is used
Camel milk is different from other ruminant milk as it is low in cholesterol,
sugar and protein but high in minerals (sodium, potassium, iron, copper, zinc
and magnesium), vitamin A
, C and E and contains a high concentration
of insulin and immunoglobulins (Kamal et al., 2007
). Further, camel milk has a high storage
room temperature capacity as compared to milk from other animals (Omer
and Eltinay, 2009
). It has no allergic properties and can be consumed by lactase-deficient
individuals and those with a weakened immune system (Inayat
et al., 2003
; Yateem et al., 2008
In fact, this milk is believed to have medicinal properties. In Sahara, fresh
butter made from camel milk is often used as a base for medicines. Other products
also developed from camel milk include cosmetics or pharmaceuticals. A series
of metabolic and autoimmune diseases are successfully being treated with camel
milk. Furthermore, in India, camel milk is used therapeutically to treat dropsy,
jaundice, problems of spleen, tuberculosis, asthma, anemia, piles and diabetes
(Rao et al., 1970
). Furthermore, a beneficial effect
of raw camel milk has been observed in chronic pulmonary tuberculosis patients
(Mal et al., 2001
). Also, in repeated trials, a
30-35% reduction in daily insulin dose required by patients with type I diabetes
was observed in response to treatment with raw camel milk (Agarwal
et al., 2002
In the present study, we investigated the treatment and protective effects of camel milk against CCl4-induced hepatotoxicity in rats by assaying liver function test enzymes (ALT, AST), alkaline phosphatase (ALP) and protein, albumin, lipid synthetic functions of liver.
MATERIALS AND METHODS
This study was carried out in four months from Jan.-Apr., 2010
Chemicals and kits: Diagnostic kits for serum alanine aminotransferase (ALT) and aspartate amino transferase (AST), alkaline phosphatase (ALP), albumin, total protein and Cholesterol were purchased from Biosystems, Barcelona (Spain). Paraffin oil was purchased from Winlab, UK and carbon tetrachloride purchased from E. Merck, Darmstadt, Germany. All other chemicals and solvents were of highest grade commercially available.
Camel milk: Camel milk samples were collected daily early in the morning from Alsalman camel milk farms in the Buraidah area of Qassim (central Saudi Arabia). Milk was collected from camels by hand milking as normally practiced by the farmers. The samples were collected in sterile screw bottles and kept in cool boxes until transported to the laboratory. The rats were given this fresh milk (400 mL/24 h/cage) as such without any further treatment.
Animals and treatment: Male albino wister rats (200-250 g) were obtained
from College of Pharmacy, King Saud University, Riyadh and acclimated for at
least 7 day before starting the experiment. All animals were housed in standard
aluminum cages (4 rats cage-1), feeding with standard laboratory
diet and tap water ad libitum. The experimental animals were housed in
air-conditioned rooms at 21-23°C and 60-65% of relative humidity and kept
on a 12 h light/dark cycle. The animals received humane care in accordance with
the Guide for the Care and Use of Laboratory Animals, published by the US National
Institute of Health.
Experimental groups and protocol: The rats were divided randomly into 5 groups comprising eight rats in each group as follows:
||Control rats fed only with diet and tap water
||Rats fed with standard diet and camel milk
||Disease control group intoxicated with CCl4 and fed with tap
water and diet
||Rats intoxicated with CCl4 on first two days of the experimental
month and then treated with camel milk
||Rats fed with camel milk and diet and intoxicated with CCl4
on the last two days of the experimental month
Induction of hepatotoxicity by CCl4: Liver disease was induced by the intraperitoneal injection of CCl4 (1 mL kg-1 b.wt.), 1:1 diluted with paraffin oil, for two successive days of the experiment. Group III received CCl4 injections on first two successive days of the month and were given tap water and standard rat feed for one month of experimental course. Similarly, Group IV rats received CCl4 injection on first two days of the experimental month but were fed with fresh and raw camel milk (400 mL/day/cage) to study the protective role of camel milk. One more group, Group V rats were fed with camel milk first for one month and then were injected with CCl4 on last two consecutive days to study how much this group resists the toxic effects caused by CCl4 intoxication. Group I and II were injected with paraffin oil only as a vehicle.
Blood and tissue collection: At the end of day 30, 24 h after the last CCl4 injection, the animals were sacrificed by cervical dislocation and the blood samples were collected directly into tubes and it was allowed to clot at room temperature for 30 min and the serum was separated by centrifugation at 1000x g for 15 min at 4°C and were saved in aliquots and stored at -80°C for further analysis. The liver was also quickly removed and washed with cold normal saline, cut and preserved in 10% neutral formalin for the pathological studies for microscopy.
Serum biochemistry: ALT, AST and ALP serum activities were measured to assess hepatotoxicity by CCl4. Protein; albumin and cholesterol activities were also measured using spectrophotometric diagnostic kits as previously described.
Histopathological examinations: Liver tissues were cut in small pieces
and placed in plastic cassettes and immersed in neutral buffered formalin for
24 h. The fixed tissues were processed routinely, embedded in paraffin, sectioned,
deparaffinized and rehydrated using the standard techniques (Bancroft
and Gamble, 2002). The extent of CCl4-induced necrosis was evaluated
by assessing the morphological changes in the liver sections stained with hematoxylin
and eosin (H and E), using standard techniques.
Statistical analysis: Results were expressed as Means±standard deviation of three replicates. The significance of differences was calculated by using student t-test p<0.05 was considered statistically significant.
CCl4 is a frequently used model substance for hepatotoxicity studies
(Weber et al., 2003). The acute toxicity study
exhibited no mortality upto a dose level of 1000 μL kg-1 b.wt.
The hepatoprotective effects of camel milk feeding against CCl4 induced
hepatotoxicity was evaluated in rats. Group III rats exhibited significant increased
ALT level, which received CCl4 only without post treatment with camel
milks (disease control group). The level of ALT in this group was observed to
reach upto a level of 225±12.9 U L-1. Post treatments of rats
after receiving CCl4 intraperitoneal injections, with fresh and raw
camel milk (Group IV) resulted in dramatically decrease in ALT level but still
its level was almost double than the control water (Group I) rats (Fig.
1). In group II rats, which were fed with camel milk only, no significant
change in ALT and AST levels were observed when compared to control (Group I)
rats (Fig. 1, 2). Group V rats were selected
to study the immunity enhancement with camel milk prior to CCl4 intoxication.
We observed that camel milk results in enhanced immunity against CCl4
intoxication (Fig. 1, 2). So In group V
rats, pre-treatment with camel milk controlled the dramatic rise of aminotransferase
level after CCl4 exposure which clearly indicates that camel milk
protects the hepatocellular integrity.
AST level was also found to follow the similar pattern of results like ALT.
AST level was significantly high in group III rats as compared to control (Group
I) rats. Its level was significantly controlled in pre- and post-treated camel
milk rats (Fig. 2). In group II rats also no change in AST
level was found. The level of ALP increased significantly in CCl4
alone (Group III) animals (167.75±13.84 U L-1) when compared
to normal control (88.97±7.68 U L-1) (Fig. 3).
The total otein and albumin levels decreased considerably in the toxic group
(Group III) when compared to normal control group I rats. Induction of hepatotoxicity
in rats with CCl4 reduced the production of total proteins. But the
rats, which were pretreated with camel, milk after taking the injection of CCl4,
its level regained (Table 1). Similarly, the level of
serum albumin production significantly dropped in rats (group III) that received
CCl4 only. The level of serum albumin was found to approach normal
values in-group IV rats (Table 1).
||Alanine aminotransferase level in serum of different groups
of rats. Changes in ALT level in different groups of rats intoxicated with
CCl4 and treated with camel milk. Group 1 (normal control fed
on tap water only), Group II (rats fed on camel milk only), Group III (disease
control received CCl4 and fed on tap water) Group IV and V (post-and
pre- treated with camel milk after CCl4 injections). Data are
presented as the Mean±standard deviation for the three independent
values (n = 8)
||Aspartate aminotransferase level in serum of different groups
of rats. AST level in different groups of rats intoxicated with CCl4
and treated with camel milk. Group1 (normal control fed on tap water only),
Group II (rats fed on camel milk only), Group III (disease control received
CCl4 and fed on tap water) Group IV and V (received CCl4
and post- and pre-treated with camel milk). Data are presented as the Mean±standard
deviation for the three independent values (n = 8)
||Alkaline phosphatase level in serum of different groups of
rats. ALP levels in different groups of rats intoxicated with CCl4
and treated with camel milk. Group I represents normal control fed
on tap water only, Group II represents rats fed on camel milk only, Group
III represents rats intoxicated with CCl4 and fed with water
only, Group IV and V represents rats post- and pre-treated with camel milk
after CCl4 dose. Data are present as the Mean±SD of three
independent values (n = 8)
Furthermore, the cholesterol level in control group (group I) was found to
be 1.64±0.26 mmol L-1 and the cholesterol levels in the serum
were increased in the rats treated with CCl4 by about 37%. Camel
milk treatment caused the fall in this level to 1.87±0.34 mmol L-1
in Group IV rats (Table 1).
||Effect of Camel milk on serum protein, albumin and cholesterol
in rats intoxicated with CCl4
|Results are Mean±SD, n = 8, *p<0.05
||Photomicrographs of the histopathological studies of livers
of various groups of rats. Photomicrographs (original magnification 100x)
of the histopathological studies of livers of various groups stained with
hematoxylin and eosin (a) normal architecture of rat liver (b) architecture
of camel milk only fed rats (c) necrosis, fatty changes and hepatocellular
degeneration of CCl4 intoxicated groups (d) marked reduction
in fatty changes, inflammatory cell infiltration and necrosis (e) less damage
of hepatocytes and low index of necrosis in camel milk pre treated rats
The histopathological studies also supported the protective roles of camel
milk. The areas of necrosis and ballooning degeneration of hepatocytes were
observed in the toxic group with vacuolar fatty change and mild inflammatory
cell infiltration (Group III). The group of animals post treated with camel
milk showed a marked protective effects with decreased necrotic zones and hepatocellular
degeneration (Group IV). The liver of rats pretreated with camel milk (group
V) showed moderate necrosis with low presence of inflammatory cells (Fig.
4e). The photomicrographs of the liver sections of all the groups is shown
is Fig. 4a-e.
The liver is the major organ responsible for the metabolism of drugs and toxic
chemicals and therefore is the primary target organ for nearly all toxic chemicals
(Kaplowitz, 2000; Bissel et al.,
2001). Liver injury induced by CCl4 is the best characterized
system of the xenobiotic-induced hepatotoxicity and is a commonly used model
for the screening the anti-hepatotoxic and hepatoprotective activity of agents
(Recknagel et al., 1989; Brautbar
and Williams, 2002). A number of drugs, chemicals and viruses have been
reported to cause severe liver necrosis, which sometimes becomes difficult to
be managed by medical therapies. So it is important to search for compounds
that can be used for better management of the hepatic failure due to severe
Literature overview shows that most of the studies on camel milk show that
it is a high quality drink and since ancient times people have used this product
for curing a number of diseases (Shabo et al., 2005;
Agarwal et al., 2007; Redwan
and Tabll, 2007). The protective effects of camel milk could be attributed
to its antioxidant activity and it may possibly have chelating effects on toxicants
(Al-Humaid et al., 2010). It has been reported
that camel milk contains high levels of vitamins A, B2, C and E ahd is very
rich in magnesium (Mg) and other trace elements (Knoess,
1979). These vitamins are antioxidants that have been found in camel milk
are useful in preventing tissue injury caused by toxic agents. Mg protects cells
from heavy metals such as aluminum, mercury lead, cadmium, beryllium and nickel,
which explains why re-mineralization is so essential for heavy metal detoxification
and chelating. In fact, Mg deficiency has been associated with production of
Reactive Oxygen Species (ROS) (Martin et al., 2003).
Additionally, Mg protects cells against oxyradical damage and assists in absorption
and metabolism of vitamin B, C and E (Barbagallo et al.,
1999). Also, it has been reported that Mg is essential for biosynthesis
of gluthaione because the enzyme, gluthathion synthetase, requires γ-glutamyl
cysteine, glycine, ATP and Mg ions to form glutathione (Minnich
et al., 1971).
Additionally, camel milk is rich in zinc (Zn) (Knoess,
1979), which is a trace element essential for living organisms. More than
300 enzymes require Zn for their activity. It also plays an important role in
DNA replication, transportation and protein synthesis, influencing cell division
and differentiation (Frederickson, 1989). It has been
noted that Zn has a relationship with many enzymes in the body and can prevent
cell damage through activation of the antioxidant system (Powell,
2000; Ozturk et al., 2003; Ozdemir
and Inanc, 2005). Zinc is an essential component of the oxidant defense
system and function at many levels (Sato and Bremner, 1993).
One study has shown that a diet deficient in zinc paves the way for cell damage
in the rat testis (Cai et al., 2001). Furthermore,
Zn deficiency increase lipid peroxidation in various rat tissues, wheras the
Zn supplementation corrects this increase (Shaheen and El-Fattah,
In the present study, we used the murine model of CCl4-induced liver injury to investigate the hepatoprotective effects of camel milk. Since, many cases of acute toxic liver damages are triggered by free radical formation and further driven by local inflammatory response, potent antioxidant and inflammatory properties of camel milk seems to be protective during these conditions.
The results of the present study show that CCl4 administration causes
severe acute liver damage in rats demonstrated by remarkable elevation of serum
ALT, AST and ALP levels (Fig. 1-3). The
increased serum levels of AST and ALT have been attributed to a damaged structural
integrity of the liver. This is because they are intracellular enzymes, released
into circulation after hepatocyte damage or necrosis (Sallie
et al., 1991). These findings were also confirmed by histological
observations (Fig. 4c). The changes mostly include hepatocellular
necrosis or apoptosis, fatty accumulation, inflammatory cells infiltration and
other histological manifestations which were also consistent with the findings
of other authors (Brattin et al., 1985; Sun
et al., 2001).
Pre-treatment and post-treatment with camel milk could ameliorate CCl4-induced
hepatotoxicity in rats, as demonstrated by the lower serum aminotransferase
activities. This effect is in agreement with the commonly accepted view that
serum levels of transaminases return to normal with the healing of hepatic parenchyma
and regeneration of hepatocytes (Thabrew et al.,
Our results were in agreement with Kumar et al.
(2009) who found that the groups of rats which received the pre-treatment
of T. cucumerina (a cucurbitaceae medicinal plant) extract significantly
controlled the change in the biochemical parameters. The extract exhibited a
sharp decrease in the serum enzyme levels and the effect was comparable with
the standard group. Pretreatment of rats with camel milk prior to CCl4
intoxication (group V) (Fig. 1,2,3)
were found to have less rise in serum aminotransferases and alkaline phosphatase
levels after CCl4 intoxications. So camel milk consumption has some
protective effects and enhances the defence system. Our results were also in
agreement with Cuciureanu et al. (2009) who found
that the groups of rats, which received pre-treatment of montelukast sodium
before the administration of CCl4 intoxication, exhibited statistically
significant lower levels of ALT, AST, TB and MDA in blood and liver homogenate
as compared to the groups that received CCl4 only. Similarly, Shen
et al. (2009) reported that Z. jujube fruit administration
prior to CCl4 intoxication significantly decreased ALT and AST and
attenuated histopathology of hepatic injury and ameliorated the oxidative stress
in hepatic tissue as compared to the groups of rats who received CCl4
In conclusion, camel milk shows a significant role in hepatoprotective effects on acute liver toxicity induced by CCl4. Camel milk seems to be a beneficial drink for the prevention of acute liver toxicity, although further studies are necessary.
Authors would like to acknowledge Tariq Ayub and Ali Babekar Yousuf for their participation in preparation of slides and imaging. Deanship of Scientific Research, Qassim University is acknowledged for financial assistance. Also we are keenly thankful to King Saud University for providing us with the animal models. Finally, we are grateful for Alsalman farms for their constant supply of freshly camel milk samples.
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