In vivo Antioxidant Potential of Momordica charantia Against Cyclophosphamide Induced Hepatic Damage in Rats
Cyclophosphamide (CP) is one among the important anti-cancer drug that could
cause hepatotoxicity due to its toxic metabolites. In the present study, in
vivo antioxidant efficacy of Momordica charantia against CP induced
liver injury in Wistar rats was evaluated. Hepatic damage in rats was induced
by injecting CP i.p. (total of 200 mg kg-1 b.wt.) for 2 days. Protective
effect of aqueous extract of Momordica charantia (MCE) was evaluated
by assessing enzymic antioxidants (superoxide dismutase, catalase, glutathione
peroxidase, glutathione-S-transferase and glutathione reductase) and lipid peroxidation
in liver and non-enzymic antioxidants (glutathione, vitamin C and vitamin E)
in serum. Administration of MCE (300 mg kg-1 b.wt.) orally for 12
days restored the activities of enzymic antioxidants in liver. Non-enzymic antioxidants
were restored to normal level with a concomitant normalized level of lipid peroxidation
that could be achieved due to the secondary metabolites, vitamins and minerals
content of Momordica charantia. Results of the present study evidenced
that supplementation of MCE protected hepatic tissues from oxidative damage
induced by CP, due to its protective and antioxidant effects.
to cite this article:
Subramanian Senthilkumar, Narayanasamy Nithya, Venkatesan Ganesan and Kalichamy Chandrakumar, 2012. In vivo Antioxidant Potential of Momordica charantia Against Cyclophosphamide Induced Hepatic Damage in Rats. International Journal of Biological Chemistry, 6: 89-96.
Received: June 29, 2012;
Accepted: September 05, 2012;
Published: October 03, 2012
Liver is the major site of intense metabolic activities which plays a pivotal
role in the removal of substances from the portal circulation that makes it
susceptible to damage by offending foreign compounds (Barriault
et al., 1998). Cyclophosphamide (CP) is the most often applied chemotherapeutic
agent in cancer and reported to cause liver injury among antitumor agents (Friedman
et al., 2003; Senthilkumar et al., 2006a).
It is catabolised to acrolein and phosphoramide mustard that causes alterations
in cell membrane integrity through lipid peroxidation resulting in hepatic damage
(Wilmer et al., 1990). Medicinal plants and folk
medicine usage has been in practice for long time in the treatment of diseases
such as jaundice, diabetes, diarrhea, arthritis, skin ulcers, gastrointestinal
disturbances etc. (Joseph and Raj, 2011; Sayyad
et al., 2011; Joseph et al., 2012).
Plant based natural compounds may provide protection against CP induced toxicities
(Senthilkumar et al., 2006b; Nithya
et al., 2012; Sati et al., 2010).
Medicinal plants have been reported to contain large amounts of antioxidants
that prevent the oxidative stress catalyzed by the free radicals (Velioglu
et al., 1998). Momordica charantia (bitter melon) is an
herbaceous plant belongs to the family Cucurbitaceae which is used as a food
as well as medicine (Nithya et al., 2012). Nutritional
content of M. charantia such as vitamin C and minerals magnesium, calcium,
sulphur, copper and other trace elements were documented (Ullah
et al., 2011; Ayoola et al., 2010).
In vitro antioxidant and free radical scavenging activities has been
evaluated in the aqueous and ethanolic extracts of wild variety of M. charantia
(Wu and Ng, 2008). Treatment with bitter melon was found
to lower blood glucose levels (Lotlikar and Rajarama Rao,
1966). Extract of this plant exert antibacterial, antineoplastic, antiviral
and antimutagenic properties (Guevara et al., 1990).
Although, M. charantia has been widely used as folk medicine and health
food, no scientific investigation had been reported regarding its in vivo
antioxidant efficacy against CP intoxicated hepatic damage. Therefore, the present
investigation has been designed to study the in vivo antioxidant potential
of aqueous extract of Momordica charantia (MCE) in CP induced liver damage.
MATERIALS AND METHODS
Drug and plant material: Cyclophosphamide (Ledoxan) was procured from Dabur
Pharma limited, New Delhi, India. All other chemicals used were of highest purity
and in analytical grade. Present study was carried out between August 2007 and
April 2008. An authentic sample of Momordica charantia fruits (unripened
edible part usable as a vegetable food) was collected in and around the farms
of Thudiyalur, Coimbatore, India, in the month of August 2007. Edible part of
the fruit (without seeds) was shade dried and coarsely powdered. Extraction
was carried out using sterile warm drinking-water for 30 h to get MCE.
Experimental animals: Wistar strain of male albino rats weighing 200±10
g were obtained from animal breeding center, Mannuthi, Kerala were used for
the study. Animals were housed in polypropylene cages under standard conditions
(25±5°C, humidity 60-70%, 12 h light: Dark cycles). Animals were
fed with standard pellet diet (AVM cattle and poultry feeds, Coimbatore, Tamil
Nadu, India) and drinking water ad libitum. Clearance from Institutional
Animal Ethics Committee was obtained prior to the experiment.
Dosage optimization: MCE dose that have maximum efficiency in a minimum
dosage determined by serum marker enzymes for tissue damage was found to be
300 mg kg-1 b.wt. (Nithya et al., 2012).
This dose was used for the whole of the present study.
Animal treatments: Rats were divided into three groups of 6 animals
||Group I: Control treated with normal saline
||Group II: Toxicity induced with CP (200 mg kg-1 b.wt.
i.p. on 2 days)
||Group III: Rats injected with cyclophosphamide (200 mg kg-1
b.wt. i.p. on 2 days) and treated with MCE (300 mg kg-1 b.wt.
p.o.) for 12 days
No drug control animal group has been maintained due to the non-toxic and edible
nature of MCE that has been proved previously (Nithya et
al., 2012). At the end of experimental period, the animals were sacrificed
by cervical decapitation after overnight fasting. Serum was isolated from blood
for biochemical assays. Liver tissue were immediately washed with ice-cold physiological
saline and homogenized in 0.1 M tris-HCl buffer (pH 7.4) and aliquots were used
for the assays.
Enzymic and non-enzymic antioxidants assays: Tissue enzymic antioxidants
such as superoxide dismutase (SOD) (Marklund and Marklund,
1974), catalase (Sinha, 1972), glutathione peroxidase
(GPx) (Rotruck et al., 1973), Glutathione Reductase
(GSH) (Beutler, 1984) and glutathione-s-transferase (GST)
(Habig et al., 1974) and serum non-enzymic antioxidants
that include glutathione (GSH) (Ellman, 1959), Vitamin
C (Omaye et al., 1979) and Vitamin E (Quaife
and Dju, 1949) were analyzed. Lipid peroxidation (Niehaus
and Samuelsson, 1968) was determined in the tissue homogenate.
Statistical analysis: Results were expressed as Mean±SD. Significant
difference between the groups was analyzed by one-way analysis of variance (ANOVA)
followed by post-hoc Least Significant Difference (LSD) test. A p<0.05 value
was considered statistically significant.
Table 1 represents the effect of MCE on the levels of enzymic
antioxidants in the liver of control and experimental groups of rats. Levels
of free radical detoxifying enzymes like SOD and CAT were decreased in the liver
during CP intoxication. Also, enzymes such as GPx, GR and GST that were involved
in the removal of products released by the above enzymes and augmented conjugation
with GSH for detoxification were found decreased during CP intoxication. On
the contrary, lipid peroxidation in CP intoxicated liver (Fig.
1) revealed a 3-fold significant increase in malondialdehyde (MDA) level,
when compared to control group. Supplementation of MCE was able to restore these
altered levels of antiperoxidative enzymes and MDA in the liver of experimental
|| Activities of enzymic antioxidants in the liver of experimental
groups of animals
|Results were expressed as Mean±SD, for six rats, SOD:
50% inhibition of nitrite formed/min/mg protein, CAT: μM of H2O2
decomposed/min/mg protein, GPx: μg GSH oxidized/min/mg protein, GR:
nM NADPH oxidized/min/mg protein and GST: nM CDNB conjugated/min/mg protein,
GSH: Reduced glutathione, NADPH : Reduced nicotinamide adenine dinucleotide
phosphate, CDNB: 1-Chloro-2,4-dinitrobenzene, *Comparison: CP with control
and CP+MCE with CP, Significant at p<0.05
||Levels of MDA in the liver of experimental groups of animals,
results were expressed as Mean±SD, for six rats, *Comparison: CP
with control and CP+MCE with CP, Significant at p<0.05
||Levels of GSH in the liver of experimental groups of animals,
results were expressed as Mean±SD, for six rats, *Comparison: CP
with control and CP+MCE with CP, Significant at p<0.05
|| Levels of vitamin C and E in the serum of experimental groups
|Results were expressed as Mean±SD for six rats, *Comparison:
CP with control and CP+MCE with CP, Significant at p<0.05
Administration of CP significantly decreased the levels of GSH (Fig.
2), Vitamin C and Vitamin E (Table 2) in the serum as
compared to control. Treatment with MCE resulted in a significant restoration
of the levels of the above non-enzymatic antioxidants.
Cyclophosphamide is a commonly used chemotherapeutic drug and well-known mutagen
and clastogen (Mohn and Ellenberger, 1976; Edwin
et al., 2002). It is an alkylating agent, producing the highly active
carbonium ion, which reacts with the extremely electron-rich area of nucleic
acids and proteins (Hochstein and Utley, 1968). Oxidative
stress induced by CP causes disturbances in the antioxidant state of the cell
leads to lipid peroxidation, protein and carbohydrate oxidation and metabolic
disorders (Pryor and Godber, 1991; Adesegun
et al., 2007). The products of lipid peroxidation such as MDA were
toxic to cells causing a devastating effect on the functional status and it
is a useful indicator of tissue damage (Raleigh, 1988;
Ohkawa et al., 1979).
Increase in LPO levels in liver induced by CP suggests enhanced lipid peroxidation
leading to tissue damage and decreased antioxidant defenses in liver (Seven
et al., 2004). Treatment with MCE showed significant protection towards
these abnormalities. This could be probably due to the hepatoprotective and
antioxidant effect of MCE.
SOD scavenges superoxide anion and reduces the toxic and deleterious effects
of the free radical. Decreased enzymatic activity of superoxide dismutase is
the most sensitive index in hepatocellular damage (Curtis
et al., 1972; Jayakumar et al., 2006).
Treatment with MCE restored SOD activity suggesting an efficient protective
role against Reactive Oxygen Species (ROS). Catalase decomposes H2O2
and protects the tissue from highly reactive hydroxyl radicals (Chance
et al., 1952). The antioxidant enzymes SOD, CAT and GPx act in coordination
to combat the formed ROS (Senthilkumar et al., 2006c)
and are directly involved in elimination of free radicals (Sabina
and Rasool, 2007). Reduction in the activity may be due to the accumulation
of free radicals causing deleterious effects to these enzymes and loss in protective
mechanism. Restoration of enzyme activities near to normal was seen in the treatment
of MCE. These findings showed that MCE could be useful to decrease oxidative
stress and lower the free radical-mediated tissue damage.
GPx is a selenium dependant enzyme have high potency in scavenging highly reactive
free radicals. A specific isozyme, phospholipid hydroperoxide glutathione peroxidase,
is the only major antioxidant enzyme that directly reduces phospholipid hydroperoxides
within membrane and lipoproteins and act together with alpha-tocopherol (vitamin
E) to inhibit lipid peroxidation (Maiorino et al.,
1991). Decrease in the activity of GPx may be due to the inactivation of
enzyme involved and insufficient availability of GSH (Venukumar
and Latha, 2002; Senthilkumar et al., 2006c).
Also, decrease in the activity of glutathione-s-transferase may be due to the
depletion in the content of glutathione in liver (Senthilkumar
et al., 2006a). Glutathione Reductase (GR) is the pivotal enzyme
for maintaining and regenerating the reduced levels of glutathione in vivo
(Senthilkumar et al., 2006b). Decrease in the
GR activity was observed in CP treatment (Senthilkumar et
al., 2006c). Restoration of the activities of these enzymes after the
administration of MCE supported its protective efficacy.
Glutathione is one of the most abundant non-enzymatic antioxidant present in
the cytosol (Valko et al., 2007). Its function
is concerned with the removal of free radical species (Struznka
et al., 2005). The depletion of GSH content in serum has to be associated
with an enhanced toxicity to chemicals including CP (Reed
and Farris, 1984; Senthilkumar et al., 2006c).
Constituents such as alkaloids, saponin, sterols, steroids, glycosides, pyrimidine
nucleoside, triterpenoids, phenolics and flavonoids has been reported to present
in M. charantia (Raman and Lau, 1996; Chen
et al., 2005, 2009; Asiamah
et al., 2011; Ullah et al., 2012).
Increase in the level of GSH during MCE administration could be due to the presence
of above constituents that helped to restore the activities of enzymic antioxidants
to prevent the tissue damage.
Vitamin C acts as a direct scavenger of free radicals and reductant in enzymatic
reactions (Nagel et al., 1997; Saalu
et al., 2010). Vitamin E is the main lipid soluble antioxidant in
membranes preventing lipid peroxidation (Fariss and Zhang,
2003). Vitamin C and Vitamin E acts synergistically in scavenging a wide
variety of ROS (Van Acker et al., 1996). Decreased
levels of vitamin C and vitamin E during CP intoxication could leads to increased
free radical damage (Lee, 1999). Significantly decreased
level of Vitamin E in CP might be due to the excessive utilization of this antioxidant
for the quenching of free radicals produced. The normalized levels of non-enzymic
antioxidants could be in-part due to its vitamin C and vitamin E content of
MCE (Wu and Ng, 2008; Ullah et
al., 2011) that helped to regenerate vitamins in vivo (Van
Acker et al., 1996). Glutathione is able to regenerate vitamin C
and E to their active form (Valko et al., 2007).
Increased level of glutathione due to supplementation of MCE could also have
contributed to the regeneration of vitamin C and E. These findings supported
the antioxidant nature of MCE.
Results obtained from the present study indicate that the MCE could be helpful
in exerting protection against cyclophosphamide-induced oxidative stress. This
study supported that CP intake induces hepatotoxicity evidenced from enhanced
lipid peroxidation and depletion of antioxidant reserves, while treatment with
MCE reverted the altered antioxidant status, thus supporting its hepatoprotective
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