Research Paper

Anticar
cinogenic and antilipidperoxidative effects of Tephrosia
Anticarcinogenic
purpurea (Linn.) Pers. in 7, 12-dimethylbenz(a)anthracene
(DMBA) induced hamster buccal pouch car
cinoma
carcinoma
K. Kavitha, S. Manoharan

ABSTRACT

Department of Biochemistry,
Faculty of Science,
Annamalai University
Annamalainagar - 608 002,
Tamil Nadu. India
Received: 11.1.2006
Revised: 21.3.2006
Accepted: 22.3.2006
Correspondence to:
S. Manoharan
E-mail : manshisak@yahoo.com

Objectives: To investigate the chemopreventive potential and antilipidperoxidative effects of ethanolic root extract of Tephrosia purpurea (Linn.) Pers. (TpEt) on 7,12dimethylbenz(a)anthracene (DMBA)- induced hamster buccal pouch carcinoma.
Materials and Methods: Oral squamous cell carcinoma was developed in the buccal
pouch of Syrian golden hamsters, by painting with 0.5% DMBA in liquid paraffin, thrice a
week, for 14 weeks. The tumor incidence, volume, and burden were determined. Oral
administration of TpEt at a dose of 300 mg/kg, b.w., to DMBA (on alternate days for
14 weeks)- painted animals significantly prevented the incidence, volume and burden of
the tumor.
Results: TpEt showed potent antilipidperoxidative effect, as well as enhanced the antioxidant status in DMBA- painted animals.
Conclusion: TpEt has potent chemopreventive efficacy and significant antilipidperoxidative
effect, in DMBA-induced oral carcinogenesis. Further studies are needed to isolate and
characterize the bioactive principle.
KEY WORDS: Chemoprevention, oral cancer, wild indigo.

Introduction
Oral squamous cell carcinoma, the fifth most common
malignancy worldwide, is predominantly a disease of men, in
the fifth to eighth decades of life. While it accounts for 3-4% of
all malignancies in western countries, India has recorded the
highest incidence, accounting about 30 - 40% of all cancers.
Cancer of the oral cavity are frequently associated with chewing
of betel quid containing tobacco, in addition to smoking and
alcohol consumption. [1] 7,12-dimethylbenz(a)anthracene
(DMBA)-induced hamster buccal pouch carcinogenesis, is a
well suited model for studying precancerous and cancerous
lesions of human oral squamous cell carcinoma, since it is
morphologically and histologically similar to human tumors,
as well as, it expresses many biochemical and molecular
markers that are expressed in humans. [2]
Lipid peroxidation, a potent reactive oxygen species (ROS)mediated chain reaction, has been implicated in the
pathogenesis of several disorders, including oral carcinoma.
Overproduction of reactive oxygen species within tissues can
damage DNA and possibly contribute to mutagenesis and
carcinogenesis. However, organisms have an array of potent
adaptive antioxidant defense mechanisms [enzymatic

antioxidants: superoxide dismutase (SOD), catalase (CAT) and

glutathione peroxidase (GPx) and non-enzymatic antioxidants:
reduced glutathione (GSH), vitamin C and vitamin E] within
the cells, to combat the deleterious effects of reactive oxygen
species- mediated oxidative damage.[3]
Cancer chemoprevention is a new promising strategy for
prevention, inhibition, or reversal of carcinogenesis, induced
by specific natural, or synthetic chemicals.[4] For a large number
of the worlds rural population, medicinal plants are the only
source for the prevention and treatment of various pathological
diseases, from time immemorial. Several medicinal plants and
their constituents have been reported, to prevent multistage
carcinogenesis.[5]
Tephrosia purpurea is a wild plant known as Sarapunkha
in Sanskrit, Purple tephrosia or Wild indigo in English and
Avuri or Kolinji in Tamil. T. purpurea has been used for
centuries in the Indian traditional medicine, for the treatment
of various inflammatory disorders. It is considered beneficial
for liver, spleen and kidney disorders. Also, it has the property
to cure all types of wounds.[6] Experimental studies suggest
that T. purpurea exerts antiulcer and antitumor promoting
effects.[7,8]
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Kavitha, et al.

To our best knowledge, there is no scientific report on the

chemopreventive efficacy and antilipidperoxidative effects of
T. purpurea in DMBA-induced, hamster buccal pouch
carcinogenesis. Hence, the present study is designed to
evaluate the effectiveness of ethanolic root extract of Tephrosia
purpurea (TpEt) in modifying the carcinogenic process, as well
as oxidative alterations in DMBA- induced hamster buccal
pouch carcinoma.
Materials and Methods
Chemicals
DMBA was obtained from Sigma-Aldrich Chemical Pvt. Ltd.,
Bangalore, India. All other chemicals used were of analytical
grade.
Animals
Male, golden Syrian hamsters 8-10 weeks old, weighing
80-120 g, were purchased from National Institute of Nutrition,
Hyderabad, India and maintained in the Central Animal House,
Rajah Muthaiah Medical College and Hospital, Annamalai
University. The animals were housed in groups of four or five
in polypropylene cages and provided standard pellet diet and
water ad libitum and maintained under controlled conditions
of temperature and humidity, with a 12 h light/dark cycle.
Plant material
Tephrosia purpurea was collected in and around Annamalai
University, Annamalai Nagar, Tamil Nadu, India, authenticated
by Botanist, R. Panneer Selvam, Department of Botany,
Annamalai University and a voucher specimen (AUO5102) was
also deposited.
Preparation of plant extract
500 g of dried finely powdered T. purpurea roots were
soaked with 1500 ml of 95% ethanol, overnight. The residue
obtained was again resuspended in equal volume of 95%
ethanol for 48 h and filtered again. The above two filtrates
were mixed and the solvents were evaporated in a rotovapour
at 40-50C, under reduced pressure. A dark semisolid material
(13%) obtained, was stored at -4C, until use. For experimental
studies, a known volume of the extract was suspended in
distilled water and orally administered to the experimental
animals by gastric intubation, using force-feeding needle.
Experimental protocol
The institutional animal ethics committee approved the
experimental design. The hamsters were randomized into four

groups of 10 animals each. Group I served as untreated control.

Groups II and III were painted with 0.5% DMBA in liquid paraffin
thrice a week, for 14 weeks on the left buccal pouches. Group
II received no other treatment. Group III were administered
TpEt (300 mg/kg, b.w.), orally starting 1 week before the
exposure to the carcinogen and continued on days alternate
to DMBA painting, until the animals are sacrified. Group IV
received oral TpEt, only throughout the experimental period.
The experiment was terminated at the end of 14 weeks and all
the animals were sacrificed by cer vical dislocation.
Biochemical studies were conducted on blood and buccal
mucosa of control and experimental animals, in each group.
For histopathological examination, buccal mucosal tissues
were fixed in 10% formalin and embedded with paraffin,
2-3 m sections were cut in a rotary microtome and stained
with haematoxylin and eosin.
Biochemical analysis
The erythrocyte membrane was prepared by the method
of Dodge et al, [9] modified by Quist. [10] Thiobarbituricacid
reactive substances (TBARS) was assayed in plasma,
erythrocytes and buccal mucosa, according to the methods
of Yagi,[11] Donnan[12] and Ohkawa et al,[13] respectively. Reduced
glutathione (GSH) was determined by the method of Beutler
and Kelley.[14] Vitamin C and E were measured according to
the methods of Omaye et al[15] and Desai,[16] respectively. The
enzymatic antioxidant activities were estimated by the
methods of Kakkar et al, [17] (SOD), Sinha [18] (CAT) and
Rotruck et al [19] (GPx), respectively.
Statistical analysis
Values are expressed as meanSD. Statistical analysis was
performed by one-way analysis of variance (ANOVA), followed
by Duncans multiple range test (DMRT). The values were
considered statistically significant, if P was less than 0.05.
Results
Table 1 depicts the effect of TpEt on the incidence, volume
and burden of tumor in DMBA- induced hamster buccal pouch
carcinoma. In DMBA- painted hamsters (Group II), a 100%
tumor formation with mean tumor volume (472 mm3) and
tumor burden (2029 mm3), was observed. Oral TpEt (300 mg/
kg, b.w.) significantly prevented the incidence, volume and
burden of tumor in DMBA- painted hamsters (Group III). No
tumor was observed in control (Group I) as well as TpEt alone
treated animals (Group IV).

Table 1
Effect of oral Tephrosia purpurea on squamous cell carcinoma in 0.5% DMBA painted golden Syrian hamsters
Parameters

Control

0.5% DMBA

0
0
0
0

100%
43/(10)
472.41 57.33
2029.61 172.75

Tumor incidence
Total number of tumors
Tumor volume (mm 3)
Tumor burden (mm 3)

Values are mean+SEM; n=10 in each group. Tumor volume was measured using the formula V =

0.5% DMBA+TpEt
(300 mg/kg)
20%
4/(2)
97.96 13.07
194.92 26.14
4
D
1
3
2

D2

D3

TpEt alone
(300 mg/kg)
0
0
0
0

where D 1, D 2 and D 3 are the three

diameters (mm) of the tumor. Tumor burden was calculated by multiplying tumor volume and the number of tumors/animal. Number in parentheses indicates
total number of animals bearing tumors. TpEt was administered orally (300 mg/kg) 1 week before DMBA painting and continued on alternate days to DMBA
painting until sacrifice. DMBA (0.5% in liquid paraffin) was painted on the left buccal pouches thrice a week for 14 weeks.

186

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Anticarcinogenic effect of Tephrosia purpurea

Table 2
Histopathological changes in oral cheek mucosa of TpEt treated and DMBA painted golden Syrian hamsters
Parameters
Keratosis
Hyperplasia
Dysplasia
Squamous cell carcinoma

Control

DMBA

DMBA+TpEt

TpEt alone

Absent
Absent
Absent
Carcinoma

Severe
Severe
Severe
Moderately differentiated

Moderate
Mild
Mild
No carcinoma

Absent
Absent
Absent
Carcinoma

n=10 in each group. TpEt was administered 1 week before and continued on alternate days to DMBA painting until sacrifice. DMBA (0.5% in liquid paraffin) was painted on
the left buccal pouches thrice a week for 14 weeks.

Table 3
Plasma TBARS and antioxidant status in TpEt treated and DMBA painted golden Syrian hamsters
Parameters

TBARS
(nmoles/ml)

GSH
(mg/dl)

Vitamin C
(mg/dl)

Vitamin E
(mg/dl)

SOD
(U*/ml)

CAT
(U**/ml)

Control
DMBA
DMBA + TpEt
TpEt alone

2.97 0.25 a
4.64 0.41b
3.41 0.36c
2.84 0.16a

28.88 2.4 a
19.71 1.31b
25.65 2.2c
30.21 2.8a

1.48 0.12 a
0.86 0.08 b
1.25 0.11c
1.50 0.12a

1.21 0.12 a
0.700.07b
1.080.10c
1.280.12a

2.87 0.22 a
1.760.19 b
2.580.20c
2.960.23a

0.43 0.04 a
0.270.02 b
0.380.03 c
0.450.04 a

133.8 12.2 a

98.3 8.6b

126.4 11.8c

138.2 12.3a

70.251
3, 36
<0.05

58.215
3, 36
<0.05

60.312
3, 36
<0.05

56.575
3, 36
<0.05

22.246
3, 36
<0.05

One-way
ANOVA

F
df
P

63.431
3, 36
<0.05

39.230
3, 36
<0.05

GPx
(U***/l)

Values are expressed as mean SD for 10 animals in each group. *The amount of enzyme required to inhibit 50% NBT reduction. **Micromoles of H2O2 utilized/sec.
***Micromoles of glutathione utilized/min. Values not sharing a common superscript letter differ significantly at P <0.05 (DMRT). DMBA (0.5% in liquid
paraffin) was painted on the left buccal pouches thrice a week for 14 weeks. TpEt was administered 1 week before and continued on alternate days to DMBA
painting until sacrifice.

Table 4
TBARS and antioxidants status in erythrocytes of TpEt treated animals
Parameters

Erythrocyte
TBARS
(pmoles/mg Hb)
1.90 0.18a
2.65 0.22b
2.16 0.19c
1.82 0.16a

Control
DMBA
DMBA + TpEt
TpEt alone
One-way
ANOVA

F
df
P

29.207
3, 36
<0.05

Erythrocyte
membrane:
TBARS (nmoles/
mg protein)

Vitamin E
(g/mg
protein)

0.34 0.03a
1.2 0.11b
0.92 0.06c
0.51 0.04a

2.320.12a
1.480.09b
2.120.2c
2.400.21a

388.585
3, 36
<0.05

60.217
3, 36
<0.05

Erythrocytes
GSH
(mg/dl)
42.35 3.8a
29.67 2.6b
38.2 3.5c
44.56 3.2a
35.942
3, 36
<0.05

Erythrocyte
lysate: SOD
(U*/mg Hb)

CAT
(U**/
mg Hb)

GPx
(U***/
g Hb)

2.170.22a
1.450.12b
1.920.17c
2.280.20a

1.240.10 a
0.820.08 b
1.120.09 c
1.300.12 a

14.63 1.14a
7.58 0.62b
11.32 1.02c
15.74 1.26a

37.141
3, 36
<0.05

41.394
3, 36
<0.05

111.794
3, 36
<0.05

Values are expressed as mean SD for 10 animals in each group. *The amount of enzyme required to inhibit 50% NBT reduction. **Micromoles of H 2O 2
utilized/ sec. ***Micromoles of glutathione utilized/min. Values not sharing a common superscript letter differ significantly at P<0.05 (DMRT). DMBA (0.5%
in liquid paraffin) was painted on the left buccal pouches thrice a week for 14 weeks. TpEt was administered 1 week before and continued on alternate days
to DMBA painting until sacrifice.

Table 2 shows the histopathological features of control

and experimental animals in each group. A myriad of
histopathological changes (severe keratosis, hyperplasia,
dysplasia and squamous cell carcinoma of the epithelium),
were observed in hamsters painted with DMBA alone (Group
II). A mild to moderate preneoplastic lesions [hyperplasia
(++), keratosis (+) and dysplasia (+)], were noticed in Group
III animals (DMBA + TpEt).
Tables 3 and 4 show the status of TBARS and antioxidant
in plasma and erythrocytes of the control and experimental

groups. The concentration of TBARS was increased, whereas

the levels of nonenzymatic antioxidants (GSH, Vitamin C and
Vitamin E) and activities of enzymatic antioxidants (SOD, CAT
and GPx), were significantly decreased in group II (DMBA
alone), as compared to control animals. Oral administration
of TpEt significantly decreased the levels of TBARS and
improved the antioxidants status in DMBA- painted hamsters.
TpEt alone- treated hamsters showed no significant difference
in TBARS and antioxidants status, as compared to control
animals.
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Kavitha, et al.

Table 5
Buccal mucosa TBARS and antioxidants status in TpEt DMBA painted golden Syrian hamsters
Parameters

TBARS (nmoles/
100mg protein)

GSH (mg/
100 g tissue)

Control
DMBA
DMBA + TpEt
TpEt alone

76.4 5.45 a
51.5 3.61b
69.2 5.23c
77.8 6.2a

8.52 0.72 a
12.020.96b
9.320.74c
8.480.85a

One-way
ANOVA

F
df
P

48.467
3, 36
<0.05

36.850
3, 36
<0.05

Vitamin E(mg/
100 mg tissue)
1.94 0.17 a
2.85 0.19b
2.28 0.27c
1.87 0.12a
45.992
3, 36
<0.05

SOD (U*/mg
protein)

CAT (U**/mg
protein)

GPx (U***/g
protein)

5.43 0.36 a
3.800.31b
4.860.38c
5.620.43a

38.2 2.9 a
24.4 1.8b
33.0 2.21c
39.5 2.1a

6.36 0.5 a
9.370.58 b
7.040.49 c
6.280.60a

43.533
3, 36
<0.05

80.143
3, 36
<0.05

63.868
3, 36
<0.05

Values are expressed as meanSD for 10 animals in each group. *The amount of enzyme required to inhibit 50% NBT reduction. **Micromoles of H2O2 utilized/
sec. ***Micromoles of glutathione utilized/min. Values not sharing a common superscript letter differ significantly at P<0.05 (DMRT). TpEt (300 mg/kg, oral)
was administered 1 week before and continued on alternate days to DMBA painting until sacrifice. DMBA (0.5% in liquid paraffin) was painted on the left
buccal pouches thrice a week for 14 weeks.

Table 5 indicates the concentration of TBARS and

antioxidants status, in the buccal mucosa of all animal groups.
Decrease in TBARS concentration and alterations in the
antioxidant status (Vitamin E, GSH and GPx were increased;
SOD and CAT were decreased), were noticed in cancer animals
(Group II) as compared to control (Group I). However, oral
administration of TpEt (Group III), reverted the concentration
of TBARS and antioxidants to near normal range in DMBA
painted animals.Hamsters treated with TpEt alone (Group IV)
showed no significant difference in TBARS and antioxidants
status, as compared to control animals.
Disscusion
The incidence and mortality rates of oral cancer vary widely
across the world, but the highest rates were reported every
year from developing countries, particularly from India. Oral
cancer is one among the few human cancers, with the vast
potential for prevention. A major target of reactive oxygen
species is cell membrane, due to the high content of
polyunsaturated fatty acids. Reactive oxygen species mediated
lipid peroxidation causes damage to cellular DNA, membrane
structure and inhibition of functions several enzymes and
alterations in the immune system.[20] In cancer, enormous
production of free radicals in the system has been reported. A
close relationship between free radical activity and neoplastic
transformation, has been shown.[21] Antioxidants (enzymatic
and non-enzymatic) play a vital role in scavenging reactive
oxygen species and protect the cells from oxidative damage.
Vitamin E, Vitamin C and reduced glutathione, are primary
defense antioxidants. They provide protection against several
reactive oxygen species, development of cancer and other
oxidative stress- mediated dysfunctions.[3] SOD, CAT and GPx,
are important antioxidant enzymes that protect cell and tissue
damage from enhanced lipid peroxidation, via elimination of
reactive oxygen species.
Elevated lipid peroxidation and poor antioxidant systems,
have been reported in oral cancer patients. Sabitha and
Shyamaladevi[22] have suggested, that a lack of antioxidant
defense is responsible for the elevated lipid peroxidation in
erythrocytes. Altered activities of enzymatic antioxidants are
reported during carcinogenesis, or after tumor formation.

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Hence, the elevated lipid peroxidation in the circulation of

cancer animals, is due to poor antioxidant defense mechanism.
Lowered nonenzymatic antioxidants (Vitamin C, Vitamin E and
GSH) in the circulation, are probably due to elevated lipid
peroxidation or sequestration by the tumor tissues for their
rapid growth.
Diminished lipid peroxidation and disturbed antioxidants
status (GSH and GPx were increased, whereas SOD and CAT
were decreased), were observed in tumor tissues, as compared
to normal tissues. Cancer cells showed decreased
susceptibility to lipid peroxidation, compared to normal
tissues. An inverse relationship between the lipid peroxidation
process and the rate of cell proliferation, has been reported.[23]
Glutathione, a biologically important tripeptide, is essential
for maintaining cell integrity, due to its reducing properties
and participation in the cell metabolism. Glutathione
peroxidase and its co-substrate glutathione, are reported to
have regulatory effects on cell proliferation. Elevated
glutathione and GPx activity, have been demonstrated in
several tumor tissues, including oral cancer. Subapriya
et al [23] have postulated that diminished lipid peroxidation
combined with enhanced glutathione-dependent antioxidant
capacity of oral tumors, facilitates cell- proliferation, offering
selective growth advantage in tumor cells over their
surrounding normal cells. Our results lend credibility to the
above observations. Decrease in SOD and catalase activities
described in tumors, is regarded as markers of malignant
transformation. Lowered activities of SOD and CAT were
reported in several cancers, including oral cavity cancer. [22,23]
Our results corroborate these observations.
The painting of 0.5% DMBA in liquid paraffin thrice a week,
for 14 weeks to the hamster buccal pouch, induced oral
carcinoma. We have also noticed the precancerous lesions in
DMBA- painted hamsters, from the 10 th week of the
experimental period. In the present study, oral administration
of TpEt at a dose of 300 mg/kg, b.w., reduced tumor incidence,
volume, burden and the number in DMBA- painted hamsters.
Our results thus indicate, that TpEt possess significant
chemopreventive potential against DMBA- induced buccal
pouch carcinoma.

Anticarcinogenic effect of Tephrosia purpurea

Furthermore, TpEt significantly reduced the levels of

TBARS and enhanced the status of antioxidants in the
circulation of DMBA- painted hamsters. We also noticed an
elevation of TBARS level and improvement in antioxidant
defense system in the buccal mucosa of DMBA-painted
hamsters, after treatment with TpEt. Johnson[24] reported that
the chemopreventive properties of plant anticarcinogens are
either due to antilipidperoxidative action, modulating
carcinogen detoxification, or by improving the antioxidant
defense system. Sharma et al,[25] have proposed that several
medicinal plants and their constituents, probably exert their
chemopreventive effect, by scavenging reactive oxygen
species and improving the antioxidant defense systems. The
present study reveals, that the chemopreventive effect of TpEt
in DMBA- painted animals, is probably due to its
antilipidperoxidative and antioxidant properties.
Acknowledgments
The authors express sincere thanks to Dr. C.R. Ramachandran, Dean, Faculty
of Dentistry and Dr. A. Thangavelu, Professor, Faculty of Dentistry, Annamalai
University, Annamalai Nagar for their valuable support and help for this study.

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