ArticlePDF Available

Anti-cancer activity of Curcuma longa linn.(Turmeric). Journal of Pharmacy Research

Authors:

Abstract and Figures

Curcuma longa Linn. (Turmeric) is used extensively in Indian cuisine and now proved to be useful in treating various types of cancers, diabetic wounds, biliary disorders etc. So the anticancer activity of turmeric was evaluated prophylactically and therapeutically (as pre-induction treatment and post-induction treatment) against the MNU induced mammary tumors. The anticancer activity was assessed using latency period, tumor incidence, tumor burden, tumor volume, tumor growth inhibition, histology and hematological parameters. Oral administration of turmeric showed anticancer activity in a dose dependent manner and it was more in pre-induction treatment than in-post induction treatment groups. Topical application of turmeric was found to be more effective in pre-induction treatment and topical treatment was more effective when compared to oral treatment. Chemo-preventive role of turmeric was more compared effective than therapeutic role of turmeric.
Content may be subject to copyright.
Journal of Pharmacy Research Vol.4.Issue 4. April 2011
Annapurna A et al. / Journal of Pharmacy Research 2011,4(4),1274-1276
1274-1276
Research Article
ISSN: 0974-6943 Available online through
http://jprsolutions.info
*Corresponding author.
Annapurna Akula,
University College of Pharmaceutical Sciences,
Andhra University, Visakhapatnam,
A.P, India-530003
Anti-cancer activity of Curcuma longa linn.(Turmeric)
Annapurna A *, Suhasin G1, Raju B Akondi2, Jaya Prakash G1 , Siva Reddy Ch1
*1College of Pharmaceutical Sciences, Andhra University, Visakhapatnam, A.P, India-530003
2Department of Pharmacology and Toxicology,St.Peters Institute of Pharmaceutical Sciences [SPIPS],Vidya Nagar,Hanamkonda,Warangal,A.P,INDIA-506001
Received on: 05-12-2010; Revised on: 14-01-2011; Accepted on:09-03-2011
ABSTRACT
Curcuma longa Linn. (Turmeric) is used extensively in Indian cuisine and now proved to be useful in treating various types of cancers, diabetic wounds, biliary disorders etc. So the anticancer
activity of turmeric was evaluated prophylactically and therapeutically (as pre-induction treatment and post-induction treatment) against the MNU induced mammary tumors. The anticancer
activity was assessed using latency period, tumor incidence, tumor burden, tumor volume, tumor growth inhibition, histology and hematological parameters. Oral administration of turmeric
showed anticancer activity in a dose dependent manner and it was more in pre-induction treatment than in-post induction treatment groups. Topical application of turmeric was found to be more
effective in pre-induction treatment and topical treatment was more effective when compared to oral treatment. Chemo-preventive role of turmeric was more compared effective than therapeutic
role of turmeric.
Key words: Curcuma longa,anticancer activity,
Experimental Design:
The SD rats were randomly divided in to 7 groups. Number of animals varies from group to
group and it ranges from 12 animals to 24 animals. The details were given as follows. Group
1 (n = 15), Control group received MNU only, Group 2 (n = 12), Prophylactic treatment of
turmeric suspension (500mg/kg, P.O), Group 3 (n = 24), Prophylactic treatment of turmeric
suspension (1000mg/kg, P.O), Group 4 (n = 24), Prophylactic treatment of turmeric suspen-
sion (200mg/rat, topical), Group 5 (n = 12), Therapeutic treatment of turmeric suspension
(500mg/kg, P.O), Group 6 (n = 12), Therapeutic treatment of turmeric suspension (1000mg/
kg, P.O), Group 7 (n = 12), Therapeutic treatment of turmeric suspension (200mg/rat, topical).
Raw turmeric powder was administered as suspension (Suspended in 1%Sodium carboxy
methyl cellulose) by two routes, orally and topically in different groups. Turmeric was
administered orally at two doses 500 mg/kg and 1000mg/kg. In topical treatment group, the
animals were shaved ventrally by using hair removing cream and turmeric suspension was
applied along the ventral side of rat by using a small brush in dose of 200 mg / rat, twice daily.
Pre-induction treatment:
Animals of groups 2 and 3 were treated with oral administration of 500 mg/kg and 1000 mg/
kg body weight of turmeric (group1: 500mg/kg body weight; group 2: 1000mg/kg body
weight) and animals of group 4 were treated with 200mg/rat turmeric topical application twice
daily from two weeks before the carcinogen treatment and continued till the end of the study (for
24 weeks after MNU treatment).
Post-induction treatment:
Animals of group 5 and 6, after 2 weeks of MNU administration were treated with oral
administration of 500 mg/kg bodyweight and 1000 mg/kg bodyweight of turmeric (group 5:
500 mg/kg body weight; group 6:1000mg /kg body weight ) and animals of group 7 were
treated with 200mg/rat turmeric topically twice daily from two weeks before the carcinogen
treatment and continued till the end of the study (for 24 weeks after MNU treatment) Follow-
ing carcinogen treatment, all rats were weighed once weekly and palpated for detection of
mammary tumors. The rats were sacrificed 24 weeks after MNU treatment. Liver and uterus
were dissected out from each of the experimental animal and weighed. The Latency period, the
number of tumor bearing animals (% incidence), the number of tumors per animal (multiplic-
ity) and tumor burden (weight/animal) were determined.
The tumor volume (V=4/3πr3),
tumor growth inhibition (TG1 %=
c
tcV)VV(
× 100) was calculated.
Hemoglobin content, RBC, WBC and platelet counts were recorded every month starting from
the experiment till the end of the experiment.
Statistical analysis
The difference in tumor volumes, latency periods, body weights, wet uterus and wet liver
weights were statistically evaluated by One–way analysis of variances (ANOVA), followed by
Tukey’s t test and the tumor incidence rates were determined using chi–square test. Values of
P<0.001, P<0.01, P<0.05 were considered significant.
RESULTS:
There was 20% mortality in control group animals whereas mortality has been significantly
reduced in prophylactic and therapeutic treatment of groups (Table 1).
INTRODUCTION
The dried Curcuma longa Linn., is the source of the spice turmeric, has been used extensively
in India for its medicinal and non medicinal uses like coloring agent, flavoring agent. Its anti
inflammatory property is known to ancient Indians and Chinese. It is also used for the
treatment of sprains and swelling caused by injury (1), for the treatment of biliary disorders,
anorexia, cough, diabetic wounds, hepatic disorders, rheumatism and sinusitis (2). It also
shows adjuvant chemoprotection in experimental stomach and oral cancer models of Swiss
mice and Syrian golden hamsters (3). Curcumin shows anti-tumour (4,5,6) and anti-
carcinogenic (7, 8, 9, 10).
Turmeric was already proved beneficial in various types of cancers like duodenal tumors (4),
tongue carcinoma (11), colon cancer (12), human breast cancer cells in-vitro (13, 14, 15, 16),
mammary tumor in-vivo (17, 18).
Few studies reported the chemopreventive effect of Curcumin. Curcumin topical application
inhibited DMBA-induced /TPA promoted skin tumors (19). So, it is logical to study the
chemo-preventive and therapeutic effects of turmeric by different routes of administration. Since
many dietary and non-dietary phytochemicals do not affect survival of normal cells and also
possess anti-tumourigenic activities, it could be a rational approach to examine the effect of
turmeric on MNU-induced mammary tumors in rats. Therefore, the present study was con-
ducted to evaluate the effect of turmeric on MNU-induced mammary tumors in rats.
MATERIALS AND METHODS:
Plant Material
Fresh raw turmeric (Curcuma longa) rhizomes were obtained from fields of Paderu,
Visakhapatnam district of Andhra Pradesh, during September 2005.They were cut down in to
small pieces, shade dried and powdered mechanically. Turmeric powder was suspended in 1%
sodium carboxy methyl cellulose and administered to rats at two dose levels orally (500mg /
Kg/B.W and 1000mg / Kg/ B.W) and topically (200mg / rat ) twice daily for 24 weeks after
MNU treatment.
Chemicals
N- methyl -N- nitrosourea (MNU) was obtained from sigma Chemical Co, St. Louis, MO,
USA. Upon arrival MNU was stored at – 200 c in the dark. All other chemicals used were of
analytical grade.
Animals
Female Sprague-Dawley rats of 4-weeks old were obtained from Mahavir Enterprises, Hyderabad.
The animals were housed in plastic cages, maintained temperature (22+/-20C) and humidity
(60+10%). Rats were maintained under 12h light/12h dark cycle and fed commercial diet
obtained from Rayan’s Bio- technology PVT – Ltd., ad libitum and water freely throughout
the study.
Induction of Mammary Carcinogenesis
For systemic exposure, MNU was dissolved immediately prior to its use in 0.9% Nacl
(Normal saline) containing 0.05% acetic acid. The intra peritoneal injection of 50mg / kg
body weight, a dose known to produce high incidence of mammary cancer (20) was made
alongthe ventral midline of the 50 days old rats.
Journal of Pharmacy Research Vol.4.Issue 4. April 2011
Annapurna A et al. / Journal of Pharmacy Research 2011,4(4),1274-1276
1274-1276
Effect of turmeric on percent incidence rates of mammary tumors:
Incidence rate of mammary tumors in control group was 83.33%. Percent incidence rates after
treatment were given in Figure 1 and Table 1. However, incidence rates were significantly
decreased in both prophylactic & therapeutic treatment of turmeric suspension. Prophylactic
treatment of turmeric has superiorly reduced the incidence rates of mammary tumor when
compared to therapeutic treatment of turmeric. Hence it is evident that per oral administration
and topical application of turmeric was more effective when administered prophylactically than
therapeutically in reducing the incidence rates when compared to control and it was dose
dependent.
topically has significantly reduced the mean tumor volume. Interestingly, prophylactic treat-
ment of turmeric at a dose of 200mg/kg topically was most effective than prophylactic oral
treatment of turmeric and both oral and topical therapeutic treatment. Therapeutic treatment of
turmeric at a dose of 500mg/kg (P<0.01) and 1000mg/kg (P<0.001) has significantly reduced
mean tumor volume but not on par with the prophylactic treatment. In addition, prophylactic
topical application of turmeric has significantly (P<0.001) reduced the mean tumor volume
when compared to therapeutic topical application of turmeric has which no significant effect on
mean tumor volume. Results of mean tumor volume were given in Figure 3 and Table 2.
Figure 1: Effect of prophylactic and therapeutic treatment of turmeric on incidence rate of
mammary tumors in female SD rats.
0
20
40
60
80
100
***p<0.05 vs Number of rats without tumors by ψ2 Chi square test
Control
Turmeric 500 mg/kg,p.o.(Prophylactic)
Turmeric 1000 mg/kg,p.o.(Prophylactic)
Turmeric 200 mg/rat, topical (Prophylactic)
Turmeric 500 mg/kg,p.o.(Therapeutic)
Turmeric 1000 mg/kg,p.o.(Therapeutic)
Turmeric 200 mg/rat, topical (Therapeutic)
83.33%
25%
8.33% 10%
60%
36.3%
63.3%
% Incidence rate
Mean ± SEM (n = 12-24)
Table 1: Effect of prophylactic and therapeutic treatment of turmeric on the incidence of
tumor development in female SD rats.
P< 0.05, * statistically significant when compared to number of rats without tumors. Ψ2 Chi
square test; S = Statistically significant; NS = Statistically insignificant
Effect of turmeric on mean latency periods for induction of mammary tumors:
Prophylactic treatment of turmeric when given orally showed dose dependent and significant
beneficial effect. Curcumin prolonged the mean latency periods for induction of mammary
tumors. Similarly, Prophylactic treatment of turmeric when used topically at a dose of 200mg/
kg has significantly increased the mean latency periods. Interestingly, prophylactic treatment
of turmeric at a dose of 200mg/kg topically was most effective than prophylactic oral treatment
and oral and topical therapeutic treatment. Therapeutic treatment of turmeric has no significant
effect on mean latency periods except at 1000 mg/kg, P.O. (P<0.001). In addition, prophylac-
tic topical application of turmeric has significantly (P<0.001) prolonged the mean latency
periods when compared to therapeutic topical application of turmeric which has no significant
effect on mean latency periods. Results of mean latency periods were given in Figure 2.
0
10
20
30
Turmeric1000 mg/kg,p.o.(Prophylactic)
Control
Turmeric 500 mg/kg,p.o.(Prophylactic)
Turmeric 200 mg/rat, topical (Prophylactic)
Turmeric 500 mg/kg,p.o.(Therapeutic)
Turmeric 1000 mg/kg,p.o.(Therapeutic)
Turmeric 200 mg/rat, topical (Therapeutic)
Mean Latency period
(Weeks) Mean ± SEM
***p<0.001 vs Control group by One way ANOVA/Tukey's test
*** ***
*** ***
Figure 2: Mean latency periods across all (control and prophylactic, therapeutic treatment) the
groups of female SD rats
Effect of turmeric on mean tumor volume:
Prophylactic treatment of turmeric when given orally, reduced the mean tumor volume
significantly (P<0.001). Similarly, Prophylactic treatment of turmeric at a dose of 200mg/kg
0
10
20
30
Turmeric1000 mg/kg,p.o.(Prophylactic)
Control
Turmeric 500 mg/kg,p.o.(Prophylactic)
Turmeric 200 mg/rat, topical (Prophylactic)
Turmeric 500 mg/kg,p.o.(Therapeutic)
Turmeric 1000 mg/kg,p.o.(Therapeutic)
Turmeric 200 mg/rat, topical (Therapeutic)
Mean Latency period
(Weeks) Mean ± SEM
***p<0.001 vs Control group by One way ANOVA/Tukey's test
*** ***
*** ***
Figure 3: Effect of prophylactic and therapeutic treatment mean tumor volume in female SD rats.
Table 2: Effect of prophylactic and therapeutic treatment on parameters of induced mammary
cancer in female SD rats
Animal Groups Total No. No. of %No. of No. of Incidence
of rats effective Mortality rats without rats with rates
rats tumors tumors
Control 15 12 20 2 10* 83.33%
Turmeric 500 mg/kg, p.o. 12 12 0 9 3* 25%
(Prophylactic)
Turmeric 1000 mg/kg, p.o. 24 24 0 22 2* 8.33%
(Prophylactic)
Turmeric 200 mg/kg, topical 24 20 16 18 2* 10%
(Prophylactic)
Turmeric 500 mg/kg, p.o. 12 10 16 4 6* 60%
(Therapeutic)
Turmeric 1000 mg/kg, p.o. 12 11 8.33 7 4* 36.36%
( Therapeutic )
Turmeric 200 mg/kg, topical 12 11 8.33 4 7* 63.36%
( Therapeutic )Effect of turmeric on percent tumor growth inhibition (% TGI):
Percent tumor growth inhibitions of prophylactic turmeric 500mg/kg, 1000mg/kg P.O. and
prophylactic turmeric 200mg/kg topical application were found to be 65.73, 73.20 and 92.83
respectively. Hence, prophylactic treatment of turmeric orally has shown percent tumor growth
inhibition dose dependently. The major finding of the study is that the highest degree of
percent growth inhibition with prophylactic topical application of turmeric (92.83) which is
significantly (P<0.001) higher than the TGI of prophylactic turmeric treatment with 500mg/
kg.p.o. Percent tumor growth inhibitions of therapeutic turmeric 500mg/kg, 1000mg/kg P.O.
and therapeutic turmeric 200mg/kg topical application were found to be 37.07, 47.35 and
20.24 respectively. In contrast to prophylactic topical application of turmeric, therapeutic
topical application of turmeric has shown lesser degree of percent tumor growth inhibition.
Results were given in the Figure 4 and Table 2.
*Tumor burden = Number of tumors per rat; Tumor growth inhibition (TGI%) = (Vc-Vt)/Vc
× 100 ; Vc = mean tumor volume in control group at any point of time, Vt = mean tumor volume
of treatment group at any point of time; Significance was given in the graphs for mean tumor
volume and tumor growth inhibition in Figure 3 and figure 4 respectively.
0
1
2
3
4
**p<0.01, ***p<0.001 vs Control group by One way ANOVA/Tukey's test
Control
Turmeric 500 mg/kg,p.o.(Prophylactic)
Turmeric 1000 mg/kg,p.o.(Prophylactic)
Turmeric 200 mg/rat, topical (Prophylactic)
Turmeric 500 mg/kg,p.o.(Therapeutic)
Turmeric 1000 mg/kg,p.o.(Therapeutic)
Turmeric 200 mg/rat, topical (Therapeutic)
*** ***
***
** ***
Mean Tumor volume (Cm
3
)
Mean± SEM
Figure 4: Effect of prophylactic and therapeutic treatment on percent tumor growth inhibition
in female SD rats.
The difference between the body weights, wet uterus, and wet liver weights between control
and treated groups were statistically insignificant (data was not shown). It was observed that
there was no statistically significant difference in hematological parameters including WBC,
RBC and hemoglobin values between control and treated groups. Hence it was evident that
Animal Groups Total No. No. of No. of Total *Tumor Mean TGI %
of rats effective rats with No. of burden tumor
rats tumors tumors volume
Control 15 12 10 17 1.41 3.21
Turmeric 500 mg/kg, p.o. 12 12 3 4 0.33 1.10 65.73
(Prophylactic)
Turmeric 1000 mg/kg, p.o. 24 24 2 1 0.08 0.86 73.20
(Prophylactic)
Turmeric 200 mg/kg, topical 24 20 2 2 0.20 0.23 92.83
(Prophylactic)
Turmeric 500 mg/kg, p.o. 12 10 6 10 1.00 2.02 37.07
(Therapeutic)
Turmeric 1000 mg/kg, p.o. 12 11 4 5 0.45 1.69 47.35
( Therapeutic )
Turmeric 200 mg/kg, topical 12 11 7 13 1.18 2.56 20.24
( Therapeutic )
Journal of Pharmacy Research Vol.4.Issue 4. April 2011
Annapurna A et al. / Journal of Pharmacy Research 2011,4(4),1274-1276
1274-1276
there was no bone marrow depression with turmeric treatment. Results of hematological
parameters, WBC, RBC and RBC were given in Table 3, Table 4 and Table 5.
Table 3: Effect of prophylactic and therapeutic treatment for six months on WBC (103/µL)
count in female SD rats
Animal Groups 0 time 1st Month 2nd Month3rd Month 4th Month 5th Month6th Month
Control 4.80±0.15 6.71±0.32 6.93±0.61 7.41±0.53 7.60±0.24 7.67±0.36 7.80±0.32
Turmeric 500 mg/kg, p.o. 4.67±0.18 6.24±0.25 6.46±0.53 6.98±0.48 7.26±0.62 7.41±0.41 7.64±0.41
(Prophylactic)
Turmeric 1000 mg/kg, p.o. 4.92±0.13 6.89±0.30 7.03±0.56 6.97±0.36 7.13±0.43 7.24±0.26 7.92±0.56
(Prophylactic)
Turmeric 200 mg/kg, topical 4.89±0.10 6.82±0.28 7.14±0.51 7.11±0.53 7.62±0.31 7.41±0.43 7.47±0.40
(Prophylactic)
Turmeric 500 mg/kg, p.o. 4.32±0.30 6.43±0.31 6.89±0.43 7.26±0.46 7.70±0.53 7.78±0.51 7.94±0.38
(Therapeutic)
Turmeric 1000 mg/kg, p.o. 4.50±0.21 6.65±0.22 6.96±0.49 7.44±0.48 7.86±0.42 7.80±0.38 7.82±0.36
( Therapeutic)
Turmeric 200 mg/kg, topical 4.72±0.14 6.96±0.26 7.16±0.54 7.38±0.38 7.52±0.63 7.52±0.43 7.77±0.43
( Therapeutic)
Table 4: Effect of prophylactic and therapeutic treatment for six months on RBC (106/µL)
count in female SD rats
Animal Groups 0 time 1stMonth 2ndMonth 3rd Month 4th Month5th Month 6th Month
Control 6.9 ±0.36 8.1±0.62 8.34±0.36 8.26±0.46 8.43±0.38 8.60±0.42 8.82±0.21
Turmeric 500 mg/kg, p.o. 7.02±0.46 8.6±0.69 8.46±0.52 8.47±0.38 8.56±0.26 8.72±0.46 8.97±0.42
(Prophylactic)
Turmeric 1000 mg/kg, p.o 7.60±0.51 8.30±0.64 8.48±0.47 8.56±0.82 8.68±0.43 8.86±0.48 8.96±0.33
.(Prophylactic)
Turmeric 200 mg/kg, topical 6.49±0.45 7.54±0.59 7.92±0.54 8.28±0.57 8.65±0.52 8.71±0.37 8.79±0.27
(Prophylactic)
Turmeric 500 mg/kg, p.o 6.36±0.26 7.89±0.43 7.99±0.38 8.03±0.48 8.16±0.61 8.11±0.34 8.3±0.36
.(Therapeutic)
Turmeric 1000 mg/kg, p.o. 7.12±0.32 7.90±0.60 8.13±0.42 8.15±0.39 8.34±0.44 8.48±0.41 8.65±0.21
( Therapeutic )
Turmeric 200 mg/kg, topical 7.32±0.52 7.92±0.52 8.22±0.48 8.34±0.40 8.58±0.39 8.73±0.31 8.68±0.46
( Therapeutic )
1. Ammon, H.P.T., Wahl, M.A., Pharmacology of Curcuma longa. Planta Med,.57(1),1991, pp. 1–
7.
2. Ammon, H. P., Anazodo, M. I., Safayhi, H., Dhawan, B. N., and Srimal, R. C., Curcumin: a potent
inhibitor of leukotriene B4 formation in rat peritoneal polymorphonuclear neutrophils
(PMNL). Planta Med.,58(2),1992, p. 226.
3. Azuine, M.A., Bhide, S.V., Adjuvant chemoprevention of experimental cancer: catechin and
dietary turmeric in fore stomach and oral cancer models. J. Ethnopharm. 44,1994, pp. 211–217.
4. Huang, M.T., Lou, Y.R., Ma, W., Newmark, H.L., Reuhl, K.R., Conney, A.H.,Inhibitory effects of
dietary curcumin on fore stomach, duodenal, and colon carcinogenesis in mice. Cancer Res., 54
(22),1994, pp.5841-5847.
5. Bhaumik, S., Jyothi, M.D., Khar, A., Differential modulation of nitric oxide production by curcumin
in host macrophages and NK cells. FEBS Letters, 483 (13),2000, pp.78–82.
6. Surh, Y.J., Chun, K.S., Cha, H.H., Han, S.S., Keum, Y.S., Park, K.K., Lee, S.S.,Molecular mecha-
nism underlying chemopreventive activities of anti-inflammatory phytochemicals: down regula-
tion of COX-2 and iNOS through suppression of NF-kB activation. Mutat Res,480(1),2001,pp.243–
268.
7. Kuo, M.L., Huang, T.S., and Lin, JK.,Curcumin, an antioxidant and anti-tumor promoter, induces
apoptosis in human leukemia cells. Biophysica Acta., 1317(2),1996, pp.95–100.
8. Goel. A., Boland, CR., Chauhan, DP.,Specific inhibition of cyclooxygenase-2(COX-2) expression
by dietary curcumin in HT29 human colon cancer cells. Cancer Lett., 172,2001,pp. 111–118.
9. Shao, Z.M., Shen, ZZ., Liu, C.H., Sartippour, M.R., Go, V.L., Heber, D., Nguyen, M.,Curcumin
exerts multiple suppressive effects on human breast carcinoma cells. Int J Cancer., 98(2),2002,
pp.234–240.
10. Choudhuri ,T., Pal. S., Aggarwal. ML., Das, T., Sa, G., Curcumin induces apoptosis in human breast
cancer cells through p53dependent Bax induction. FEBS Letters., 512 (1-3) 2002,pp.334–340.
11. Tanaka, T., Makita, H., Ohnishi, M.,Chemoprevention of 4-nitroquinoline 1-oxide-induced oral
carcinogenesis by dietary curcumin and hesperidin: comparison with the protective effect of beta-
carotene. Cancer Res., 54(17),1994, pp.4653-4659.
12. Rao, C.V., Rivenson, A., Simi, B., Reddy, B.S.,Chemoprevention of colon carcinogenesis by dietary
curcumin, a naturally occurring plant phenolic compound. Cancer Res.,55(2), 1995,pp.259-66.
13. Jee, S.H., Shen, S.C., Tseng, C.R., Chiu, H.C., Kuo, M.L.,Curcumin induces a p53-dependent apoptosis
in human basal cell carcinoma cells. J Invest Dermatol., 111(4),1998, pp.656-661.
14. Kim,M.S., Kang, H.J., Moon, A.,Inhibition of invasion and induction of apoptosis by curcumin in
H-ras-transformed MCF10A human breast epithelial cells. Archives of Pharmacal Research.,
24(4), 2001,pp 349-354.
15. Simon, A., Allais, DP., Duroux, J.L., Basly, J.P., Durand-Fontanier S., Delage, C.,Inhibitory effect
of curcuminoids on MCF-7 cell proliferation and structure-activity relationships. Cancer
Lett,129(1),1998, 111-6.
16. Holy, J.M., Curcumin disrupts mitotic spindle structure and induces micronucleation in MCF-7
breast cancer cells. Mutat Res., 518(1),2002, pp.71-84.
17. Huang, M.T., Lou, Y.R., Xie, J.G., Ma, W., Lu, Y,P., Yen, P., Zhu, B.T., Newmark, H., Ho, C.T.,Effect
of dietary curcumin and dibenzoylmethane on formation of 7,12 dimethyl benz[a] anthracene
induced mammary tumours and lymphoma/leukemias in Sencar mice. Carcinogenesis, 19(9),1998,
pp.1697-1700.
18. Huang, M.T., Wang, Z.Y., Georgiadis, C.A., Laskin, J.D., Conney, A.H.,Inhibitory effects of curcumin
on tumor initiation by benzo [a] pyrene and 7,12- dimethylbenz[a]anthrecene. Carcinogenesis,
13(11),1992, pp.2183-2186.
19. Huang, M.T., Ma,W., Yen, P., Xie, J.G., Han, J., Frenkel, K., Grunberger, D.,Conney, A.H.,Inhibitory
effects of topical application of low doses of curcumin on 12-O-tetradecanoylphorbol-13-acetate
induced tumor promotion and oxidized DNA bases in mouse epidermis. Carcinogenesis, 18(1),1997,
pp.83-88.
20. Mc Cormick DL, Adamowski CB, Fiks A, Moon RC.,Lifetime dose response relationships for
mammary tumor induction by a single administration of N methyl-N-nitrosourea. Cancer Res.,
41,(5),1981,pp.1690-1694.
21. Kuttan, R., Sudheeran, P.C., Josph, C.D.,Turmeric and curcumin as topical agents in cancer therapy.
Tumori.,73,1987,pp.29-31.
22. Huang, M.T., Smart, R.C., Wong, Ch. Q., Conney, A.H.,Inhibitory effect of curcumin, chlorogenic
acid, caffeic acid, and ferulic acid on tumor promotion in mouse skin by 12-O-tetradecanoylphorbol-
13-acetate. Cancer Res., 48,1988, pp.5941–5946.
23. Chen, H.W., Huang, HC.,Effect of curcumin on cell cycle progression and apoptosis in vascular
smooth cells. Br J Pharmacol.,124(6),1998,pp.1029–1040.
Table 5: Effect of prophylactic and therapeutic treatment for six months on Hemoglobin (g/
dl) in female SD rats
DISCUSSION AND CONCLUSION
In the present study, turmeric was evaluated for its ability to modulate the MNU induced
mammary cancer in rats over a period of 24 weeks. The anticancer activity of turmeric was
evaluated prophylactically and therapeutically i.e., pre-induction treatment and post -induction
treatment respectively, by two different routes of administration i.e., per oral and topical
application. Though post-induction per oral treatment with turmeric demonstrated a signifi-
cant anticancer activity against MNU-induced mammary cancer in rats, the degree of anticancer
activity was more prominent in prophylactic treatment groups and was more effective particu-
larly with topical application. It was clearly evidenced by the decreased drastic reduction in
mean tumor volume and higher degree of tumor growth inhibition in prophylactic topical
application of turmeric when compared to the therapeutic treatment of groups. Our study
demonstrated similar results with the previous work reported (21).
Prophylactic topical application of turmeric has shown superior efficacy when compared to all
other groups in reduction of the incidence rates of tumor induction, prolongation of mean
latency periods of tumor development, reversal of mean tumor volume and inhibition of tumor
growth. Hence, interesting findings in this study are i) Preventive role of turmeric against
MNU induced mammary cancer was more predominant than the therapeutic role of turmeric on
MNU induced mammary cancer. ii) Preventive role of turmeric was more pronounced with
topical application though it has demonstrated moderate prophylactic effect with per oral
administration of turmeric. In an in-vivo study, dietary administration of 1% turmeric, 0.05%
ethanol extract of turmeric, when administered during initiation and post initiation periods
significantly inhibited the 7, 12 – dimethyl benz (a) anthracene (DMBA) induced mammary
tumorigenesis by reducing tumor multiplicity, tumor burden and tumor incidence. Simulta-
neous administration of 1% curcumin-free aqueous turmeric extract as the sole source of
drinking water during the initiation phase did not suppress DMBA-induced mammary tum-
origenesis but suppressed the DMBA-induced mammary tumorigenesis when administered
during post initiation period by reducing tumor multiplicity and tumor burden but not the
tumor incidence.
Till date, there was no evidence of anticancer activity with topical application of turmeric in
breast cancer model. In two in vivo studies reported earlier, topical application of 100 or 3000
nmol curcumin in CD-1 mice and 0.2% or 1% curcumin in diet significantly reduced the tumor
incidence and tumor volume in dimethyl benz (a) anthracene (DMBA) initiated and 12,0-
tetradecanoylphorbal -13-acetate (TPA) promoted skin tumors (22).
The general anti-carcinognic effect of Curcumin involves the mechanisms like induction of
apoptosis and inhibits cell-cycle progression, both of which are instrumental in preventing
cancerous cell growth in rat aortic smooth muscle cells (23). The antiproliferative effect is
mediated partly through inhibition of protein tyrosine kinase and c-myc mRNA expression and
the apoptotic effect may partly be mediated through inhibition of protein tyrosine kinase,
protein kinase C, c-myc mRNA expression and bcl-2 mRNA expression (23). Specifically,
Curcumin suppresses human breast carcinoma through multiple pathways. Its antiproliferative
effect is estrogendependent in ER (estrogen receptor)-positive MCF-7 cells and estrogen-
independent in ER-negative MDA-MB-231 cells (9). Curcumin also down regulates matrix
metalloproteinase (MMP)-2 and upregulates tissue inhibitor of metalloproteinase (TIMP)-1,
two common effector molecules involved in cell invasion (9). It also induces apoptosis
through P53-dependent Bax induction in human breast cancer cells (10).
Since major side effect of anti-cancer drugs is bone marrow depression, the present study has
investigated the effect of chronic turmeric treatment on hematological parameters. There was no
significant difference in hematological parameters among the different treatment groups and
control group. Hence it was evident that no bone marrow depression with turmeric treatment
was observed, which is a major side effect with cytotoxic chemotherapy.
In conclusion, the turmeric acts effectively both orally and topically initiation stage of mam-
mary cancer than in the promotion stage of mammary carcinoma. This stage specificity of
turmeric’s anticancer activity must be established by further investigations.
REFERENCES:
Source of support: Nil, Conflict of interest: None Declared
Animal Groups 0 time 1stMonth 2ndMonth 3rd Month 4th Month5th Month 6th Month
Control 6.9 ±0.36 8.1±0.62 8.34±0.36 8.26±0.46 8.43±0.38 8.60±0.42 8.82±0.21
Turmeric 500 mg/kg, p.o. 7.02±0.46 8.6±0.69 8.46±0.52 8.47±0.38 8.56±0.26 8.72±0.46 8.97±0.42
(Prophylactic)
Turmeric 1000 mg/kg, p.o 7.60±0.51 8.30±0.64 8.48±0.47 8.56±0.82 8.68±0.43 8.86±0.48 8.96±0.33
.(Prophylactic)
Turmeric 200 mg/kg, topical 6.49±0.45 7.54±0.59 7.92±0.54 8.28±0.57 8.65±0.52 8.71±0.37 8.79±0.27
(Prophylactic)
Turmeric 500 mg/kg, p.o 6.36±0.26 7.89±0.43 7.99±0.38 8.03±0.48 8.16±0.61 8.11±0.34 8.3±0.36
.(Therapeutic)
Turmeric 1000 mg/kg, p.o. 7.12±0.32 7.90±0.60 8.13±0.42 8.15±0.39 8.34±0.44 8.48±0.41 8.65±0.21
( Therapeutic )
Turmeric 200 mg/kg, topical 7.32±0.52 7.92±0.52 8.22±0.48 8.34±0.40 8.58±0.39 8.73±0.31 8.68±0.46
( Therapeutic )
... Chemo-preventive role of turmeric was more potent against mammary tumors. [18] Curcumin has cancer chemo preventive activity in preclinical animal models and human hepato cellular liver carcinoma cell line. The study of anticancer activity of the curcumin ethanolic extract was done in vitro on cell line and in vivo on mice. ...
Article
Cancer is abnormal growth of cells in the body; cancer almost affects any one at any age. Cancer affects most of the people; the mortality rate of cancer is high when compared to any other disease. With emerging trends in herbal medicine and complementary alternative medicine India is considered to be one of the largest producer of herbal medicine in the world. Scientists and researchers are inventing many synthetic analogs with anticancer activity these allopathic medicines have severe side effects and become toxic to many patients suffering with cancer. The treatment or chemotherapy given for cancer patient is costly so the treatment should be non-toxic and economic. There are anticancer medicinal plants abundantly present in India there are many active constituents which can be isolated and patented. Scientists and researchers are meticulously working to invent new compounds with anticancer activity. India is having an unexplored data of hidden treasure of medicinal plants. These plants can be explored in future and will be helpful for the researchers who are working on anticancer medicinal plants. This review has been compiled from various sources and reports few plants collected from various literatures containing anticancer activities. This review contains few medicinal plants the type of extract, different type of cell lines and the assay methods used. Cancer will become the most dreadful disease affecting many people in the world in future so this review on cancer has been chosen and compiled from many literatures. This review will be helpful for researchers around the globe in finding new entities and new molecules from easily available plants for the treatment of cancer.
Article
Bacterial resistance is a growing health problem worldwide that has serious economic and social impacts, compromising public health, and the therapeutic action of current antibiotics. Therefore, the search for new compounds with antimicrobial properties is relevant in modern studies, particularly against bacteria of clinical interest. In the present study, in vitro antibacterial activity of the ethanol extract and essential oil of Curcuma longa (Zingiberaceae) was evaluated against nosocomial bacteria, using the microdilution method. Escherichia coli strains, Pseudomonas aeruginosa, Klebsiella pneumoniae, Proteus sp. were used, Salmonella sp. and Bacillus sp., isolated from nosocomial infections in a hospital in the city of Monteria and reference strains of S. aureus ATCC 43300, S. aureus ATCC 29213, S. aureus ATCC 25923, P. aeruginosa ATCC 27853, E. coli ATCC 25922 and K. pneumonia ATCC 700603. The ethanol extract antibacterial profile was more efficient at higher concentrations (1 000 ppm), obtaining significant percentages of reduction of more than 50 % against K. pneumoniae ATCC 700603 and a clinical isolate of E. coli; while compared to Bacillus clinical isolate, was more active than the essential oil. For the rest of microorganisms, the reduction percentages obtained at a concentration of 1 000 ppm varied between 17 and 42 % with ethanolic extract, and 8 to 43 % with essential oil. At concentrations of 100 and 500 ppm antibacterial activity of the extracts was lower. The results indicated that the ethanolic extract and essential oil of C. longa rhizomes have active compounds with antibacterial properties that could be used in future research as a therapeutic alternative for the treatment of infections caused by nosocomial pathogens.
Article
Turmeric (Curcuma longa L) rhizome extracts were evaluated for their antidiabetic, antihypertensive and antioxidant potentials. α-Glucosidase (0.4 μg/mL) and α-amylase (0.4 μg/mL) inhibitory potential of turmeric ethyl acetate extract was significantly higher than those of the reference drug acarbose (17.1 μg/mL and 290.6 μg/mL respectively). Protein glycation inhibitory potential of ethyl acetate extract was 800 times higher than that of ascorbic acid. High potential of ethyl acetate extract to scavenge free radicals and to reduce LDL oxidation and cellular oxidative stress was also revealed. The positive correlation obtained between the free radical scavenging capacity of the extracts and their antiglycation potential further confirmed the role of antioxidants in controlling glycation reactions. Ethyl acetate extract was also found as effective in reducing hy-pertension by inhibiting angiotensin converting enzyme (ACE). Antidiabetic, ACE inhibitory and antioxidant capac-ities of the extracts were in the order of their curcumin contents.
Data
Turmeric (Curcuma longa L) rhizome extracts were evaluated for their antidiabetic, antihypertensive and antioxidant potentials. α-Glucosidase (0.4 μg/mL) and α-amylase (0.4 μg/mL) inhibitory potential of turmeric ethyl acetate extract was significantly higher than those of the reference drug acarbose (17.1 μg/mL and 290.6 μg/mL respectively). Protein glycation inhibitory potential of ethyl acetate extract was 800 times higher than that of ascorbic acid. High potential of ethyl acetate extract to scavenge free radicals and to reduce LDL oxidation and cellular oxidative stress was also revealed. The positive correlation obtained between the free radical scavenging capacity of the extracts and their antiglycation potential further confirmed the role of antioxidants in controlling glycation reactions. Ethyl acetate extract was also found as effective in reducing hy-pertension by inhibiting angiotensin converting enzyme (ACE). Antidiabetic, ACE inhibitory and antioxidant capac-ities of the extracts were in the order of their curcumin contents.
Article
Full-text available
Dose-response relationships for the induction of mammary tumors by a single i.v. injection of N-methyl-N-nitrosourea (MNU) were studied. At 50 days of age, groups of 20 virgin female Sprague-Dawley rats received single doses of 50, 45, 40, 35, 30, 25, 20, 15, or 10 mg MNU per kg body weight; a group of 10 control rats received 0.85% NaCl solution only. Animals were observed for the appearance of mammary tumors over their life span or until 600 days after carcinogen administration. Both malignant and benign mammary tumors appeared in all groups; however, malignant tumors appeared earlier and at a faster rate than did benign tumors. Incidence of cancer and number of cancers per animal increased with increasing MNU dose; the latent period for cancer increased with decreasing dose. The number of benign tumors induced as a percentage of total tumors increased with decreasing dose, ranging from approximately 10% in groups receiving more than 30 mg MNU per kg to 58% in the group receiving 10 mg/kg. Foci of metastatic mammary carcinoma were found in lungs of animals in several MNU dose groups. Data from the present study indicate that a single i.v. administration of MNU induces mammary cancer in a dose-related fashion, with little toxicity and a short latent period; induced cancers metastasize to distant sites. The single-dose MNU model thus appears to be superior to both the 7,12-dimethylbenz(a)anthracene and multiple-dose MNU models, particularly for use in studies of modification of mammary carcinogenesis.
Article
Full-text available
Human epidemiological and laboratory animal model studies have suggested that nonsteroidal antiinflammatory drugs reduce the risk of development of colon cancer and that the inhibition of colon carcinogenesis is mediated through the alteration in cyclooxygenase metabolism of arachidonic acid. Curcumin, which is a naturally occurring compound, is present in turmeric, possesses both antiinflammatory and antioxidant properties, and has been tested for its chemopreventive properties in skin and forestomach carcinogenesis. The present study was designed to investigate the chemopreventive action of dietary curcumin on azoxymethane-induced colon carcinogenesis and also the modulating effect of this agent on the colonic mucosal and tumor phospholipase A2, phospholipase C gamma 1, lipoxygenase, and cyclooxygenase activities in male F344 rats. At 5 weeks of age, groups of animals were fed the control (modified AIN-76A) diet or a diet containing 2000 ppm of curcumin. At 7 weeks of age, all animals, except those in the vehicle (normal saline)-treated groups, were given two weekly s.c. injections of azoxymethane at a dose rate of 15 mg/kg body weight. All groups were continued on their respective dietary regimen until the termination of the experiment at 52 weeks after the carcinogen treatment. Colonic tumors were evaluated histopathologically. Colonic mucosa and tumors were analyzed for phospholipase A2, phospholipase C gamma 1, ex vivo prostaglandin (PG) E2, cyclooxygenase, and lipoxygenase activities. The results indicate that dietary administration of curcumin significantly inhibited incidence of colon adenocarcinomas (P < 0.004) and the multiplicity of invasive (P < 0.015), noninvasive (P < 0.01), and total (invasive plus noninvasive) adenocarcinomas (P < 0.001). Dietary curcumin also significantly suppressed the colon tumor volume by > 57% compared to the control diet. Animals fed the curcumin diet showed decreased activities of colonic mucosal and tumor phospholipase A2 (50%) and phospholipase C gamma 1 (40%) and levels of PGE2 (> 38%). The formation of prostaglandins such as PGE2, PGF2 alpha, PGD2, 6-keto PGF1 alpha, and thromboxane B2 through the cyclooxygenase system and production of 5(S)-, 8(S)-, 12(S)-, and 15(S)-hydroxyeicosatetraenoic acids via the lipoxygenase pathway from arachidonic acid were reduced in colonic mucosa and tumors of animals fed the curcumin diet as compared to control diet. Although the precise mechanism by which curcumin inhibits colon tumorigenesis remains to be elucidated, it is likely that the chemopreventive action, at least in part, may be related to the modulation of arachidonic acid metabolism.
Article
1The possible mechanisms of the antiproliferative and apoptotic effects of curcumin (diferuloylmethane), a polyphenol in the spice turmeric, on vascular smooth muscle cells were studied in rat aortic smooth muscle cell line (A7r5).2The proliferative response was determined from the uptake of [3H]-thymidine. Curcumin (10−6–10−4m) inhibited serum-stimulated [3H]-thymidine incorporation of both A7r5 cells and rabbit cultured vascular smooth muscle cells in a concentration-dependent manner. Cell viability, as determined by the trypan blue dye exclusion method, was unaffected by curcumin at the concentration range 10−6 to 10−5m in A7r5 cells. However, the number of viable cells after 10−4m curcumin treatment was less than the basal value (2×105 cells).3To analyse the various stages of the cell cycle, [3H]-thymidine incorporation into DNA was determined every 3 h. After stimulation with foetal calf serum, quiescent A7r5 cells started DNA synthesis in 9 to 12 h (G1/S phase), then reached a maximum at 15 to 18 h (S phase). Curcumin (10−6–10−4m) added during either the G1/S phase or S phase significantly inhibited [3H]-thymidine incorporation.4Following curcumin (10−6–10−4m) treatment, cell cycle analysis utilizing flow cytometry of propidium iodide stained cells revealed a G0/G1 arrest and a reduction in the percentage of cells in S phase. Curcumin at 10−4m also induced cell apoptosis. It is suggested that curcumin arrested cell proliferation and induced cell apoptosis, and hence reduced the [3H]-thymidine incorporation.5The apoptotic effect of 10−4m curcumin was also demonstrated by haematoxylin-eosin staining, TdT-mediated dUTP nick end labelling (TUNEL), and DNA laddering. Curcumin (10−4m) induced cell shrinkage, chromatin condensation, and DNA fragmentation.6The membranous protein tyrosine kinase activity stimulated by serum in A7r5 cells was significantly reduced by curcumin at the concentration range 10−5 to 10−4m. On the other hand, the cytosolic protein kinase C activity stimulated by phorbol ester was reduced by 10−4m curcumin, but unaffected by lower concentrations (10−6–10−5m).7The levels of c-myc, p53 and bcl-2 mRNA were analysed using a reverse transcription-polymerase chain reaction (RT-PCR) technique. The level of c-myc mRNA was significantly reduced by curcumin (10−5–10−4m) treatment. And, the level of bcl-2 mRNA was significantly reduced by 10−4m curcumin. However, the alteration of the p53 mRNA level by curcumin (10−5–10−4m) treatment did not achieve significance. The effects of curcumin on the levels of c-myc and bcl-2 mRNA were then confirmed by Northern blotting.8Our results demonstrate that curcumin inhibited cell proliferation, arrested the cell cycle progression and induced cell apoptosis in vascular smooth muscle cells. Curcumin may be useful as a template for the development of drugs to prevent the pathological changes of atherosclerosis and post-angioplasty restenosis. Our results suggest that the antiproliferative effect of curcumin may partly be mediated through inhibition of protein tyrosine kinase activity and c-myc mRNA expression. And, the apoptotic effect may partly be mediated through inhibition of protein tyrosine kinase activity, protein kinase C activity, c-myc mRNA expression and bcl-2 mRNA expression.British Journal of Pharmacology (1998) 124, 1029–1040; doi:10.1038/sj.bjp.0701914
Article
The effects of topical administration of curcumin on the formation of benzo[a]pyrene (B[a]P)–DNA adducts and the tumorigenic activities of B[a]P and 7,12-dimethyl-benz[a]anthracene (DMBA) in epidermis were evaluated in female CD-1 mice. Topical application of 3 or 10 μmol curcumin 5 min prior to the application of 20 nmol [3H]B[a]P inhibited the formation of [3H]B[a]P—DNA adducts in epidermis by 39 or 61% respectively. In a two-stage skin tumorigenesis model, topical application of 20 nmol B[a]P to the backs of mice once weekly for 10 weeks followed a week later by promotion with 15 nmol 12-O-tetradecanoylpborbol-13-acetate (TPA) twice weekly for 21 weeks resulted in the formation of 7.1 skin tumors per mouse, and 100% of the mice had tumors. In a parallel group of mice, in which the animals were treated with 3 or 10 μmol curcumin 5 min prior to each application of B[a]P, the number of tumors per mouse was decreased by 58 or 62% respectively. The percentage of tumor-bearing mice was decreased by 18–25%. In an additional study, topical application of 3 or 10 μmol curcumin 5 min prior to each application of 2 nmol DMBA once weekly for 10 weeks followed a week later by promotion with 15 nmol TPA twice weekly for 15 weeks decreased the number of tumors per mouse by 37 or 41% respectively.
Article
The data reviewed indicate that extracts of Curcuma longa exhibit anti-inflammatory activity after parenteral application in standard animal models used for testing anti-inflammatory activity. It turned out that curcumin and the volatile oil are at least in part responsible for this action. It appears that when given orally, curcumin is far less active than after i.p. administration. This may be due to poor absorption, as discussed. Data on histamine-induced ulcers are controversial, and studies on the secretory activity (HCl, pepsinogen) are still lacking. In vitro, curcumin exhibited antispasmodic activity. Since there was a protective effect of extracts of Curcuma longa on the liver and a stimulation of bile secretion in animals, Curcuma longa has been advocated for use in liver disorders. Evidence for an effect on liver disease in humans is not yet available. From the facts that after oral application only traces of curcumin were found in the blood and that, on the other hand, most of the curcumin is excreted via the faeces it may be concluded that curcumin is absorbed poorly by the gastrointestinal tract and/or underlies pre-systemic transformation. Systemic effects therefore seem to be questionable after oral application except that they occur at very low concentrations of curcumin. This does not exclude a local action in the gastrointestinal tract.
Article
An ethanol extract of turmeric ("Curcuma longa") as well as an ointment of curcumin (its active ingredient) were found to produce remarkable symptomatic relief in patients with external cancerous lesions. Reduction in smell were noted in 90% of the cases and reduction in itching in almost all cases. Dry lesions were observed in 70% of the cases, and a small number of patients (10%) had a reduction in lesion size and pain. In many patients the effect continued for several months. An adverse reaction was noticed in only one of the 62 patients evaluated.
Article
The effects of topically applied curcumin, chlorogenic acid, caffeic acid, and ferulic acid on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced epidermal ornithine decarboxylase activity, epidermal DNA synthesis, and the promotion of skin tumors were evaluated in female CD-1 mice. Topical application of 0.5, 1, 3, or 10 mumol of curcumin inhibited by 31, 46, 84, or 98%, respectively, the induction of epidermal ornithine decarboxylase activity by 5 nmol of TPA. In an additional study, the topical application of 10 mumol of curcumin, chlorogenic acid, caffeic acid, or ferulic acid inhibited by 91, 25, 42, or 46%, respectively, the induction of ornithine decarboxylase activity by 5 nmol of TPA. The topical application of 10 mumol of curcumin together with 2 or 5 nmol of TPA inhibited the TPA-dependent stimulation of the incorporation of [3H]-thymidine into epidermal DNA by 49 or 29%, respectively, whereas lower doses of curcumin had little or no effect. Chlorogenic acid, caffeic acid, and ferulic acid were less effective than curcumin as inhibitors of the TPA-dependent stimulation of DNA synthesis. Topical application of 1, 3, or 10 mumol of curcumin together with 5 nmol of TPA twice weekly for 20 weeks to mice previously initiated with 7,12-dimethylbenz[a]anthracene inhibited the number of TPA-induced tumors per mouse by 39, 77, or 98%, respectively. Similar treatment of mice with 10 mumol of chlorogenic acid, caffeic acid, or ferulic acid together with 5 nmol of TPA inhibited the number of TPA-induced tumors per mouse by 60, 28, or 35%, respectively, and higher doses of the phenolic acids caused a more pronounced inhibition of tumor promotion. The possibility that curcumin could inhibit the action of arachidonic acid was evaluated by studying the effect of curcumin on arachidonic acid-induced edema of mouse ears. The topical application of 3 or 10 mumol of curcumin 30 min before the application of 1 mumol of arachidonic acid inhibited arachidonic acid-induced edema by 33 or 80%, respectively.
Article
Catechin and dietary turmeric (Curcuma longa) were used as chemopreventive agents in benzo[a]pyrene induced forestomach tumors in Swiss mice and methyl-(acetoxymethyl)-nitrosamine induced oral mucosal tumors in Syrian golden hamsters. Catechin in drinking water and dietary turmeric significantly inhibited the tumor burden and tumor incidence in both tumor models. The induction of oral tumors in golden hamsters was delayed by catechin and dietary turmeric. Adjuvant chemoprevention utilising both catechin and dietary turmeric inhibited both the gross tumor yield and burden more effectively than when compared to individual components in both tumor models. A single i.p. injection of catechin to male Swiss mice induced increased forestomach and hepatic glutathione S-transferase (GST) activity when compared to controls. These findings suggest that catechin and turmeric which are regularly consumed natural products, are effective in mice or golden hamsters as chemopreventive agents.
Article
Curcumin (diferuloylmethane), a yellow pigment that is obtained from the rhizomes of Curcuma longa Linn., is a major component of turmeric and is commonly used as a spice and food-coloring agent. The inhibitory effects of feeding commercial grade curcumin (77% curcumin, 17% demethoxycurcumin, and 3% bisdemethoxycurcumin) in AIN 76A diet on carcinogen-induced tumorigenesis in the forestomach, duodenum, and colon of mice were evaluated. Administration p.o. of commercial grade curcumin in the diet inhibited benzo(a)pyrene-induced forestomach tumorigenesis in A/J mice, N-ethyl-N'-nitro-N-nitrosoguanidine-induced duodenal tumorigenesis in C57BL/6 mice, and azoxymethane (AOM)-induced colon tumorigenesis in CF-1 mice. Dietary commercial grade curcumin was given to mice at: (a) 2 weeks before, during, and for 1 week after carcinogen administration (during the initiation period); (b) 1 week after carcinogen treatment until the end of the experiment (during the postinitiation period); or (c) during both the initiation and postinitiation periods. Feeding 0.5-2.0% commercial grade curcumin in the diet decreased the number of benzo(a)pyrene-induced forestomach tumors per mouse by 51-53% when administered during the initiation period and 47-67% when administered during the postinitiation period. Feeding 0.5-2.0% commercial grade curcumin in the diet decreased the number of N-ethyl-N'-nitro-N-nitrosoguanidine-induced duodenal tumors per mouse by 47-77% when administered during the postinitiation period. Administration of 0.5-4.0% commercial grade curcumin in the diet both during the initiation and postinitation periods decreased the number of AOM-induced colon tumors per mouse by 51-62%. Administration of 2% commercial grade curcumin in the diet inhibited the number of AOM-induced colon tumors per mouse by 66% when fed during the initiation period and 25% when fed during the postinitiation period. The ability of commercial grade curcumin to inhibit AOM-induced colon tumorigenesis is comparable to that of pure curcumin (purity greater than 98%). Administration of pure or commercial grade curcumin in the diet to AOM-treated mice resulted in development of colon tumors which were generally smaller in number and size as compared to the control group of AOM-treated mice. These results indicate that not only did curcumin inhibit the number of tumors per mouse and the percentage of mice with tumors but it also reduced tumor size. Histopathological examination of the tumors showed that dietary curcumin inhibited the number of papillomas and squamous cell carcinomas of the forestomach as well as the number of adenomas and adenocarcinomas of the duodenum and colon.