See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/283863862

Chemical constituents and biological activities of turmeric (Curcuma longa L.) -

A review

Article  in  Journal of Food Science and Technology -Mysore- · March 2008

CITATIONS READS

81 56,675

2 authors:

Abhishek Niranjan Dhan Prakash Prof

National Botanical Research Institute - India Amity University
65 PUBLICATIONS   1,016 CITATIONS    135 PUBLICATIONS   4,213 CITATIONS   

SEE PROFILE SEE PROFILE

Some of the authors of this publication are also working on these related projects:

Economic & social upliftment of rural women through value added products from aromatic plants View project

Herbal drugs View project

All content following this page was uploaded by Abhishek Niranjan on 17 December 2018.

The user has requested enhancement of the downloaded file.

 J Food Sci Technol, 2008, 45(2), 109–116

Chemical constituents and biological activities of turmeric (Curcuma longa L.) -

A review
Abhishek Niranjan*, Dhan Prakash
Nutraceutical Chemistry, National Botanical Research Institute, Lucknow-226 001, India
*E-mail:abhishek_niranjan@yahoo.co.in

Turmeric (Curcuma longa) is used as spice, preservative, colouring matter and has wide range of medicinal and
pharmacological applications. It exhibits anti-inflammatory, anti-HIV, anti-bacterial, antioxidant, nematocidal, anti-
parasitic, antispasmodic and anticarcinogenic activities. It is a potent scavenger of a variety of reactive oxygen species
(ROS) including superoxide anion, hydroxyl radical, singlet oxygen, peroxynitrite and nitric oxide. It is a inhibitor of
ROS generating enzymes, cyclooxygenase and lipoxygenase and plays active role in the inhibition of COX-I and COX-
II enzymes that are involved in the inflammatory reaction. The turmeric extract protects lipids, haemoglobin, and red
blood cells from lipid peroxidation induced by hydrogen peroxide. It prevents oxidative damage and inhibits binding
to toxic metabolites to DNA. Safety evaluation studies indicate that turmeric is well tolerated at very high dose (0.5
to 1.5 g/day/person) without any toxic effects. Turmeric contains 3-6% polyphenolic compounds, collectively known as
curcuminoids, which is a mixture of curcumin, demethoxycurcumin and bisdemethoxycurcumin. Curcuminoids are major
components responsible for various biological actions. Pure curcumin has more potent superoxide anion scavenging
activity than demethoxycurcumin or bisdemethoxycurcumin. Curcumin acts as a pro-oxidant in the presence of transition
metal ions (Cu and Fe) and is a potent bioprotectant with a potentially wide range of therapeutic applications.
Keywords: Curcuma longa, Turmeric, Curcuminoids, Curcumin, Structure-activity relationship, Biological activity,
Toxicity

Turmeric (Curcuma longa L. syn C.
domestica Val.) belongs to family
Zingiberaceae, which is extensively culti-
vated for its rhizomes. It is a perennial
herb distributed throughout tropical and
sub-tropical regions of the world includ-
ing India, Pakistan, Bangladesh and Sri
Lanka. Its rhizomes are harvested, washed
and boiled in mild alkaline water to soften
and dried in sun or in electric driers. It
is used as colouring agent in pharmacy,
confectionery, food industry, for dyeing
wool, silk, cotton and in combination with
other natural dyes to get different shades
(Bakshi et al 1999). Rhizomes are used as
cosmeceutical, expectorant, antiseptic,
anthelmintic, blood purifier, in leprosy,
spleen disorders, rheumatism, bronchitis,
cough and cold, insecticide, spasmolytic,
hypotensive, cholera and syphilis (Kapoor
1990, Yu et al 2002). It is a minor ingre-
dient of ‘Ayurvedic’ drug for malarial
fever; indigenous antifatigue drug
Geriforte (Geri care/stress care), Unani
drug majnoon-e-falsfa, vitafix, opthacare,
purime (hemo care), V-gel, fem care gel,
Acne-n-pimple cream, anti-wrinkle cream,
blood purifier capsules and syrup, foot
care cream, dibecon (gluco care),
curcumin-97 and curcumin 900 MG. In
the modern pharmaceutical products, it is
an ingredient of Geriforte effective in
senile pruritis, anti-fungal, anti-inflamma-
tory, anti-bacterial and to fight decaying
metabolism to prevent cancer (Chopra et
al 1999, Niranjan et al 2003).
Chemical constituents of turmeric
Curcumin, demethoxycurcumin and
bisdemethoxycurcumin collectively known
as curcuminoids (3-6%) are major polyphe-
nolic compounds in turmeric rhizomes
(Ravindranath and Satyanarayan 1980,
Satyawati et al 1976). The main colouring
principle of turmeric rhizome was isolated
in 19th century and named as ‘Curcumin’.
Its chemical structure was determined by
Roughley and Whiting (1973). Other phe-
nolic compounds present in turmeric rhi-
zome are 1-hydroxy-1, 7-bis (4-hydroxy-3-
methoxyphenyl)-(6E)-6-heptene-3, 5-dione;
1-(4- hydroxy-3, 5-dimethoxyphenyl)-7-(4-
hydroxy-3-methoxyphenyl)-(1E, 6E)-1, 6-
heptadiene-3, 4-dione; 1, 5-bis (4-hydroxy-
3-methoxyphenyl)-penta-(1E, 4E)-1, 4-dien-
3-one; 1-(4-hydroxy-3-methoxyphenyl-5-(4-
hydroxyphenyl)-penta-(1E, 4E)-1, 4-dien-
3-one; 1-(4-hydroxy-3-methoxyphenyl)-7-
(3, 4-dihydroxyphenyl)-1, 6-heptadiene-3,
5-dione and 1, 7-bis (4-hydroxyphenyl)-1,
4, 6-heptatrien-3-one. The pale yellow to
orange-yellow volatile oil (4-6%) obtained
from turmeric consists of a number of
mono- and sesquiterpenes. The sesquiter-
penes were named as curcumenone;
dehydrocurdione; (4 S, 5 S)-germacrone 4,
5-epoxide; bisabola 3, 10-diene 2-one; ar-
turmerone (Roth et al 1998); bisacumol;
bisacurone; curcumenol; isoprocurcumenol;
zedoaronediol; procurcumenol;
epiprocurcumenol; germacrone-13-al; 4-
hydroxybisabola-2, 10-diene-9-one; 4, 5-
dihydrobisabola-2, 10-diene; 4-methoxy-
5-hydroxybisabola-2, 10-diene-9-one; 2,
5-dihydroxybisabola-3, 10-diene and
procurcumadiol (Ohshiro et al 1990).
Some other compounds named as curlone
(Kiso et al 1983); α-turmerone; β-
turmerone; terpinolene; α-phellandrene;
curcumadiol; labda-8 (17)-diene-15, 16-
dial and three acidic polysaccharides iso-
lated on a column of DEAE Sephadex A-
25 were named as Ukon A, B and C.
They were composed of L-arabinose, D-
xylose, D-galactose, D-glucose, L-rham-
nose, D-galacturonic acid in the molar
ratio 12:4:12:1:4:10 (Ukon A),
12:4:12:1:2:4 (Ukon B) and 8:3:614:2:3
(Ukon C). The polysaccharide, named as
Ukon D is composed of L-arabinose, D-
galactose, D-glucose and D-mannose in
the molar ratio of 1:1:12:2. The water
soluble peptide is named as turmerin with
an amino acid composition as aspartic
acid/aspargine, glutamic acid/glutamine,
serine, glysine, argenine, proline, alanine,
tyrosine, valine, methionine, leucine, iso-

109
110
leucine and phenylalanine in the ratio:
1:2:3:8:1:1:1:3:2:6:3:4:5:3 (Rastogi and
Mehrotra 1993, 1998, Srinivas et al 1992).
Niranjan et al (2003) reported that the
leaves are excellent natural sources of
carotenoids with maximum amount present
in the middle followed by lower and upper
leaves.
Biological activity of turmeric
A great variety of pharmacological
activities of turmeric have been reported.
Curcumin is one of its major components
being responsible for its various biologi-
cal actions. It exhibits anti-parasitic,
antispasmodic, anti-inflammatory, antic
arcinogenic and gastrointestinal
effects in vitro whereas it has shown anti-
parasitic and anti-inflammatory activity
through oral application in animal models
(Araujo and Leon 2001, Davis et al 2007,
Thangapazham et al 2007). The variou
pharmacological activities of turmeric/
compounds/extracts are shown in Table 1.
Anti-inflammatory activity
Chronic inflammation leads to de-
struction of normal tissue injury. Produc-
tion of inflammation mediators through
up-regulation of several inducible gene
products, such as inducible nitric acid
(iNOS) and cyclo-oxygenase-2 (COX-2),
contribute to inflammatory responses and
tissue damage. Lee et al (2005) have
prepared 4 diarylheptanoid and a series of
new diarylheptalamine analogues deriva-
tives from curcumin and evaluated anti-
inflammatory activity by using LPS-stimu-
lated macrophages for induction of iNOS
and COX-2 as a model system.
Mukhophadhyay et al (1982) studied the
anti-inflammatory activity of curcumin,
diacetyl curcumin, triethyl curcumin,
tetrahydrocurcumin and phenylbutazone by
using carrageenin-induced rat paw oedema.
The curcumin analogues decrease the
carrageenin induced paw oedema.
Yamamoto et al (1997) hypothesized that
the anti-inflammatory action of curcumin
was partly due to the inhibition of the
enzyme G protein mediated phospholi-
pase D (PLD). The authors studied the
effects of curcumin on a number of phos-
pholipases in a cell free system and re-
ported that it inhibits 12-O tetradeco
noylphorbel-13 in a dose dependent man-
ner. It suggests that PLD inhibition may
contribute to the mechanism of
chemopreventive action of curcumin. Xu
et al (1997) evaluated the effects of
curcumin on chemotactic cytokines or
chemokine expression in bone marrow
cells. Regulatory effects on chemokine
expression by IL-1 alpha lowered mRNA
levels by inhibition of the transcription of
chemokine genes, effecting immunomodu-
lation. Awasthi (1996) studied the effi-
cacy of turmeric in the local application
in the eye in which twenty-five cases were
used in inflammatory condition and bac-
terial conjunctivitis of eye. Clinical symp-
toms like eye redness or burning sensa-
tion started subsiding from the third day
treatment. The author reported that 23 out
of 25 patients were completely relieved
from the condition during the six-day
treatment. Barquero et al (2007) reported
that inhibition of Mitogen-activated pro-
tein kinases (MAPK) p38 signaling by
curcumin (50-100 mg/kg body weight)
explain the reduced COX-2 and iNOS
immunosignals and the nitrite production
in colonic mucosa reducing the develop-
ment of chronic colonic inflammation.
Woo et al (2007) reported that curcumin
suppresses obesity-induced inflammatory
responses by suppressing adipose tissue
macrophage accumulation or activation
and inhibiting MCP-1 release from
adipocytes. It has a potential to improve
chronic inflammatory conditions in obe-
sity.
Antioxidant activity
Unnikrishnan and Rao (1995) re-
ported protection of heamoglobin from
oxidation at low concentration (0.08 mM
of curcumin), inhibition of lipid
peroxidation in rat liver microsomes, eryth-
rocyte membranes and brain homogenates.
The curcumin is capable of scavenging
oxygen free radicals such as superoxide
anions and hydroxyl radicals, which are
important to inhibit the lipid peroxidation
(Selvem et al 1995, Sreejayan and Rao
1994, 1996, 1997, Stano et al 2000).
Jayaprakasha et al (2006) and Ramsewak
et al (2000) reported in vitro antioxidant
activity of individual curcuminoids in
phosphomolybdenum and linoleic acid
peroxidation methods. Its capacity as
ascorbic acid equivalent (µmol/g) was in
the order of curcumin> demethoxy -
curcumin> bisdemethoxycurcumin. The
methoxy and phenolic group on the phe-
J Food Sci Technol, 2008, 45(2), 109–116
nyl ring and the 1, 3-diketone systems
seem to play a major role and potent
legend for metals. The antioxidant activ-
ity of curcumin increases when phenolic
and methoxy groups are on the ortho
position. Venkatesan and Rao (2000) and
Masuda et al (1999) showed that the
phenolic group is the most important for
mechanism and radical reaction of
curcumin that enhances antioxidant prop-
erties to a significant extent. Commandeur
and Vermeulen (1996) averred that
curcuminoids are proven to have a dual
pronged mechanism of antioxidant action
viz., inhibiting the formation as well as
propagation of free radicals. Jarula et al
(1998) in the subsequent study reported
that curcumin exerts a glutathione inde-
pendent mechanism of cell protection.
Cousins et al (2007) showed the antioxi-
dant capacities of methanolic extracts of
fresh and dried rhizomes for their ability
to scavenge the DPPH radical and chelate
ferrous ion whereas Jang et al (2007)
reported activity in curcumin, acetone,
methanol and hot water extracts using
DPPH, FRAP and FTC assays. Kurien
and Scofield (2007) reported that in vitro
curcumin suppresses the HNE-protein (4-
hydroxy-2-nonenal) modification signifi-
cantly (65%) in the presence of an in-
ducer, sodium hydroxide. Xu et al (2007)
reported the relaxing effect of curcumin
on porcine coronary arteries, which re-
lates to its antioxidant effect and protect
from oxidative stress by blocking the pro-
duction of superoxide anoin and promote
nitric oxide release.
Anti-tumor and anti-cancer activity
Huang et al (1988, 1991, 1992) re-
ported that turmeric inhibits the epider-
mal ornithine decarboxylase (ODC) and
epidermal DNA synthesis on tumor pro-
motion in mouse skin. According to Lin
et al (2000) and Johnson and Mukhtar
(2007) curcumin enhances cytotoxicity of
chemotherapeutic agents in prostate can-
cer cells and has ability to block colon
tumor initiation. Synergistic effects were
observed when curcumin was combined
with standard chemotherapeutic agents. It
effectively inhibited UV radiation induced
cellular damage and thereby reduced the
incidence of skin cancer by virtue of its
free radical quenching action. Curcumin
was found to inhibit the proliferation of
 111

Table 1. Biological activity of turmeric compounds and extracts

Turmeric/compounds/extracts Activity References
Curcumin Anti-inflammatory Araujo and Leon 2001, Barquero et al 2007, Davis
et al 2007, Lee et al 2005, Mukhophadhyay et al
1982, Thangapazham et al 2007, Woo et al 2007,
Xu et al 1997, Yamamoto et al 1997
Antioxidant Jang et al 2007, Jayaprakasha et al 2006, Kurien and
Scofield 2007, Masuda et al 1999, Ramsewak et al
2000, Selvem et al 1995, Sreejayan and Rao 1994,
1996, 1997, Stano et al 2000, Unnikrishnan and Rao
1995, Venkatesan and Rao 2000, Xu et al 2007
Anti-tumor and anti-cancer Lin et al 2000, Azuin and Bhide 1994, Kuo et al
1996, Soudamini and Kuttan 1988, Lal et al 2000,
Ozaki et al 2000, Johnson and Mukhtar 2007, Wahl
et al 2007, Zhang et al 2007
Anti-HIV De Clereq 2000, Eigner and Scholz 1999, Mazumber
et al 1995, 1997, Rafael et al 1993, Rithaporn et al
2003, Santo et al 2005, Vlietinck et al 1998
Antimutagenic Khajavi et al 2007, Li et al 1998, Shukla et al 2002
Anti-fungal Nose et al 1998
Antidiabetic Arun and Nalini 2002, Hussain 2002, Murugan and
Pari 2007
Antifibrinogenic Kang et al 2002
Wound healing Panchatcharam et al 2006, Phan et al 2001, Sidhu et
al 1998, Thangapazham et al 2007
Lipid lowering Asai and Miyasawa 2001, Peschel et al 2007, Shalini
and Srinivas 1987, Sreejayan and Rao 1996,
Venkatesan 1998
Radioprotective Cheng et al 2001, Inano and Onada 2002, Khafif et
al 2005, Kunwar et al 2007, Thresiamma 1996,
Varadkar et al 2001
Immunomodulating Bright 2007, Feruguson and Philpott 2007, South et
al 1997
Demethoxycurcumin Antioxidant Ramsewak et al 2000
Bisdemethoxycurcumin Antioxidant Ramsewak et al 2000
Diacetyl curcumin Anti-inflammatory Araujo and Leon 2001, Lee et al 2005,
Mukhophadhyay et al 1982, Xu et al 1997,
Yamamoto et al 1997
Triethyl curcumin Anti-inflammatory Mukhophadhyay et al 1982
Tetrahydrocurcumin Anti-inflammatory Mukhophadhyay et al 1982
Antidiabetic Murugan and Pari 2007
Turmeric oil Anti-bacterial, anti-fungal Apisariyakul et al 1995, Bhavani and Murthy 1979
Turmeric powder Antidiabetic Arun and Nalini 2002, Hussain 2002
Anti-inflammatory Awasthi 1996
Anti-tumor and anti-cancer Huang et al 1988, 1991, 1992
Ethanol extract Anti-protozoal Rasmussen et al 2000
Anti-fungal Khattaka et al 2005
Acetone extract Anti-fungal Lee et al 2007
Antioxidant Jang et al 2007
Methanol extract Antioxidant Cousins et al 2007, Jang et al 2007
Water extract Antioxidant Jang et al 2007

J Food Sci Technol, 2008, 45(2), 109–116

112
human breast cancer cells in vitro models
(Azuin and Bhide 1994, Kuo et al 1996,
Soudamini and Kuttan 1988, Zhang et al
2007). The development of cancerous and
precancerous lesions in the glandular stom-
ach was decreased by exposure to pure
curcumin and exerted chemopreventive
effects in rats (Lal et al 2000). Ozaki et
al (2000) observed curcumin to be a potent
inhibitor of the transcriptional factors
activated protein 1 and nuclear factor
kappa B. These factors were known to
play important functional roles in the
survival of osteoclast. Curcumin was
shown to stimulate osteoclast apoptosis in
a dose dependent and time dependent
manner. It exhibits osteoclastic bone re-
sorption supporting the results that it stimu-
lates osteoclasts apoptosis. Wahl et al
(2007) reported that curcumin in conjuga-
tion with Apo2L/TRAIL, the chemoresi-
stant phenotype seen in many ovarian
cells could be overcome by activating the
apoptotic pathways through both the ex-
trinsic and intrinsic pathways.
Anti-HIV activity
Vlietinck et al (1998) reported the
inhibition of the virus cell fusion stage in
the replication cycle of HIV. Mazumber
et al (1995, 1997) and De Clereq (2000)
demonstrated the antiviral activity, being
a HIV-1 integrase inhibitor (IC50=40µM)
and suggested that its analogs such as
dicaffeoylmethane and rosmarinic acid
may be developed as anti-HIV drugs.
Eigner and Scholz (1999) and Rafael et
al (1993) claimed in patent application
that curcumin has anti-HIV-1 and HIV-2
activities. Rithaporn et al (2003) reported
that curcumin is noval intravaginal sper-
micidal agent for contraception and HIV
prevention. Santo et al (2005) reported
that curcumin and compounds containing.
3,4,5 trihydroxyphenyl group with car-
boxylic group function are potent
integrase (IN) inhibitor active against HIV
replication.
Antimutagenic potential
Li et al (1998) and Shukla et al
(2002) evaluated the antimutagenic ef-
fects in vitro by using chromosomal ab-
erration assay in Wistar rats induced by
cyclophosphamide, a known carcinogen.
The aberrant cells were found to be re-
duced with 100 and 200 mg/kg body
weight doses of curcumin when compared
to a control group treated with
phosphamide alone for 7 consecutive days.
The authors concluded that curcumin has
antigenotoxic potential against cyclophos-
phamide induced chromosomal mutations.
Findings of Khajavi et al (2007) indicate
that curcumin treatment is sufficient to
relieve the toxic effect of mutant aggre-
gation-induced apoptosis and improves the
neuropathologic phenotype in an animal
model of human neuropathy, suggesting a
potential therapeutic role in selected forms
of inherited peripheral neuropathies.
Anti-bacterial, anti-fungal and anti-
protozoal activity
Turmeric oil showed inhibition of
Staphylococcus aureus growth in the
concentration of 1 to 5000 ppm. Khattaka
et al (2005) reported that ethanol extract
of turmeric has good anti-fungal activity.
Total inhibition of intestinal Lactobacilli
growth was reduced with the treatment of
turmeric extract. Anti-fungal effect against
Candida albicans, C. kruseii, C.
parapsilosis, isolates of dermatophytes,
yeast and pathogenic moulds was reported
by Apisariyakul et al (1995) and Bhavani
and Murthy (1979). Nose et al (1998)
found the weak growth and toxicogenesis
of selected Aspergillus flavus strains on
curcumin, indicating its anti-fungal effects
and inhibition of aflatoxin production. It
has marked antiparasitic activity in vitro
showing cytotoxicity against African try-
panosomes. Saleheen et al (2002) showed
curcumin to have an IC50 of 5.3 µM against
prostagotes of various leishmanial strains
that was much lower as compared to
pentamidine. Anti-protozoal activity was
reported in the ethanolic extract of tur-
meric against Plasmodium falciparum and
Leishmania major. It was able to inhibit
the in vitro growth of these parasites
(Rasmussen et al 2000). Lee et al (2007)
reported that acetone extract of turmeric
inhibits effectively Phyllosticta caricae
with the minimum inhibitory value of 6.7
mg/ml.
Antidiabetic activity
Administration of turmeric or
curcumin or tetrahydrocurcumin to dia-
betic rats reduced the blood sugar and
glycosylated haemoglobin level signifi-
cantly (Arun and Nalini 2002, Hussain
2002, Murugan and Pari 2007). Oxidative
stress was reduced by turmeric and
J Food Sci Technol, 2008, 45(2), 109–116
curcumin as determined by the standard
TBARS test. The authors postulated that
this could be due to decrease of glucose
in polyol pathway, leading to an increased
NADPH/NADP ratio and elevated activ-
ity of the antioxidant enzyme glutathione
peroxidase.
Antifibrinogen activity
Kang et al (2002) reported the ef-
fects of curcumin on the production of
collagen and smooth muscle alpha pro-
teins. Alpha (1) collagen mRNA in vivo
and in vitro was found to reduce DNA
synthesis at a concentration of 5 µg/ml. It
was concluded that curcumin might prove
as a valuable antifibrinogenic agent.
Wound healing activity
Tissue repair and wound healing
are complex processes that involve in-
flammation, granulation and remolding
of the tissue. Sidhu et al (1998) ob-
served that the localization of trans-
forming growth factor beta and
fibronectin, which are important criteria
in wound healing, showed increase in
curcumin treated wounds as compared
to untreated wounds. Phan et al (2001)
investigated the effects of curcumin on
hydrogen peroxide and hypoxanthine-
xanthine oxidase induced damage to
cultured human keratinocytes and fibro-
blasts in an effort to elucidate the mecha-
nism of wound healing action of
curcumin. It was observed that exposure
of human keratinocytes to curcumin (10
µg/ml) offered significant protection
against hydrogen peroxide. However, no
protective effects were observed against
hypoxanthine-xanthine oxidase injury.
The authors concluded that curcumin is
a powerful inhibitor of damage to
human keratinocytes and fibroblasts.
Thangapazham et al (2007) showed the
beneficial effect of curcumin as
proangiogenic agent in wound healing
by inducing transforming growth
factor-beta, which induces both
angiogenesis and accumulation of
extracellular matrix and continues
through the remodeling phase of wound
repair. Panchatcharam et al (2006) found
that curcumin treated wound heal much
as indicated by improved rates of
epithelialisation, wound contraction and
increased tensile strength confirmed by
histopathological examinations.

Lipid lowering activity
The effects of diet supplemented
curcuminoids (commercial grade curcumin:
a mixture of curcumin (73.4%), demethoxy-
curcumin (16.1%)and bisd emethoxy-
curcumin (10.5%)) showed encouraging
effects on triacylglycerol and cholesterol
concentrations with lipid-lowering potency
(Asai and Miyasawa 2001, Shalini and
Srinivas 1987). Sreejayan and Rao (1996)
reported the ability of curcumin to scav-
enge electrophilic reactive intermediate
found by metabolic activation of drug and
lipid peroxidation. Venkatesan (1998) stud-
ied the protective effect against acute
adriamycin myocardial toxicity. Curcumin
treatment for 7 days before and 2 days
after adriamysin treatment at the level of
200 mg/kg body weight significantly inhib-
ited the lipid peroxidation and increased
the levels of endogenous antioxidants.
Peschel et al (2007) studied the effect of
curcumin on hepatic gene expression using
the human hepatoma cell line HepG2 as a
model system for hypocholesterolemic
activity on molecular basis. They found
that the curcumin treatment caused up to
seven fold concentration dependent increase
in LDL-receptor m-RNA whereas m-RNA
of the genes encoding the sterol biosyn-
thetic enzymes HMG CoA reductase and
farnesyle diphosphate synthase were only
slightly increased at high curcumin con-
centrations, where cell viability was re-
duced.
Radioprotective activity
Curcumin was effective in inhibiting
radiation-induced protein kinase C (PKC)
activity and was potentially useful as a
chemo preventive agent. Activation of PKC
is reported to be the means of conferring
radio resistance on a tumor cell. Therefore
suppression of PKC by curcumin may be
means of preventing the development of
radio resistance following radiotherapy. It
is beneficial in reducing the risk of devel-
oping cancer; it has also protective effect
on radiation-induced toxicity and also prob-
ably against the harmful effects of orga-
nochlorine pesticides (Cheng et al 2001,
Thresiamma 1996). Varadkar et al (2001)
reported curcumin to be potentially useful
in preventing the development of radio
resistance following radiotherapy. Inano
and Onada (2002) reported the protective
action of curcumin to reduce the incidence
of mammary and pituitary tumors against
the long-term effect of radiation in preg-
nant rats. Khafif et al (2005) found that
curcumin (3.75 µM) exhibits radio-sensi-
tizing effects on squamous cell carcinoma
(SCC) cells. Kunwar et al (2007) reported
that curcumin and its mononuclear copper
complex are very effective in protecting
the cells against radiation-induced suppres-
sion of glutathione peroxidase, catalase and
superoxide dismutase (SOD) activities.
Immunomodulating activity
South et al (1997) attributed the
beneficial actions of natural compounds
to their immunomodulating effects. The
effect of curcumin on 3 major types of
immune function in rats, antibody (IgG)
production, delayed-type hypersensitivity
and natural killer cell activity were evalu-
ated after 5 weeks of dietary exposure to
1, 20 or 40 mg/kg of curcumin. The
highest dose of curcumin significantly
enhanced IgG levels. Neither delayed type
hypersensitivity nor natural killer cell
activity was different from control values
at any dietary concentration of curcumin.
In vitro incubation of tumor cells (YAC-
1 and EL-4-types) and normal spleenocytes
with varying concentration of curcumin
for different periods of time revealed the
differences between cell types and its
effects on cell proliferations and viability.
No toxic effects were seen in EL-4 cells
treated with 125 µg/ml curcumin even
after incubation for 48 h. Cell prolifera-
tion was reduced by almost 50% after 24
h. YAC-1 cell viability and cell numbers
were diminished at longer cell incuba-
tions. A lower curcumin concentration
(1.25 µg/ml) enhanced cell growth in the
YAC-1 cells at 24 and 48 h. This en-
hancement was not seen in spleen and
EL-4 cells. Feruguson and Philpott (2007)
reported that curcumin effectively targets
the immune response by preventing can-
cer. According to Bright (2007) curcumin
inhibits autoimmune diseases by regulat-
ing inflammatory cytokines such as IL-
1beta, IL-6, IL-12, TNF-alpha and IFN-
gamma and associated JAK-STAT, AP-1,
and NF-kappaB signaling pathways in
immune cells.
Structure–activity relationships
Curcumin belongs to class of
curcuminoids and is very similar to
diarylheptanoids. The anti-inflammatory
J Food Sci Technol, 2008, 45(2), 109–116
113
activity of curcumin and its derivatives is
due to the presence of hydroxyl and phenol
groups in the molecule that being essential
for the inhibition of prostaglandins (PG
synthetase) and leucotrienes (LT) (Araujo
and Leon 2001). On the other hand, some
authors suggested that due to the existence
of β-dicarbonylic system having the con-
jugated double bonds (dienes) is respon-
sible for anti-inflammatory activity (Barclay
et al 2000). The presence of diene and
keto system provide lipophilicity to the
compounds and thus probably has better
skin penetration. The presence of diketone
moiety in the curcumin molecule seems to
be essential for the inhibitory activity
(Kiuchi et al 1993). Many research groups
have taken curcumin as a starting material
of drug discovery. One widely used struc-
tural modification truncates the central con-
jugated beta-diketone in curcumin to the
monocarbonyl dienone used against cancer
related cell lines (Mosley et al 2007).
Authors reported that dienone drugs, per-
mit a double-pronged attack with the po-
tential to destroy a tumor directly by
apoptosis. Somparn et al (2007) reported
that the demethoxy derivatives
(demethoxycurcumin and bisdemethoxy
curcumin) of curcumin have lower antioxi-
dant activity suggesting that the ortho-
methoxyphenolic groups of curcumin are
involved in antioxidant activities. Authors
studied that hydrogenation at conjugated
double bonds of the central seven carbon
chain and β-diketone of curcumin to
tetrahydro curcumin, hexahydrocurcumin
and octahydrocurcumin remarkably enhance
antioxidant activity.
Pharmacodynamic and
pharmacokinetic studies
A dose escalation pilot study of a
novel standardized turmeric extract in
proprietary capsule form was performed
at doses between 440 and 2200 mg/day,
containing 36-180 mg of curcumin. Fif-
teen patients with advanced colorectal
cancer refractory to standard chemothera-
pies received turmeric extract daily up to
4 months. Indices of damage including
glutathione S-transferase levels, levels of
a DNA adduct formed by lipid
peroxidation end products (leukocyte M
(1)(G) and prostaglandin biosynthesis in
the blood cells of the patients were mea-
sured (Sharma et al 2001). Curcumin was
114
not detected in the blood or urine of the
patients. Ingestion of 440 mg of turmeric
extract for 29 days induced a 59% de-
crease in lymphocytic glutathione S-trans-
ferase activity, and the effect was not
observed at higher dose levels. Leukocyte
M (1) G levels did not change and radio-
logically stable disease was demonstrated
in five patients for 2-4 months treatment.
Sharma et al (2001) concluded that tur-
meric extract could be administered safely
to patients at doses of up to 2.2 g daily,
equivalent to approximately 180 mg of
curcumin. Curcumin has low oral
bioavailability in humans and may un-
dergo intestinal metabolism (Sharma et al
2001). Curcumin when added to isolated
hepatocytes is quickly metabolized and
the major biliary metabolites are glucu-
ronides of tetrahydrocurcumin and
hexahydrocurcumin. After metabolism in
the liver it is mainly excreted through
bile. Sharma et al (2007) reported that
daily oral dose of 3.6 g of curcumin is
compatible with detectable levels of the
parent compound in colorectal tissue from
patients with cancer. The levels demon-
strated might be sufficient to exert phar-
macological activity.
Clinical studies of turmeric and
curcumin
Clinical trail in 18 patients with defi-
nite rheumatoid arthritis showed that pa-
tient receiving either turmeric at 1200
mg/day or phenylbutazone at 30 mg/day
had significant improvement in morning
stiffness, walking time and joint swelling
after 2 weeks of therapy (Deodhar et al
1980). Oral administration of the drug to
116 patients having acid and randomized
dyspepsia and flatulence were found sig-
nificant relief. Two other clinical trials
measure the effect of the drug on peptic
ulcers. Oral administration of the drug
showed the promotion in ulcer healing
and reduction in abdominal pain.
Curcumin exhibits free radical scavenging
ability when administered to humans. In
an open (uncontrolled) clinical trial, 18
healthy individuals ranging in age from
27 to 67 years consumed turmeric extract,
at a dose supplying 20 mg curcuminoids
for 45 days. Before and after blood tests
showed a statistically significant decrease
in lipid peroxides (Ammon and Wahl
1991).
Safety and dosage
No significant toxicity has been re-
ported in administration of turmeric pow-
der, extracts or curcumin at high doses.
Average consumption of 0.5 to 1.5 g/day/
person turmeric by Asians showed no
toxic symptoms (Eigner and Scholz 1999).
Administration of turmeric at higher doses
(2.5 g/kg body weight) to male and fe-
male guinea pigs, monkeys and Wistar
rats showed no changes in the appearance
and weight of kidney, liver and heart
(Chattopadhyay et al 2004). Wu (2003)
reported in a phase 1 human trial with 25
subjects using up to 8000 mg of curcumin
per day for 3 months found no toxicity.
In five other human trials using 1125-
2500 mg of curcumin per day have also
found it to be safe. The human studies
were used in anti-inflammatory activity of
curcumin. Aggarwal et al (2003) reported
that human clinical trials have no dose
limiting toxicity when curcumin was ad-
ministered at dose up to 10 g/day.
Conclusion
Turmeric has been used in Ayurveda,
Unani and Siddha systems of medicines
from ancient times. Literature survey
shows wide spectrum of pharmacological
activities of turmeric either in the form of
powder, extracts or in its isolated com-
pounds with minimum side effects. The
methoxy group on the phenyl ring, phe-
nolic, and 1, 3-diketone systems in the
curcumin play important role for various
pharmacological activities. Several prod-
ucts have been launched in National and
International markets for various diseases
fortified with curcumin or turmeric. Ex-
tensive work has been reported on this
plant, but still it requires to explore more
work for drug development. Curcumin is
safe, non-toxic and strong natural antioxi-
dant in comparison with other phyto-an-
tioxidants.
References
Aggarwal BB, Kumar A, Bharti AC 2003.
Anticancer potential of curcumin: preclini-
cal and clinical studies. Anticancer Res
23:363-398
Ammon HPT, Wahl MA 1991. Pharmacology
of Curcuma longa. Planta Medica 57:1-7
Apisariyakul A, Vanittanakom N, Buddhasukh
D 1995. Anti-fungal activity of turmeric
oil extracted from Curcuma longa
(Zingiberaceae). J Ethnopharmacol
49:163-169
J Food Sci Technol, 2008, 45(2), 109–116
Araujo CAC, Leon LL 2001. Biological ac-
tivities of Curcuma longa L. Mem Inst
Oswaldo Cruz Rio de Janeiro 96:723-728
Arun N, Nalini N 2002. Efficacy of turmeric
on blood sugar and polyol pathway in
diabetic albino rats. Plant Food Hum Nutr
57:41-52
Asai A, Miyasawa T 2001. Dietary
curcuminoids prevent high fat diet in-
duced lipid accumulation in rat liver and
epididymal adipose tissue. J Nutr
131:2932-2935
Awasthi S 1996. Curcumin protects against 4-
hydroxy-2-transnonenal-induced cataract
formation in rat lenses. Am J Clin Nutr
64:761-766
Azuine MA, Bhide SV 1994. Adjuvant
chemoprevention of experimental cancer:
catechin and dietary turmeric in forestom-
ach and oral cancer models. J
Ethnopharmcol 44:211-217
Bakshi DNG, Sensarma P, Pal DC 1999. A
lexicon of medicinal plants in India. Naya
Prakash, Calcutta.
Barclay LR, Vinqvist MR, Mukai K, Goto H,
Hashimoto Y, Yokunaga A, Uno H 2000.
On the antioxidant mechanism of
curcumin: Classical methods are needed
to determine antioxidant mechanism and
activity. Org Lett 2:2841-2843
Barquero LC, Villegas I, Sanchez-Calvo JM,
Talero E, Sanchez-Fidalgo S, Motilva V,
Lastra CA 2007. Curcumin, a Curcuma
longa constituent, acts on MAPK p38
pathway modulating COX-2 and iNOS
expression in chronic experimental colitis.
Int Immunopharm 7:333–342
Bhavani STN, Murthy S 1979. Effect of tur-
meric (Curcuma longa) fractions on the
growth of some intestinal and pathogenic
bacteria in vitro. Indian J Exp Biol
17:1363-1366
Bright JJ 2007. Curcumin and autoimmune
disease. Adv Exp Med Biol 595:425-451
Chattopadhyay I, Biawas K, Bandyopadhyay
I, Banerjee RK 2004. Turmeric and
curcumin: Biological actions and medici-
nal applications. Curr Sci 87:44-53
Cheng A-L, Hsu C-H, Lin JK 2001. Phase-
I clinical trail of curcumin, a
chemopreventive agent in patients with
high risk or premalignant lesions. Anti-
cancer Res 27:2895-2900
Chopra RN, Nayar SL, Chopra IC 1999.
Glossary of Indian medicinal plants.
NISCOM, CSIR, New Delhi,
Commandeur JN, Vermeulen NP 1996. Cyto-
toxicity and cytoprotectivity activities of
natural compounds. The case of curcumin.
Xenobiotics 26:667-680
Cousins M, Adelberg J, Chenb F, Rieck J
2007. Antioxidant capacity of fresh and

dried rhizomes from four clones of tur-
meric (Curcuma longa L.) grown in vitro.
Ind Crop Prod 25:129–135
Davis JM, Murphy EA, Carmichael MD,
Zielinski MR, Groschwitz CM, Brown AS,
Gangemi JD, Ghaffar A, Mayer EP 2007.
Curcumin effects on inflammation and
performance recovery following eccentric
exercise-induced muscle damage. Am J
Physiol Regul Integr Comp Physiol
292:2168-2173
De Clereq E 2000. Current lead natural prod-
ucts for the chemotherapy of human im-
munodeficiency virus (HIV) infection. Med
Res Rev 20:323-349
Deodhar SD, Sethi R, Srimal RC 1980. Pre-
liminary study on antirheumatic activity
of curcumin (diferuloylmethane). Indian J
Med Res 71:632-634
Eigner D, Scholz D 1999. Ferula asafoetida
and Curcuma longa in traditional medical
treatment and diet in Nepal. J
Ethnopharmacol 67:1-6
Ferguson LR, Philpott M 2007. Cancer pre-
vention by dietary bioactive components
that target the immune response. Curr
Cancer Drug Targets 7:459-464
Huang HC, Jan TR, Yeh SF 1992. Inhibitory
effect of curcumin, an anti-inflammatory
agent, on vascular smooth muscle cell pro-
liferation. Eur J Pharmacol 221:381-384
Huang MT, Lysz T, Ferraro T, Abidi TF,
Laskin JD, Conney AH 1991. Inhibitory
effects of curcumin on in vitro
lipoxygenase and cyclooxygenase activi-
ties in mouse epidermis. Cancer Res
51:813-819
Huang MT, Smart RC, Wong CQ, Conney
AH 1988. 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 48:5941-5946
Hussain HEM 2002. Hypoglycemic,
hypolipidemic and antioxidant properties
of combination of curcumin from Cur-
cuma longa Linn and partially purified
product from Abroma auguesta Linn in
streptozotocin induced diabetes. Indian J
Clin Biochem 17:33-43
Inano H, Onoda M 2002. Prevention of radia-
tion-induced mammary tumors. Int J Radiat
Oncol Biol Phys 52:212-223
Jang HD, Chang KS, Huang YS, Hsu CL, Lee
SH, Su MS 2007. Principal phenolic
phytochemicals and antioxidant activities
of three Chinese medicinal plants. Food
Chem 103:749–756
Jaruga E, Bielak-Zmijewska A, Sikora E,
Skierski J, Radziszewska E, Pioweka K,
Bartoz G 1998. Glutathione-independent
mechanism of apoptosis inhibited by
curcumin in rat thymocytes. Biochem
Pharmacol 56:961-965
Jayaprakasha GK, Rao LJ, Sakariah KK 2006.
Antioxidant activities of curcumin,
demethoxycurcumin and bisdemethoxy
curcumin. Food Chem 98:720-724
Johnson JJ, Mukhtar H 2007. Curcumin for
chemoprevention of colon cancer. Can Lett
255:170–181
Kang HC, Nan JX, Park PH 2002. Curcumin
inhibits collagen synthesis and hepatic
stellate cell activation in vivo and in
vitro. J Pharm Pharmacol 54:119-126
Kapoor LD 1990. Hand book of ayurvedic
medicinal plants. CRC Press, Boca
Raton, FL
Khafif A, Hurst R, Kyker K, Fliss DM, Gil
Z, Medina JE 2005. Curcumin: a new
radio-sensitizer of squamous cell carci-
noma cells. Otolaryngol Head Neck Surg
132:317-321
Khajavi M, Shiga K, Wiszniewski W, He F,
Shaw CA, Yan J, Wensel TG, Snipes GJ,
Lupski JR 2007. Oral curcumin mitigates
the clinical and neuropathologic pheno-
type of the trembler-j mouse: a potential
therapy for inherited neuropathy. Am J
Hum Genet 81:438-453
Khattaka S, Rehmana S, Shahb HU, Ahmade
W, Ahmad M 2005. Biological effects of
indigenous medicinal plants Curcuma
longa and Alpinia galanga. Fitoterapia
76:254–257
Kiso Y, Suzuki Y, Oshima Y, Hikino H 1983.
Stereostructure of curlone
sesquiterpenoid of Curcuma longa Rhi-
zomes. Phytochem 22:596-597
Kiuchi F, Goto Y, Sugimoto N, Akao N, Kondo
K, Tsuda Y 1993. Nematocidal activity of
turmeric: synergistic action of curcuminoids.
Chem Pharm Bull 41:1640-1643
Kunwar A, Narang H, Priyadarsini KI, Krishna
M, Pandey R, Sainis KB 2007. Delayed
activation of PKCdelta and NFkappa B
and higher radioprotection in splenic lym-
phocytes by copper (II)-curcumin (1:1)
complex as compared to curcumin. J Cell
Biochem 102:1214-1224
Kuo ML, Huang TS, Lin JK 1996. Curcumin
an antioxidant and anti-tumor promoter,
induces apoptosis in human leukemia cells.
Biochem Biophys Acta 15:95-100
Kurien BT, Scofield RH 2007. Curcumin/tur-
meric solubilized in sodium hydroxide in-
hibits HNE protein modification-An in vitro
study. J Ethnopharmacol 110:368-373
Lal B, Kapoor AK, Agarwal PK, Asthana OP,
Srimal RC 2000. Role of curcumin in
idiopathic inflammatory orbital
pseudotumours. Phytother Res 14:443-447
Lee SH, Chang KS, Su MS, Huang YS, Jang
HD 2007. Effects of some Chinese me-
115
dicinal plant extracts on five different
fungi. Food Control 18:1547–1554
Lee SL, Huang WJ, Lin WW, Lee SS and
Chen CH 2005. Preparation and anti-in-
flammatory activities of diarylheptanoid
and diarylheptylamine analogs. Bioorganic
Med Chem 13:6175-6181
Li X, Song Q, Chen B 1998. Study on the
antimutagenicity of curcumin. Wei Sheng
Yan Jiu 27:163-165
Lin JK, Pan MH, Lin-Shiau SY 2000. Recent
studies on the biofunctions and biotransfor-
mations of curcumin. Biofactors 13:153-158
Masuda T, Hidaka K, Shinohara A, Maikawa
T, Takeda Y, Yamaguchi H 1999. Chemi-
cal studies on antioxidant mechanism of
curcuminoid: analysis of radical reaction
products from curcumin. J Agric Food
Chem 47:71-77
Mazumber A, Neamati N, Sunder S, Schulz
J, Pertz H, Eich E, Pommier Y 1997.
Curcumin analogs with altered potencies
against HIV-I integrase as probes for
biochemicals mechanisms of drug action.
J Med Chem 40:3057-3063
Mazumber A, Raghavan K, Weinstein J, Kohn
KW, Pommer Y 1995. Inhibition of hu-
man immunodeficiency virus type-1
integrase by curcumin. Biochem Pharmacol
49:1165-1170
Mosley CA, Liotta DC, Snyder JP 2007.
Highly active anticancer curcumin ana-
logues. Adv Exp Med Biol 595:77-103
Mukhophadhyay A, Basu N, Ghatak N, Gujral
a PK 1982. Anti-inflammatory and irritant
activities of curcumin analogues in rats.
Agents Actions 12:508-515
Murugan P, Pari L 2007. Influence of
tetrahydrocurcumin on erythrocyte mem-
brane bound enzymes and antioxidant
status in experimental type 2 diabetic rats.
J Ethnopharmacol 113:479-486
Niranjan A, Prakash D, Tewari SK, Pande A,
Pushpangadan P 2003. Chemistry of spe-
cies of Curcuma cultivated on sodic soil.
J Med Aromatic Plant Sci 25:69-75
Nose M, Koide T, Ogihara Y, Yabu Y, Ohta
N 1998. Trypanocidal effects of curcumin
in vitro. Biol Pharm Bull 21:643-645
Ohshiro M, Kuroyanagi M, Ueno A 1990.
Structures of sesquiterpenes from Cur-
cuma longa. Phytochem 29:2201-2205
Ozaki K, Kawata Y, Amano S, Hanazawa S
2000. Stimulatory effect of curcumin on
osteoclast apoptosis. Biochem Pharmacol
59:1577-1581
Panchatcharam M, Miriyala S, Gayathri VS,
Suguna L 2006. Curcumin improves
wound healing by modulating collagen
and decreasing reactive oxygen species.
Mol Cell Biochem 290:87-96
Peschel D, Koerting R, Nass N 2007.
J Food Sci Technol, 2008, 45(2), 109–116
 116
Curcumin induces changes in expression
of genes involved in cholesterol homeo-
stasis. J Nutr Biochem 18:113–119
Phan TT, See P, Lee ST, Chan SY 2001.
Protective effects of curcumin against
oxidative damage on skin cells in vitro: its
implication for wound healing. J Trauma
51:927-931
Rafael Z, Salto R, Li J, Craik C, Montellano
de PRO 1993. Inhibition of HIV-1 and
HIV-2 proteases by curcumin and
curcumin boron complexes. Bioorg Med
Chem 1:415-422
Ramsewak RS, De Witt DL, Nair MG 2000.
Cytotoxicity, antioxidant and anti-inflam-
matory activities of curcumins I-III from
Curcuma longa. Phytomed 7:303-308
Rasmussen HB, Christensen SB, Kvist LP,
Karazmi A 2000. A simple and efficient
separation of the curcumins, the
antiprotozoal constituents of Curcuma
longa. Planta Med 66:396-398
Rastogi RP, Mehrotra BN 1993. Compen-
dium of Indian medicinal plants. Central
Drug Research Institute, Lucknow and
National Institute of Science Communica-
tion, New Delhi. 3:220-221
Rastogi RP, Mehrotra BN 1998. Compen-
dium of Indian medicinal plants. Central
Drug Research Institute, Lucknow and
National Institute of Science Communica-
tion, New Delhi. 5:260-271
Ravindranath V, Satyanarayana MN 1980. An
unsymmetrical diarylheptanoid from Cur-
cuma longa. Phytochem 19:2031-2032
Rithaporna T, Mongaa M, Rajasekarana M
2003. Curcumin: a potential vaginal con-
traceptive. Contraception 68:219-223
Roth GN, Chandra A, Nair MG 1998. Noval
bioactivities of Curcuma longa constitu-
ents. J Nat Prod 61:542-545
Roughley PJ, Whiting DA 1973. Experi-
ments in the biosynthesis of curcumin. J
Chem Soc 20:2379-2388
Saleheen D, Ali SA, Ashfaq K, Sissiqui AA,
Aga A, Yasinzai MM 2002. Latent activ-
ity of curcumin against leshmaniasis in
vitro. Biol Pharma Bull 25:386-389
Santo RD, Costi R, Artico M, Ragno R,
Greco G, Novellino E, Marchand C,
Pommier Y 2005. Design, synthesis and
biological evaluation of heteroaryl
diketohexenoic and diketobutanoic acids
as HIV-1 integrase inhibitors endowed
with antiretroviral activity Il. Farmaco
60:409–417
Satyavati GV, Raina MR, Sharma M 1976.
Medicinal plants of India. Indian Council
of Medical Research, New Delhi
Selvem R, Subramanium L, Gayathri R,
Angayarkanni N 1995. The antioxidant
Received 03 April 2006; revised 17 September 2007; accepted 20 September 2007
View publication stats
activity of turmeric (Curcuma longa). J
Ethnopharmacol 47:59-67
Shalini VK, Srinivas L 1987. Lipid peroxide
induced DNA damage: protection by tur-
meric (Curcuma longa). Mol Cell Biochem
77:3-10
Sharma RA McLelland HR, Hill KA, Ireson
CR, Euden SA, Manson MM, Pirmohamed
M, Marnett LJ, Gescher AJ, Steward W
2001. Pharmacodynamic and pharmacoki-
netic study of oral Curcuma extract in
patients with colorectal cancer. Clin Can-
cer Res 7:1894-1900
Sharma RA, Steward WP, Gescher AJ 2007.
Pharmacokinetics and pharmacodynamics of
curcumin. Adv Exp Med Biol 595:453-470
Shukla Y, Arora A, Taneja P 2002. Antimu-
tagenic potential of curcumin on chromo-
somal aberrations in Wistar rats. Mutat
Res 575:197-202
Sidhu GS, Singh AK, Thaloor D, Banaudha
KK, Patniak GK, Srimal RC, Maheshwari
RK 1998. Enhancement of wound healing
by curcumin in animals. Wound Repair
Reg 6:167-177
Somparn P, Phisalaphong C, Nakornchai S,
Unchern S, Morales NP 2007. Compara-
tive antioxidant activities of curcumin and
its demethoxy and hydrogenated deriva-
tives. Biol Pharm Bull 30:74-78
Soudamini, Kuttan R 1988. Cytotoxic and
tumor reducing properties of curcumin.
Indian J Pharmacol 20:95-101
South EH, Exon JH, Hendrix K 1997. Dietary
curcumin enhances antibody response in
rats. Immunopharmacol Immunotoxicol
19:105-119
Sreejayan N, Rao MN 1994. Curcuminoids as
potent inhibitors of lipid peroxidation. J
Pharm Pharmacol 46:1013-1016
Sreejayan N, Rao MN 1996. Free radical
scavenging activity of curcuminoids.
Arzneimittelforschung 46:169-171
Sreejayan N, Rao MN 1997. Nitric acid oxide
scavenging by curcuminoids. J Pharmacol
49:105-107
Srinivas L, Shalini VK, Shylaja M 1992.
Turmerin: a water soluble antioxidant
peptide from turmeric. Arch Biochem
Biophys 292:617-623
Stano J, Grancai D, Neubert K, Kresanek J
2000. Curcumin as a potential antioxi-
dant. Ceska Slov Farm 49:168-170
Thangapazham RL, Sharma A, Maheshwari
RK 2007. Beneficial role of curcumin in
skin diseases. Adv Exp Med Biol 595:343-
357
Thresiamma KC 1996. Protective effect of
curcumin, ellagic acid and bixin on radia-
tion induced toxicity. Indian J Exp Biol
34:845-847
J Food Sci Technol, 2008, 45(2), 109–116
Unnikrishnan MK, Rao MN 1995. Inhibition
of nitrite induced oxidation of heamoglobin
by curcuminoids. Pharmazie 50:490-492
Varadkar P, Dubey P, Krishna M, Vermal NC
2001. Modulation of radiation induced
protein kinase and activity by phenolics.
J Radio Prot 21:261-370
Venkatesan N 1998. Curcumin attenuation of
acute adriyamycin mycocardial toxicity in
rats. Br J Pharmacol 124:425-427
Venkatesan P, Rao MN 2000. Structure activ-
ity relationships for the inhibition of lipid
peroxidation and the scavenging of free
radicals by synthetic symmetric curcumin
analogues. J Pharm Pharmacol
52:1123-1128
Vlietinck A, de Bruyne T, Apers S, Pieters L
1998. Plant-derived leading compounds
for chemotherapy of HIV infection. Planta
Med 64:97-109
Wahl H, Tan L, Griffith K, Choi M, Liu JR
2007. Curcumin enhances Apo2L/TRAIL-
induced apoptosis in chemoresistant ovarian
cancer cells Gynecol Oncol 105:104–112
Woo HM, Kang JH, Kawada T, Yoo H, Sung
MK, Yu R 2007. Active spice-derived
components can inhibit inflammatory re-
sponses of adipose tissue in obesity by
suppressing inflammatory actions of mac-
rophages and release of monocyte
chemoattractant protein-1 from adipocytes.
Life Sci 80:926–931
Wu NC 2003. Safety and anti-inflammatory
activity of curcumin: A component of
turmeric (Curcuma longa). J Alter Comp
Med 9:161-168
Xu PH, Long Y, Dai F, Liu ZL 2007. The
relaxant effect of curcumin on porcine
coronary arterial ring segments. Vasc
Pharmacol 47:25–30
Xu YX, Pindolia KR, Janakiraman N, Noth
CJ, Chapman RA, Gautam SC 1997.
Curcumin, a compound with anti-inflam-
matory and antioxidant properties,
downregulates Chemokine expressions in
bone marrow stromal cells. Exp Hematol
25:413-422
Yamamoto H, Mizutami T, Nomura H 1997.
Inhibitory effects of curcumin on mamma-
lian phospholipase D activity. FEBS Lett
417:196-198
Yu ZF, Kong LD, Chen Y 2002. Antidepres-
sant activity of aqueous extracts of Cur-
cuma longa in mice. J Ethnopharmacol
83:161-165
Zhang HG, Kim H, Liu C, Yu S, Wang J,
Grizzle WE, Kimberly RP, Barnes S 2007.
Curcumin reverses breast tumor exosomes
mediated immune suppression of NK cell
tumor cytotoxicity. Biochim Biophys Acta
1773:1116–1123