| Curcumin (diferuloyl methane) Benefits |
| Curcumin (diferuloyl methane), is a major component of Curcuma species, which is commonly used as a yellow coloring and flavoring agent in foods. |
Curcuminoids, a group of phenolic compounds isolated from the roots of Curcuma
longa (Zingiberaceae), exhibit a variety of beneficial effects on health and on events
that help in preventing certain diseases. [10]
Curcumin has been widely used for centuries in the Asian countries without any toxic
effects. [6] Epidemiological data also suggest that curcumin may be responsible for
the lower rate of colorectal cancer in these countries. [6] Curcumin is a naturally
occurring powerful anti-inflammatory medicine and some researchers suggested to
use curcumin as an agent to reverse or inhibit the malignant transformation of colon
cancer cells and to prevent invasion and metastasis*. [11]
*More studies are needed to support this suggestion.
CURCUMIN FUNCTIONAL STRUCTURE
Analysis of curcumin (diferuloylmethane) structure revealed the presence of
beta-diketone moiety and phenolic hydroxy groups that were believed to contribute to
antioxidation. [8]
ANTI-CANCER ACTIVITIES
Curcumin has shown anti-carcinogenic activity in animals as indicated by its ability to
block colon tumor initiation by azoxymethane and skin tumor promotion induced by
phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA). The structurally related
compounds chlorogenic acid, caffeic acid and ferulic acid are less potent inhibitors on
12-O-tetradecanoylphorbol-13-acetate (TPA)-induced tumor promotion in mouse skin.
Curcumin possesses anti-inflammatory activity and is a potent inhibitor of reactive
oxygen-generating enzymes such as lipoxygenase/cyclooxygenase, xanthine
dehydrogenase/oxidase and inducible nitric oxide synthase. Curcumin is also a
potent inhibitor of protein kinase C, EGF-receptor tyrosine kinase and IkappaB kinase.
Subsequently, curcumin inhibits the activation of NFkappaB and the expressions of
c-jun, c-fos, c-myc and iNOS. It is proposed that curcumin may suppress tumor
promotion through blocking signal transduction pathways in the target cells. [1,2, 5]
MORE DETAILS Curcumin inhibits lipooxygenase activity and is a specific inhibitor of
cyclooxygenase-2 expression. Curcumin inhibits the initiation of carcinogenesis by
inhibiting the cytochrome P-450 enzyme activity and increasing the levels of
glutathione-S-transferase. Curcumin inhibits the promotion/progression stages of
carcinogenesis. The anti-tumor effect of curcumin has been attributed in part to the
arrest of cancer cells in S, G2/M cell cycle phase and induction of apoptosis. [6]
In a study, when mouse fibroblast cells were treated with TPA alone, PKC
translocated from the cytosolic fraction to the particulate fraction. Treatment with 15 or
20 microM curcumin for 15 min inhibited TPA-induced protein kinase C activity in the
particulate fraction by 26-60%. Curcumin also inhibited protein kinase C activity in vitro
by competing with phosphatidylserine. Curcumin (10 microM) suppressed the
expression of c-jun in TPA-treated cells. [3]
Commercial curcumin isolated from the rhizome of the plant Curcuma longa Linn
contains 3 major curcuminoids (approximately 77% curcumin, 17%
demethoxycurcumin, and 3% bisdemethoxycurcumin). [4]
Commercial curcumin, pure curcumin, and demethoxycurcumin are about equipotent
as inhibitors of TPA-induced tumor promotion in mouse skin, whereas
bisdemethoxycurcumin is somewhat less active. Topical application of curcumin
inhibits tumor initiation by benzo[a]pyrene and tumor promotion by TPA in mouse skin.
Dietary curcumin (commercial grade) inhibits benzo[a]pyrene -induced stomach
cancer, N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG)-induced duodenal cancers, and
azoxymethane (AOM)-induced colon cancers. [4]
SPECULATION Cystic fibrosis (CF), the most-common lethal hereditary disease in the
white population, is caused by mutations in the cystic fibrosis transmembrane
conductance regulator (CFTR) gene. The mutation that is most frequently responsible
for the disease, DeltaF508, causes misfolding and retention of the CFTR protein in
the endoplasmic reticulum. This leads to a series of cellular dysfunctions and results
in a multi-organ disease. The activation of mutant forms of the cystic fibrosis
transmembrane conductance regulator (CFTR), particularly the most frequent mutant
allele (DeltaF508), is a potential strategy for the treatment of the disease cystic
fibrosis (CF). Scientists are interested to find if curcumin is able to restore function to
this allele, both in heterologous expression systems and in DeltaF508 CF mice. [12,
13]
TOXICITY AND SAFETY
A phase 1 human trial with 25 subjects using up to 8000 mg of curcumin per day for 3
months found no toxicity from curcumin. Five other human trials using 1125-2500 mg
of curcumin per day have also found it to be safe. [7] Human clinical trials indicated no
dose-limiting toxicity when administered at doses up to 10 g/day. [9]
METABOLISM
Curcumin was first biotransformed to dihydrocurcumin and tetrahydrocurcumin and
that these compounds subsequently were converted to monoglucuronide conjugates
(in an animal study). [5]
SUGGESTED READING
Lin JK Suppression of protein kinase C and nuclear oncogene expression as
possible action mechanisms of cancer chemoprevention by Curcumin. Arch Pharm
Res. 2004 Jul;27(7):683-92.
Duvoix A Chemopreventive and therapeutic effects of curcumin. Cancer Lett. 2005 Jun
8;223(2):181-90. Epub 2004 Nov 11
Karunagaran D et al Induction of apoptosis by curcumin and its implications for
cancer therapy. Curr Cancer Drug Targets. 2005 Mar;5(2):117-29.
HOME
THIS ARTICLE IS FOR YOUR REFERENCE ONLY. IF YOU HAVB QUESTIONS, PLEASE<
DISCUSS WITH YOUR DOCTOR.
ALL RIGHT RESERVED 2008.
REFERENCES
[1] Conney AH et al, Inhibitory effect of curcumin and some related dietary compounds on tumor
promotion and arachidonic acid metabolism in mouse skin. Adv Enzyme Regul. 1991;31:385-96.
[2] Conney AH et al, Some perspectives on dietary inhibition of carcinogenesis: studies with
curcumin and tea. Proc Soc Exp Biol Med. 1997 Nov;216(2):234-45. [3] Lin JK et al Suppression of
protein kinase C and nuclear oncogene expression as possible molecular mechanisms of cancer
chemoprevention by apigenin and curcumin. J Cell Biochem Suppl. 1997;28-29:39-48 [4] Huang
MT et al, Inhibitory effects of curcumin on tumorigenesis in mice. J Cell Biochem Suppl.
1997;27:26-34. [5] Lin JK et al, Recent studies on the biofunctions and biotransformations of
curcumin. Biofactors. 2000;13(1-4):153-8. [6] Chauhan DP et al Chemotherapeutic potential of
curcumin for colorectal cancer., Curr Pharm Des. 2002;8(19):1695-706. [7] Chainani-Wu N Safety
and anti-inflammatory activity of curcumin: a component of tumeric (Curcuma longa). J Altern
Complement Med. 2003 Feb;9(1):161-8. [8] Leu TH The molecular mechanisms for the
antitumorigenic effect of curcumin. Curr Med Chem Anti-Canc Agents. 2002 May;2(3):357-70. [9]
Aggarwal BB Anticancer potential of curcumin: preclinical and clinical studies. Anticancer Res.
2003 Jan-Feb;23(1A):363-98. [10] Joe B et al Biological properties of curcumin-cellular and
molecular mechanisms of action. Crit Rev Food Sci Nutr. 2004;44(2):97-111. [11] Narayan S
Curcumin, a multi-functional chemopreventive agent, blocks growth of colon cancer cells by
targeting beta-catenin-mediated transactivation and cell-cell adhesion pathways. J Mol Histol.
2004 Mar;35(3):301-7. [12] Davis PB et al, Some like it hot: curcumin and CFTR. Trends Mol Med.
2004 Oct;10(10):473-5. [13] Mall M Correction of the CF defect by curcumin: hypes and
disappointments. Bioessays. 2005 Jan;27(1):9-13.
longa (Zingiberaceae), exhibit a variety of beneficial effects on health and on events
that help in preventing certain diseases. [10]
Curcumin has been widely used for centuries in the Asian countries without any toxic
effects. [6] Epidemiological data also suggest that curcumin may be responsible for
the lower rate of colorectal cancer in these countries. [6] Curcumin is a naturally
occurring powerful anti-inflammatory medicine and some researchers suggested to
use curcumin as an agent to reverse or inhibit the malignant transformation of colon
cancer cells and to prevent invasion and metastasis*. [11]
*More studies are needed to support this suggestion.
CURCUMIN FUNCTIONAL STRUCTURE
Analysis of curcumin (diferuloylmethane) structure revealed the presence of
beta-diketone moiety and phenolic hydroxy groups that were believed to contribute to
antioxidation. [8]
ANTI-CANCER ACTIVITIES
Curcumin has shown anti-carcinogenic activity in animals as indicated by its ability to
block colon tumor initiation by azoxymethane and skin tumor promotion induced by
phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA). The structurally related
compounds chlorogenic acid, caffeic acid and ferulic acid are less potent inhibitors on
12-O-tetradecanoylphorbol-13-acetate (TPA)-induced tumor promotion in mouse skin.
Curcumin possesses anti-inflammatory activity and is a potent inhibitor of reactive
oxygen-generating enzymes such as lipoxygenase/cyclooxygenase, xanthine
dehydrogenase/oxidase and inducible nitric oxide synthase. Curcumin is also a
potent inhibitor of protein kinase C, EGF-receptor tyrosine kinase and IkappaB kinase.
Subsequently, curcumin inhibits the activation of NFkappaB and the expressions of
c-jun, c-fos, c-myc and iNOS. It is proposed that curcumin may suppress tumor
promotion through blocking signal transduction pathways in the target cells. [1,2, 5]
MORE DETAILS Curcumin inhibits lipooxygenase activity and is a specific inhibitor of
cyclooxygenase-2 expression. Curcumin inhibits the initiation of carcinogenesis by
inhibiting the cytochrome P-450 enzyme activity and increasing the levels of
glutathione-S-transferase. Curcumin inhibits the promotion/progression stages of
carcinogenesis. The anti-tumor effect of curcumin has been attributed in part to the
arrest of cancer cells in S, G2/M cell cycle phase and induction of apoptosis. [6]
In a study, when mouse fibroblast cells were treated with TPA alone, PKC
translocated from the cytosolic fraction to the particulate fraction. Treatment with 15 or
20 microM curcumin for 15 min inhibited TPA-induced protein kinase C activity in the
particulate fraction by 26-60%. Curcumin also inhibited protein kinase C activity in vitro
by competing with phosphatidylserine. Curcumin (10 microM) suppressed the
expression of c-jun in TPA-treated cells. [3]
Commercial curcumin isolated from the rhizome of the plant Curcuma longa Linn
contains 3 major curcuminoids (approximately 77% curcumin, 17%
demethoxycurcumin, and 3% bisdemethoxycurcumin). [4]
Commercial curcumin, pure curcumin, and demethoxycurcumin are about equipotent
as inhibitors of TPA-induced tumor promotion in mouse skin, whereas
bisdemethoxycurcumin is somewhat less active. Topical application of curcumin
inhibits tumor initiation by benzo[a]pyrene and tumor promotion by TPA in mouse skin.
Dietary curcumin (commercial grade) inhibits benzo[a]pyrene -induced stomach
cancer, N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG)-induced duodenal cancers, and
azoxymethane (AOM)-induced colon cancers. [4]
SPECULATION Cystic fibrosis (CF), the most-common lethal hereditary disease in the
white population, is caused by mutations in the cystic fibrosis transmembrane
conductance regulator (CFTR) gene. The mutation that is most frequently responsible
for the disease, DeltaF508, causes misfolding and retention of the CFTR protein in
the endoplasmic reticulum. This leads to a series of cellular dysfunctions and results
in a multi-organ disease. The activation of mutant forms of the cystic fibrosis
transmembrane conductance regulator (CFTR), particularly the most frequent mutant
allele (DeltaF508), is a potential strategy for the treatment of the disease cystic
fibrosis (CF). Scientists are interested to find if curcumin is able to restore function to
this allele, both in heterologous expression systems and in DeltaF508 CF mice. [12,
13]
TOXICITY AND SAFETY
A phase 1 human trial with 25 subjects using up to 8000 mg of curcumin per day for 3
months found no toxicity from curcumin. Five other human trials using 1125-2500 mg
of curcumin per day have also found it to be safe. [7] Human clinical trials indicated no
dose-limiting toxicity when administered at doses up to 10 g/day. [9]
METABOLISM
Curcumin was first biotransformed to dihydrocurcumin and tetrahydrocurcumin and
that these compounds subsequently were converted to monoglucuronide conjugates
(in an animal study). [5]
SUGGESTED READING
Lin JK Suppression of protein kinase C and nuclear oncogene expression as
possible action mechanisms of cancer chemoprevention by Curcumin. Arch Pharm
Res. 2004 Jul;27(7):683-92.
Duvoix A Chemopreventive and therapeutic effects of curcumin. Cancer Lett. 2005 Jun
8;223(2):181-90. Epub 2004 Nov 11
Karunagaran D et al Induction of apoptosis by curcumin and its implications for
cancer therapy. Curr Cancer Drug Targets. 2005 Mar;5(2):117-29.
HOME
THIS ARTICLE IS FOR YOUR REFERENCE ONLY. IF YOU HAVB QUESTIONS, PLEASE<
DISCUSS WITH YOUR DOCTOR.
ALL RIGHT RESERVED 2008.
REFERENCES
[1] Conney AH et al, Inhibitory effect of curcumin and some related dietary compounds on tumor
promotion and arachidonic acid metabolism in mouse skin. Adv Enzyme Regul. 1991;31:385-96.
[2] Conney AH et al, Some perspectives on dietary inhibition of carcinogenesis: studies with
curcumin and tea. Proc Soc Exp Biol Med. 1997 Nov;216(2):234-45. [3] Lin JK et al Suppression of
protein kinase C and nuclear oncogene expression as possible molecular mechanisms of cancer
chemoprevention by apigenin and curcumin. J Cell Biochem Suppl. 1997;28-29:39-48 [4] Huang
MT et al, Inhibitory effects of curcumin on tumorigenesis in mice. J Cell Biochem Suppl.
1997;27:26-34. [5] Lin JK et al, Recent studies on the biofunctions and biotransformations of
curcumin. Biofactors. 2000;13(1-4):153-8. [6] Chauhan DP et al Chemotherapeutic potential of
curcumin for colorectal cancer., Curr Pharm Des. 2002;8(19):1695-706. [7] Chainani-Wu N Safety
and anti-inflammatory activity of curcumin: a component of tumeric (Curcuma longa). J Altern
Complement Med. 2003 Feb;9(1):161-8. [8] Leu TH The molecular mechanisms for the
antitumorigenic effect of curcumin. Curr Med Chem Anti-Canc Agents. 2002 May;2(3):357-70. [9]
Aggarwal BB Anticancer potential of curcumin: preclinical and clinical studies. Anticancer Res.
2003 Jan-Feb;23(1A):363-98. [10] Joe B et al Biological properties of curcumin-cellular and
molecular mechanisms of action. Crit Rev Food Sci Nutr. 2004;44(2):97-111. [11] Narayan S
Curcumin, a multi-functional chemopreventive agent, blocks growth of colon cancer cells by
targeting beta-catenin-mediated transactivation and cell-cell adhesion pathways. J Mol Histol.
2004 Mar;35(3):301-7. [12] Davis PB et al, Some like it hot: curcumin and CFTR. Trends Mol Med.
2004 Oct;10(10):473-5. [13] Mall M Correction of the CF defect by curcumin: hypes and
disappointments. Bioessays. 2005 Jan;27(1):9-13.
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Acetyl-L Carnitine
Acidophilus
Almond
Bladderwrack
Bilberry
Chromium
CLA
Cod Liver Oil
Coenzyme Q
Colostrum
Dandelion
EGCG
Echinacea
Eleuthero
Ellagic Acid
Eve. Primrose Oil
Fish Oil
Flaxseed
Garlic
Ginger
Ginseng
Ginkgo Biloba
Glucosamine
Gotu Kola
Guar Gum
Hyaluronic acid
Lecithin
Lycopene
Milk Thistle
Nattokinase
Passion Flower
Probiotics
Policosanol /
Polycosanol
Pycnogenol
Reishi / Lingzhi
Resveratrol
Rhodiola
Royal Jelly
Stevia
Whey
Xylitol
More Supplements
| THIS ARTICLE IS FOR YOUR REFERENCE ONLY. IF YOU HAVE ANY QUESTION, YOU SHOULD CONSULT WITH YOUR DOCTOR. ALL RIGHT RESERVED 2008 zhion. DO NOT COPY NOR TRANSFER THE CONTENT TO OTHER WEBSITES NOR OTHER TYPES OF PUBLICATIONS. |