| red chili pepper-benefits / side effects |
RED CHILI PEPPER BENEFITS- FIGHT AGAINST CANCER?
In a recent study, researchers found that red chili pepper appear to be effective
inhibitors of the cancer process. They looked at the chemotherapeutic potential
of capsaicin, the "hot" ingredient in red chili pepper that is often associated with
antioxidative and anti-inflammatory activities. In the study, it exhibited
anticancer activity against pancreatic cancer cells. It disrupted the mitochondrial
function resulting in the release of cytochrome c, which induced apoptosis, or
programmed cell death, in the cancerous cells without affecting normal
pancreatic cells.
Capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide) is the main pungent
principle of hot pepper, which is consumed in high quantities by humans
worldwide. The capsaicin content of some chili varieties ranges up to 0.53%. [2]
Some people believe that red pepper /capsaicin provides multiple health
benefits for various chronic inflammatory diseases such as cancer,
atherosclerosis, myocardial infarction, diabetes, allergy, asthma, arthritis,
Crohn's disease, multiple sclerosis, Alzheimer's disease, osteoporosis, psoriasis,
septic shock, and AIDS. It is because these chronic inflammatory diseases are
associated with the activation of nuclear transcription factor kappaB. While,
capsaicin derived from red pepper has been shown to be able to interrupt the
pathway activating this transcription factor. [1,6,7,10,14, 16]
RESEARCH FINDINGS
I. Capsaicin causes inhibition of the activity of the transcription factors AP-1 and
NF-kappaB, thus inhibiting cell proliferation and enhancing apoptosis. [3]
II. Capsaicin targets tNOX, a tumor (cancer)-specific surface hydroquinone
(NADH) oxidase with protein disulfide-thiol interchange activity (ECTO-NOX
protein). Accordingly vector-forced over expression of tNOX in MCF-10A
mammary epithelia or COS cells that lack tNOX or in COS cells that underexpress
tNOX enhanced the susceptibility of growth and apoptosis to capsaicin.
Additionally, the tNOX-transfected MCF-10A cells proliferated in Matrigel, a
measure of invasiveness. In contrast, oligomeric antisense tNOX DNA abrogated
growth inhibition by capsaicin and reduced anchorage-dependent growth of
HeLa (human cervical carcinoma) cells that naturally overexpress tNOX.
The findings show cell surface expression of tNOX as both necessary and
sufficient for the cellular anticancer activities attributed to capsaicin. [4]
III. Capsaicin induced apoptotic MBT-2 murine bladder tumor cell death in a
time- and dose-dependent manner. In addition to the caspase-3 activation,
capsaicin also induced cytochrome c release and decrease in Bcl-2 protein
expression with no changes in the level of Bax. Furthermore, capsaicin at the
concentration of inducing apoptosis also markedly reduced the level of reactive
oxygen species and lipid peroxidation, implying that capsaicin may enhance the
antitumor effect of BCG in bladder cancer treatment. [5]
IV Capsaicin selectively induces apoptosis in H-ras-transformed MCF10A human
breast epithelial cells but not in their normal cell counterparts. [8]
V. Treatment with capsaicin or the PPARgamma ligand troglitazone induced
apoptotic cell death in a dose-dependent manner in HT-29 human colon cancer
cells. Thus, capsaicin-induced apoptotic cell death in HT-29 human colon cancer
cells could be associated with the Peroxisome proliferator-activated receptor
gamma pathway without the involvement of the vanilloid receptor. [9]
VI Capsaicin suppressed the growth of leukemic cells, but not normal bone
marrow mononuclear cells, via induction of G(0)-G(1) phase cell cycle arrest and
apoptosis. Capsaicin-induced apoptosis was in association with the elevation of
intracellular reactive oxygen species production. Interestingly,
capsaicin-sensitive leukemic cells were possessed of wild-type p53, resulting in
the phosphorylation of p53 at the Ser-15 residue by the treatment of capsaicin.
Abrogation of p53 expression by the antisense oligonucleotides significantly
attenuated capsaicin-induced cell cycle arrest and apoptosis. Pretreatment with
the antioxidant N-acetyl-L-cystein and catalase, but not superoxide dismutase,
completely inhibited capsaicin-induced apoptosis by inhibiting phosphorylation of
Ser-15 residue of p53. Moreover, capsaicin effectively inhibited tumor growth
and induced apoptosis in vivo using NOD/SCID mice with no toxic effects. [11]
VII Studies have demonstrated that capsaicin induces apoptotic cell death in
human gastric cancer cells (SNU-1) in vitro which may be possibly mediated by
the overexpression of p53 and/or c-myc genes. [21]
RED CHILI PEPPER (CAPSAICIN) PROMOTING CANCER? -- SIDE EFFECTS?
Most findings discussed in the last section were done in either test-tube or
animal studies only. Now, we move on to see what impact of red chili pepper or
capsaicin onthe human health.
OBSERVATION I-GASTRIC CANCER IN MEXICO
Gastric cancer incidence was high in Mexico. A population-based case-control
study was conducted in Mexico City during 1989-1990 to evaluate the relation
between chili pepper consumption and gastric cancer risk. The study included
220 incident cases and 752 controls randomly selected from the general
population. Information was collected by interview. Chili pepper consumers
were at high risk for gastric cancer compared with non-consumers. [17]
A few years later, researchers from Mexico National Institute of Public Health
conducted a survey to check if the intake of capsaicin (chili peppers) increases
the risk of gastric cancer again. They studied 234 cases of gastric cancer and
468 matched controls in three areas of Mexico from 1994-1996. They acquired
information about chili pepper intake and determined the capsaicin amount by
gas chromatography for each individual; they concluded that the risk of gastric
cancer was linked to high consumption of capsaicin. [12]
OBSERVATION II-GASTRIC AND LIVER CANCERS IN FOUR SUB-POPULATIONS
There are four cookeries in the United States have high pepper content:
Mexican-American, Cajun, white Creole, and black Creole. Each is largely
confined to a single ethnic-cultural group which is concentrated in some
counties. Researchers from the University of Utah found that significantly higher
rates for stomach and liver cancer in counties inhabited by these four
ethnic-cultural groups than in matched control counties. From statistical
analysis, they conclude that the odds ratio was above 5 for the stomach cancer
association with capsaicin pepper. [15]
OBSERVATION III-ESOPHAGEAL CANCER IN NORTHEN IRAN
Cancer of the esophagus has a more varied geographical distribution and
incidence than any other commonly occurring cancer. In the high-risk region of
northern Iran, where the frequency of esophageal cancer is higher among
women than men, the main food during pregnancy contains strong black pepper
and sharp crushed pomegranate seeds, which irritate the esophagus. [18]
Researchers from Sungkyunkwan University, Korea, proposed that capsaicin
altered the metabolism of chemical carcinogens and may promote
carcinogenesis at high doses. [13]
OBSERVATION IV-STOMACH CANCER IN TRIVANDRUM, INDIA
Researchers conducted a prospective case-control study of 194 patients
suffered from stomach cancer during the period 1988-1991 in Trivandrum, India.
They collected information such as socio-demographic/economic background,
tobacco chewing, tobacco smoking and alcohol habits from the patients and
controls. They analyzed the data using a multiple logistic regression model, and
they concluded that increased risks were associated with higher consumption of
chili. [19]
OBSERVATION IV-GALLBLADDER CANCER IN INDIA
Cancer of the gallbladder is rare but fatal, and has an unusual geographic and
demographic distribution. Gallstones and obesity have been suggested as
possible risk factors. Researchers conducted a case-control study of 165
diagnosed cases of gallstones or gallbladder cancer. The researchers evaluated
their dietary habits and they found an increase in the odds with consumption of
capsicum (OR 2.2), beef (OR 2.58), tea (OR 1.98), red chilli (OR 1.29) and mutton
(OR 1.2). [20]
SCIENTIFIC SUPPORTS
There are actually a few experiments supporting the view that a large
consumption of capsicum or hot pepper chili is linked to cancer. Mexican
researchers dosed mouse with capsaicin at 1.46 and 1.94 mg/kg via i.p. route
for 32 days. Based on the frequency of micronucleated normochromatic
erythrocytes, the researchers detected the genotoxic response at dose of 1.94
mg/kg appeared on day 16 and that at dose of 1.46 mg/kg on day 32. While,
based on sister chromatid exchanges frequency, they detected the genotoxic
response only with the higher dose. These results suggest that excessive
consumption of capsicum (hot pepper chili) is linked to gastric cancer. [22] In
another study, researchers administered 6 weeks old Swiss mice with capsaicin
in a semisynthetic powdered diet at 0.03125% level. They observed that 22% of
females and 14% of males developed cecum tumors while only 8% incidences
happened in the controls. [23]
CONCLUSION
It is not sure if capsaicin is carcinogenic or anti-cancer. But, there are some
indications that large consumption of hot pepper chili is linked to stomach
cancers.
THIS ARTICLE IS FOR YOUR REFERENCE ONLY. IF YOU HAVE QUESTIONS, YOU SHOULD
CONSULT WITH YOUR DOCTOR. ALL RIGHT RESERVED 2008 zhion. DO NOT COPY NOR
TRANSFER THE CONTENT TO OTHER WEB-SITES OR OTHER TYPES OF PULBICATIONS.
REFERENCE [1] Aggarwal BB and Shishodia S Suppression of the nuclear factor-kappaB
activation pathway by spice-derived phytochemicals: reasoning for seasoning. Ann N Y
Acad Sci. 2004 Dec;1030:434-41. [2] Toth B and Gannett P, Carcinogenicity of lifelong
administration of capsaicin of hot pepper in mice. In Vivo. 1992 Jan-Feb;6(1):59-63. [3]
Shimizu M and Weinstein IB Modulation of signal transduction by tea catechins and related
phytochemicals. Mutat Res. 2005 Jun 28. [4] Chueh PJ et al, tNOX is both necessary and
sufficient as a cellular target for the anticancer actions of capsaicin and the green tea
catechin (-)-epigallocatechin-3-gallate. Biofactors. 2004;20(4):235-49. [5] Lee JS et al,
Capsaicin-induced apoptosis and reduced release of reactive oxygen species in MBT-2
murine bladder tumor cells. Arch Pharm Res. 2004 Nov;27(11):1147-53. [6] Dorai T and
Aggarwal BB Rol e of chemopreventive agents in cancer therapy. Cancer Lett. 2004 Nov
25;215(2):129-40. [7] Aggarwal BB, Takada Y and Oommen OV. From chemoprevention
to chemotherapy: common targets and common goals. Expert Opin Investig Drugs. 2004
Oct;13(10):1327-38. [8] Kim S and Moon A Capsaicin-induced apoptosis of
H-ras-transformed human breast epithelial cells is Rac-dependent via ROS generation.
Arch Pharm Res. 2004 Aug;27(8):845-9. [9] Kim CS et al, Capsaicin, a spicy component
of hot pepper, induces apoptosis by activation of the peroxisome proliferator-activated
receptor gamma in HT-29 human colon cancer cells. J Med Food. 2004 Fall;7(3):267-73.
[10] Lee YS et al, Involvement of NADPH oxidase-mediated generation of reactive oxygen
species in the apototic cell death by capsaicin in HepG2 human hepatoma cells. Free Radic
Res. 2004 Apr;38(4):405-12. [11] Ito K et al, Induction of apoptosis in leukemic cells by
homovanillic acid derivative, capsaicin, through oxidative stress: implication of
phosphorylation of p53 at Ser-15 residue by reactive oxygen species. Cancer Res. 2004
Feb 1;64(3):1071-8. [12] Lopez-Carrillo L et al, Capsaicin consumption, Helicobacter
pylori positivity and gastric cancer in Mexico. Int J Cancer. 2003 Aug 20;106(2):277-82.
[13] Lee BM and Park KK, Beneficial and adverse effects of chemopreventive agents.
Mutat Res. 2003 Feb-Mar;523-524:265-78. [14] Surh YJ et al, Inhibitory effects of
curcumin and capsaicin on phorbol ester-induced activation of eukaryotic transcription
factors, NF-kappaB and AP-1. Biofactors. 2000;12(1-4):107-12. [15] Archer VE and Jones
DW, Capsaicin pepper, cancer and ethnicity Med Hypotheses. 2002 Oct;59(4):450-7. [16]
Teel RW and Huynh HT Lack of the inhibitory effect of intragastrically administered
capsaicin on NNK-induced lung tumor formation in the A.J mouse. In Vivo. 1999
May-Jun;13(3):231-4. [17] Lopez-Carrillo L et al, Chili pepper consumption and gastric
cancer in Mexico: a case-control study. Am J Epidemiol. 1994 Feb 1;139(3):263-71. [18]
Ghadirian P et al, Food habits and esophageal cancer: an overview. Cancer Detect Prev.
1992;16(3):163-8. [19] Mathew A et al, Diet and stomach cancer: a case-control study in
South India. Eur J Cancer Prev. 2000 Apr;9(2):89-97. [20] Pandey M and Shukla VK, Diet
and gallbladder cancer: a case-control study. Eur J Cancer Prev. 2002 Aug;11(4):365-8.
[21] Kim JD et al, Capsaicin can alter the expression of tumor forming-related genes
which might be followed by induction of apoptosis of a Korean stomach cancer cell line,
SNU-1. Cancer Lett. 1997 Dec 9;120(2):235-41. [22] Diaz Barriga Arceo S et al, Genotoxic
effects produced by capsaicin in mouse during subchronic treatment. Mutat Res. 1995
Dec;345(3-4):105-9. [23] Toth B and Gannett P Carcinogenicity of lifelong administration
of capsaicin of hot pepper in mice. In Vivo. 1992 Jan-Feb;6(1):59-63.
In a recent study, researchers found that red chili pepper appear to be effective
inhibitors of the cancer process. They looked at the chemotherapeutic potential
of capsaicin, the "hot" ingredient in red chili pepper that is often associated with
antioxidative and anti-inflammatory activities. In the study, it exhibited
anticancer activity against pancreatic cancer cells. It disrupted the mitochondrial
function resulting in the release of cytochrome c, which induced apoptosis, or
programmed cell death, in the cancerous cells without affecting normal
pancreatic cells.
Capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide) is the main pungent
principle of hot pepper, which is consumed in high quantities by humans
worldwide. The capsaicin content of some chili varieties ranges up to 0.53%. [2]
Some people believe that red pepper /capsaicin provides multiple health
benefits for various chronic inflammatory diseases such as cancer,
atherosclerosis, myocardial infarction, diabetes, allergy, asthma, arthritis,
Crohn's disease, multiple sclerosis, Alzheimer's disease, osteoporosis, psoriasis,
septic shock, and AIDS. It is because these chronic inflammatory diseases are
associated with the activation of nuclear transcription factor kappaB. While,
capsaicin derived from red pepper has been shown to be able to interrupt the
pathway activating this transcription factor. [1,6,7,10,14, 16]
RESEARCH FINDINGS
I. Capsaicin causes inhibition of the activity of the transcription factors AP-1 and
NF-kappaB, thus inhibiting cell proliferation and enhancing apoptosis. [3]
II. Capsaicin targets tNOX, a tumor (cancer)-specific surface hydroquinone
(NADH) oxidase with protein disulfide-thiol interchange activity (ECTO-NOX
protein). Accordingly vector-forced over expression of tNOX in MCF-10A
mammary epithelia or COS cells that lack tNOX or in COS cells that underexpress
tNOX enhanced the susceptibility of growth and apoptosis to capsaicin.
Additionally, the tNOX-transfected MCF-10A cells proliferated in Matrigel, a
measure of invasiveness. In contrast, oligomeric antisense tNOX DNA abrogated
growth inhibition by capsaicin and reduced anchorage-dependent growth of
HeLa (human cervical carcinoma) cells that naturally overexpress tNOX.
The findings show cell surface expression of tNOX as both necessary and
sufficient for the cellular anticancer activities attributed to capsaicin. [4]
III. Capsaicin induced apoptotic MBT-2 murine bladder tumor cell death in a
time- and dose-dependent manner. In addition to the caspase-3 activation,
capsaicin also induced cytochrome c release and decrease in Bcl-2 protein
expression with no changes in the level of Bax. Furthermore, capsaicin at the
concentration of inducing apoptosis also markedly reduced the level of reactive
oxygen species and lipid peroxidation, implying that capsaicin may enhance the
antitumor effect of BCG in bladder cancer treatment. [5]
IV Capsaicin selectively induces apoptosis in H-ras-transformed MCF10A human
breast epithelial cells but not in their normal cell counterparts. [8]
V. Treatment with capsaicin or the PPARgamma ligand troglitazone induced
apoptotic cell death in a dose-dependent manner in HT-29 human colon cancer
cells. Thus, capsaicin-induced apoptotic cell death in HT-29 human colon cancer
cells could be associated with the Peroxisome proliferator-activated receptor
gamma pathway without the involvement of the vanilloid receptor. [9]
VI Capsaicin suppressed the growth of leukemic cells, but not normal bone
marrow mononuclear cells, via induction of G(0)-G(1) phase cell cycle arrest and
apoptosis. Capsaicin-induced apoptosis was in association with the elevation of
intracellular reactive oxygen species production. Interestingly,
capsaicin-sensitive leukemic cells were possessed of wild-type p53, resulting in
the phosphorylation of p53 at the Ser-15 residue by the treatment of capsaicin.
Abrogation of p53 expression by the antisense oligonucleotides significantly
attenuated capsaicin-induced cell cycle arrest and apoptosis. Pretreatment with
the antioxidant N-acetyl-L-cystein and catalase, but not superoxide dismutase,
completely inhibited capsaicin-induced apoptosis by inhibiting phosphorylation of
Ser-15 residue of p53. Moreover, capsaicin effectively inhibited tumor growth
and induced apoptosis in vivo using NOD/SCID mice with no toxic effects. [11]
VII Studies have demonstrated that capsaicin induces apoptotic cell death in
human gastric cancer cells (SNU-1) in vitro which may be possibly mediated by
the overexpression of p53 and/or c-myc genes. [21]
RED CHILI PEPPER (CAPSAICIN) PROMOTING CANCER? -- SIDE EFFECTS?
Most findings discussed in the last section were done in either test-tube or
animal studies only. Now, we move on to see what impact of red chili pepper or
capsaicin onthe human health.
OBSERVATION I-GASTRIC CANCER IN MEXICO
Gastric cancer incidence was high in Mexico. A population-based case-control
study was conducted in Mexico City during 1989-1990 to evaluate the relation
between chili pepper consumption and gastric cancer risk. The study included
220 incident cases and 752 controls randomly selected from the general
population. Information was collected by interview. Chili pepper consumers
were at high risk for gastric cancer compared with non-consumers. [17]
A few years later, researchers from Mexico National Institute of Public Health
conducted a survey to check if the intake of capsaicin (chili peppers) increases
the risk of gastric cancer again. They studied 234 cases of gastric cancer and
468 matched controls in three areas of Mexico from 1994-1996. They acquired
information about chili pepper intake and determined the capsaicin amount by
gas chromatography for each individual; they concluded that the risk of gastric
cancer was linked to high consumption of capsaicin. [12]
OBSERVATION II-GASTRIC AND LIVER CANCERS IN FOUR SUB-POPULATIONS
There are four cookeries in the United States have high pepper content:
Mexican-American, Cajun, white Creole, and black Creole. Each is largely
confined to a single ethnic-cultural group which is concentrated in some
counties. Researchers from the University of Utah found that significantly higher
rates for stomach and liver cancer in counties inhabited by these four
ethnic-cultural groups than in matched control counties. From statistical
analysis, they conclude that the odds ratio was above 5 for the stomach cancer
association with capsaicin pepper. [15]
OBSERVATION III-ESOPHAGEAL CANCER IN NORTHEN IRAN
Cancer of the esophagus has a more varied geographical distribution and
incidence than any other commonly occurring cancer. In the high-risk region of
northern Iran, where the frequency of esophageal cancer is higher among
women than men, the main food during pregnancy contains strong black pepper
and sharp crushed pomegranate seeds, which irritate the esophagus. [18]
Researchers from Sungkyunkwan University, Korea, proposed that capsaicin
altered the metabolism of chemical carcinogens and may promote
carcinogenesis at high doses. [13]
OBSERVATION IV-STOMACH CANCER IN TRIVANDRUM, INDIA
Researchers conducted a prospective case-control study of 194 patients
suffered from stomach cancer during the period 1988-1991 in Trivandrum, India.
They collected information such as socio-demographic/economic background,
tobacco chewing, tobacco smoking and alcohol habits from the patients and
controls. They analyzed the data using a multiple logistic regression model, and
they concluded that increased risks were associated with higher consumption of
chili. [19]
OBSERVATION IV-GALLBLADDER CANCER IN INDIA
Cancer of the gallbladder is rare but fatal, and has an unusual geographic and
demographic distribution. Gallstones and obesity have been suggested as
possible risk factors. Researchers conducted a case-control study of 165
diagnosed cases of gallstones or gallbladder cancer. The researchers evaluated
their dietary habits and they found an increase in the odds with consumption of
capsicum (OR 2.2), beef (OR 2.58), tea (OR 1.98), red chilli (OR 1.29) and mutton
(OR 1.2). [20]
SCIENTIFIC SUPPORTS
There are actually a few experiments supporting the view that a large
consumption of capsicum or hot pepper chili is linked to cancer. Mexican
researchers dosed mouse with capsaicin at 1.46 and 1.94 mg/kg via i.p. route
for 32 days. Based on the frequency of micronucleated normochromatic
erythrocytes, the researchers detected the genotoxic response at dose of 1.94
mg/kg appeared on day 16 and that at dose of 1.46 mg/kg on day 32. While,
based on sister chromatid exchanges frequency, they detected the genotoxic
response only with the higher dose. These results suggest that excessive
consumption of capsicum (hot pepper chili) is linked to gastric cancer. [22] In
another study, researchers administered 6 weeks old Swiss mice with capsaicin
in a semisynthetic powdered diet at 0.03125% level. They observed that 22% of
females and 14% of males developed cecum tumors while only 8% incidences
happened in the controls. [23]
CONCLUSION
It is not sure if capsaicin is carcinogenic or anti-cancer. But, there are some
indications that large consumption of hot pepper chili is linked to stomach
cancers.
THIS ARTICLE IS FOR YOUR REFERENCE ONLY. IF YOU HAVE QUESTIONS, YOU SHOULD
CONSULT WITH YOUR DOCTOR. ALL RIGHT RESERVED 2008 zhion. DO NOT COPY NOR
TRANSFER THE CONTENT TO OTHER WEB-SITES OR OTHER TYPES OF PULBICATIONS.
REFERENCE [1] Aggarwal BB and Shishodia S Suppression of the nuclear factor-kappaB
activation pathway by spice-derived phytochemicals: reasoning for seasoning. Ann N Y
Acad Sci. 2004 Dec;1030:434-41. [2] Toth B and Gannett P, Carcinogenicity of lifelong
administration of capsaicin of hot pepper in mice. In Vivo. 1992 Jan-Feb;6(1):59-63. [3]
Shimizu M and Weinstein IB Modulation of signal transduction by tea catechins and related
phytochemicals. Mutat Res. 2005 Jun 28. [4] Chueh PJ et al, tNOX is both necessary and
sufficient as a cellular target for the anticancer actions of capsaicin and the green tea
catechin (-)-epigallocatechin-3-gallate. Biofactors. 2004;20(4):235-49. [5] Lee JS et al,
Capsaicin-induced apoptosis and reduced release of reactive oxygen species in MBT-2
murine bladder tumor cells. Arch Pharm Res. 2004 Nov;27(11):1147-53. [6] Dorai T and
Aggarwal BB Rol e of chemopreventive agents in cancer therapy. Cancer Lett. 2004 Nov
25;215(2):129-40. [7] Aggarwal BB, Takada Y and Oommen OV. From chemoprevention
to chemotherapy: common targets and common goals. Expert Opin Investig Drugs. 2004
Oct;13(10):1327-38. [8] Kim S and Moon A Capsaicin-induced apoptosis of
H-ras-transformed human breast epithelial cells is Rac-dependent via ROS generation.
Arch Pharm Res. 2004 Aug;27(8):845-9. [9] Kim CS et al, Capsaicin, a spicy component
of hot pepper, induces apoptosis by activation of the peroxisome proliferator-activated
receptor gamma in HT-29 human colon cancer cells. J Med Food. 2004 Fall;7(3):267-73.
[10] Lee YS et al, Involvement of NADPH oxidase-mediated generation of reactive oxygen
species in the apototic cell death by capsaicin in HepG2 human hepatoma cells. Free Radic
Res. 2004 Apr;38(4):405-12. [11] Ito K et al, Induction of apoptosis in leukemic cells by
homovanillic acid derivative, capsaicin, through oxidative stress: implication of
phosphorylation of p53 at Ser-15 residue by reactive oxygen species. Cancer Res. 2004
Feb 1;64(3):1071-8. [12] Lopez-Carrillo L et al, Capsaicin consumption, Helicobacter
pylori positivity and gastric cancer in Mexico. Int J Cancer. 2003 Aug 20;106(2):277-82.
[13] Lee BM and Park KK, Beneficial and adverse effects of chemopreventive agents.
Mutat Res. 2003 Feb-Mar;523-524:265-78. [14] Surh YJ et al, Inhibitory effects of
curcumin and capsaicin on phorbol ester-induced activation of eukaryotic transcription
factors, NF-kappaB and AP-1. Biofactors. 2000;12(1-4):107-12. [15] Archer VE and Jones
DW, Capsaicin pepper, cancer and ethnicity Med Hypotheses. 2002 Oct;59(4):450-7. [16]
Teel RW and Huynh HT Lack of the inhibitory effect of intragastrically administered
capsaicin on NNK-induced lung tumor formation in the A.J mouse. In Vivo. 1999
May-Jun;13(3):231-4. [17] Lopez-Carrillo L et al, Chili pepper consumption and gastric
cancer in Mexico: a case-control study. Am J Epidemiol. 1994 Feb 1;139(3):263-71. [18]
Ghadirian P et al, Food habits and esophageal cancer: an overview. Cancer Detect Prev.
1992;16(3):163-8. [19] Mathew A et al, Diet and stomach cancer: a case-control study in
South India. Eur J Cancer Prev. 2000 Apr;9(2):89-97. [20] Pandey M and Shukla VK, Diet
and gallbladder cancer: a case-control study. Eur J Cancer Prev. 2002 Aug;11(4):365-8.
[21] Kim JD et al, Capsaicin can alter the expression of tumor forming-related genes
which might be followed by induction of apoptosis of a Korean stomach cancer cell line,
SNU-1. Cancer Lett. 1997 Dec 9;120(2):235-41. [22] Diaz Barriga Arceo S et al, Genotoxic
effects produced by capsaicin in mouse during subchronic treatment. Mutat Res. 1995
Dec;345(3-4):105-9. [23] Toth B and Gannett P Carcinogenicity of lifelong administration
of capsaicin of hot pepper in mice. In Vivo. 1992 Jan-Feb;6(1):59-63.
| A few test-tube studies suggest that spices like red chili pepper, may provide a cancer-fighting benefit by slowing or preventing the growth of cancerous tumor cells. The findings have been published in various nationwide scientific journals. |
THIS WEBSITE TALKS ABOUT THE SIDE EFFECTS AND THE POTENTIAL HEALTH BENEFITS OF HERBS, SUPPLEMENTS,
PHYTONUTRIENTS AND DRUG PRODUCTS. THIS WEBSITE ALSO TALKS ABOUT SOME POPULAR HEALTH ISSUES AND DISEASES.
ARTICLES IN THIS WEB SITE IS FOR YOUR REFERENCE ONLY. IF YOU HAVE ANY QUESTION, YOU SHOULD CONSULT WITH YOUR
DOCTOR IMMEDIATELY. ALL RIGHTS RESERVED 2008. DO NOT COPY NOR TRANSFER ARTICLES TO OTHER WEBSITES NOR OTHER
FORMS OF PUBLICATIONS. Privacy Policy. ARTICLE INDEX
PHYTONUTRIENTS AND DRUG PRODUCTS. THIS WEBSITE ALSO TALKS ABOUT SOME POPULAR HEALTH ISSUES AND DISEASES.
ARTICLES IN THIS WEB SITE IS FOR YOUR REFERENCE ONLY. IF YOU HAVE ANY QUESTION, YOU SHOULD CONSULT WITH YOUR
DOCTOR IMMEDIATELY. ALL RIGHTS RESERVED 2008. DO NOT COPY NOR TRANSFER ARTICLES TO OTHER WEBSITES NOR OTHER
FORMS OF PUBLICATIONS. Privacy Policy. ARTICLE INDEX
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