| 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 2005 zhion inc.
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 2005 zhion inc.
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. |
