Citations on Ellagic Acid and Raspberries
- an anticancer agent - it protects the DNA from mutation
- shrinks tumors within 72 hours (if cancer not caused by mutation in
p53 or WAF 1/p21 genes)
- an antioxidant
- an anti bacterial and antiviral agent
- helps ulcers (antibacterial properties)
- protects liver and heart
- inhibits enzyme necessary for cholesterol biosynthesis
- reduces blood sugar levels
Free Radic Res 2002 Sep;36(9):1023-31
Anti-angiogenic property of edible berries.
Roy S, Khanna S, Alessio HM, Vider J, Bagchi D, Bagchi M, Sen CK.
Laboratory of Molecular Medicine, Department of Surgery, 512 Heart and
Lung Research Institute, Ohio State University Medical Center, 473 W.
12th Avenue, Columbus, OH 43210, USA.
Recent studies show that edible berries may have potent chemopreventive
properties. Anti-angiogenic approaches to prevent and treat cancer represent
a priority area in investigative tumor biology. Vascular endothelial growth
factor (VEGF) plays a crucial role for the vascularization of tumors.
The vasculature in adult skin remains normally quiescent. However, skin
retains the capacity for brisk initiation of angiogenesis during inflammatory
skin diseases such as psoriasis and skin cancers. We sought to test the
effects of multiple berry extracts on inducible VEGF expression by human
HaCaT keratinocytes. Six berry extracts (wild blueberry, bilberry, cranberry,
elderberry, raspberry seed, and strawberry) and a grape seed proanthocyanidin
extract (GSPE) were studied. The extracts and uptake of their constituents
by HaCaT were studied using a multi-channel HPLC-CoulArray approach. Antioxidant
activity of the extracts was determined by ORAC. Cranberry, elderberry
and raspberry seed samples were observed to possess comparable ORAC values.
The antioxidant capacity of these samples was significantly lower than
that of the other samples studied. The ORAC values of strawberry powder
and GSPE were higher than cranberry, elderberry or raspberry seed but
significantly lower than the other samples studied. Wild bilberry and
blueberry extracts possessed the highest ORAC values. Each of the berry
samples studied significantly inhibited both H2O2 as well as TNF alpha
induced VEGF expression by the human keratinocytes. This effect was not
shared by other antioxidants such as alpha-tocopherol or GSPE but was
commonly shared by pure flavonoids. Matrigel assay using human dermal
microvascular endothelial cells showed that edible berries impair angiogenesis.
Mutat Res 2001 Sep 1;480-481:97-108
Effect of chemopreventive agents on DNA adduction induced by the
potent mammary carcinogen dibenzo[a,l]pyrene in the human breast cells
MCF-7.
Smith WA, Freeman JW, Gupta RC.
Graduate Center for Toxicology, 354 Health Sciences Research Building,
University of Kentucky Medical Center, Lexington, KY 40536-0305, USA.
Over 1500 structurally diverse chemicals have been identified which have
potential cancer chemopreventive properties. The efficacy and mechanisms
of this growing list of chemoprotective agents may be studied using short-term
bioassays that employ relevant end-points of the carcinogenic process.
In this study, we have examined the effects of eight potential chemopreventive
agents, N-acetylcysteine (NAC), benzylisocyanate (BIC), chlorophyllin,
curcumin, 1,2-dithiole-3-thione (D3T), ellagic acid, genistein, and oltipraz,
on DNA adduction of the potent mammary carcinogen dibenzo[a,l]pyrene (DBP)
using the human breast cell line MCF-7. Bioactivation of DBP by MCF-7
cells resulted in the formation of one predominant (55%) dA-derived and
several other dA- or dG-derived DNA adducts. Three test agents, oltipraz,
D3T, and chlorophyllin substantially (>65%) inhibited DBP-DNA adduction
at the highest dose tested (30 microM). These agents also significantly
inhibited DBP adduct levels at a lower dose of 15 microM, while oltipraz
was effective even at the lowest dose of 5 microM. Two other agents, genistein
and ellagic acid were moderate (45%) DBP-DNA adduct inhibitors at the
highest dose tested, while NAC, curcumin, and BIC were ineffective. These
studies indicate that the MCF-7 cell line is an applicable model to study
the efficacy of cancer chemopreventive agents in a human setting. Moreover,
this model may also provide information regarding the effect of the test
agents on carcinogen bioactivation and detoxification enzymes.
Eur J Drug Metab Pharmacokinet 1999 Apr-Jun;24(2):183-9
Tannins, xenobiotic metabolism and cancer chemoprevention in experimental
animals.
Nepka C, Asprodini E, Kouretas D.
Cytopathology Laboratory, Serres, Greece.
Tannins are plant polyphenolic compounds that are contained in large quantities
in food and beverages (tea, red wine, nuts, etc.) consumed by humans daily.
It has been shown that various tannins exert broad cancer chemoprotective
activity in a number of animal models. This review summarizes the recent
literature regarding both the mechanisms involved, and the specific organ
cancer models used in laboratory animals. An increasing body of evidence
demonstrates that tannins act as both anti-initiating and antipromoting
agents. In view of the fact that tannins may be of valid medicinal efficacy
in human clinical trials, the present review attempts to integrate results
from animal studies, and considers their possible application in humans.
Carcinogenesis 1996 Apr;17(4):821-8
The effects of dietary ellagic acid on rat hepatic and esophageal
mucosal cytochromes P450 and phase II enzymes.
Ahn D, Putt D, Kresty L, Stoner GD, Fromm D, Hollenberg PF.
Department of Surgery, Wayne State University, Detroit, MI 48201, USA.
Ellagic acid (EA), a naturally occurring plant polyphenol possesses broad
chemoprotective properties. Dietary EA has been shown to reduce the incidence
of N-2-fluorenylacetamide-induced hepatocarcinogenesis in rats and N-nitrosomethylbenzylamine
(NMBA)-induced rat esophageal tumors. In this study changes in the expression
and activities of specific rat hepatic and esophageal mucosal cytochromes
P450 (P450) and phase II enzymes following dietary EA treatment were investigated.
Liver and esophageal mucosal microsomes and cytosol were prepared from
three groups of Fisher 344 rats which were fed an AIN-76 diet containing
no EA or 0.4 or 4.0 g/kg EA for 23 days. In the liver total P450 content
decreased by up to 25% and P450 2E1-catalyzed p-nitrophenol hydroxylation
decreased by 15%. No changes were observed in P450 1A1, 2B1 or 3A1/2 expression
or activities or cytochrome b5 activity. P450 reductase activity decreased
by up to 28%. Microsomal epoxide hydrolase (mEH) expression decreased
by up to 85% after EA treatment, but mEH activities did not change. The
hepatic phase II enzymes glutathione S-transferase (GST), NAD(P)H:quinone
reductase ?NAD-(P)H:QR? and UDP glucuronosyltransferase (UDPGT) activities
increased by up to 26, 17 and 75% respectively. Assays for specific forms
of GST indicated marked increases in the activities of isozymes 2-2 (190%),
4-4 (150%) and 5-5 (82%). In the rat esophageal mucosa only P450 1A1 could
be detected by Western blot analysis and androstendione was the only P450
metabolite of testosterone detectable. However, there were no differences
in the expression of P450 1A1, the formation of androstendione or NAD(P)H:QR
activities between control and EA-fed rats in the esophagus. Although
there was no significant decrease in overall GST activity, as measured
with 1-chloro-2,4-dinitrobenzene (CDNB), there was a significant decrease
in the activity of the 2-2 isozyme (66% of control). In vitro incubations
showed that EA at a concentration of 100 microM inhibited P450 2E1, 1A1
and 2B1 activities by 87, 55 and 18% respectively, but did not affect
3A1/2 activity. Using standard steady-state kinetic analyses, EA was shown
to be a potent non-competitive inhibitor of both liver microsomal ethoxyresorufin
O-deethylase and p-nitrophenol hydroxylase activities, with apparent Ki
values of approximately 55 and 14 microM respectively. In conclusion,
these results demonstrate that EA causes a decrease in total hepatic P450
with a significant effect on hepatic P450 2E1, increases some hepatic
phase II enzyme activities ?GST, NAD-(P)H:QR and UDPGT? and decreases
hepatic mEH expression. It also inhibits the catalytic activity of some
P450 isozymes in vitro. Thus the chemoprotective effect of EA against
various chemically induced cancers may involve decreases in the rates
of metabolism of these carcinogens by phase I enzymes, due to both direct
inhibition of catalytic activity and modulation of gene expression, in
addition to effects on the expression of phase II enzymes, thereby enhancing
the ability of the target tissues to detoxify the reactive intermediates
Cancer Lett 1999 Mar 1;136(2):215-21
p53/p21(WAF1/CIP1) expression and its possible role in G1 arrest
and apoptosis in ellagic acid treated cancer cells.
Narayanan BA, Geoffroy O, Willingham MC, Re GG, Nixon DW.
Cancer Prevention Program, Hollings Cancer Center, Medical University
of South Carolina, Charleston 29425, USA. bhagavati@musc.edu
Ellagic acid is a phenolic compound present in fruits and nuts including
raspberries, strawberries and walnuts. It is known to inhibit certain
carcinogen-induced cancers and may have other chemopreventive properties.
The effects of ellagic acid on cell cycle events and apoptosis were studied
in cervical carcinoma (CaSki) cells. We found that ellagic acid at a concentration
of 10(-5) M induced G arrest within 48 h, inhibited overall cell growth
and induced apoptosis in CaSki cells after 72 h of treatment. Activation
of the cdk inhibitory protein p21 by ellagic acid suggests a role for
ellagic acid in cell cycle regulation of cancer cells.
Cancer Res 2001 Aug 15;61(16):6112-9
Chemoprevention of esophageal tumorigenesis by dietary administration
of lyophilized black raspberries.
Kresty LA, Morse MA, Morgan C, Carlton PS, Lu J, Gupta A, Blackwood M,
Stoner GD.
Division of Environmental Health Sciences, School of Public Health, Comprehensive
Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA.
Fruit and vegetable consumption has consistently been associated with
decreased risk of a number of aerodigestive tract cancers, including esophageal
cancer. We have taken a "food-based" chemopreventive approach
to evaluate the inhibitory potential of lyophilized black raspberries
(LBRs) against N-nitrosomethylbenzylamine (NMBA)-induced esophageal tumorigenesis
in the F344 rat, during initiation and postinitiation phases of carcinogenesis.
Anti-initiation studies included a 30-week tumorigenicity bioassay, quantification
of DNA adducts, and NMBA metabolism study. Feeding 5 and 10% LBRs, for
2 weeks prior to NMBA treatment (0.25 mg/kg, weekly for 15 weeks) and
throughout a 30-week bioassay, significantly reduced tumor multiplicity
(39 and 49%, respectively). In a short-term bioassay, 5 and 10% LBRs inhibited
formation of the promutagenic adduct O(6)-methylguanine (O(6)-meGua) by
73 and 80%, respectively, after a single dose of NMBA at 0.25 mg/kg. Feeding
5% LBRs also significantly inhibited adduct formation (64%) after NMBA
administration at 0.50 mg/kg. The postinitiation inhibitory potential
of berries was evaluated in a second bioassay with sacrifices at 15, 25,
and 35 weeks. Administration of LBRs began after NMBA treatment (0.25
mg/kg, three times per week for 5 weeks). LBRs inhibited tumor progression
as evidenced by significant reductions in the formation of preneoplastic
esophageal lesions, decreased tumor incidence and multiplicity, and reduced
cellular proliferation. At 25 weeks, both 5 and 10% LBRs significantly
reduced tumor incidence (54 and 46%, respectively), tumor multiplicity
(62 and 43%, respectively), proliferation rates, and preneoplastic lesion
development. Yet, at 35 weeks, only 5% LBRs significantly reduced tumor
incidence and multiplicity, proliferation indices and preneoplastic lesion
formation. In conclusion, dietary administration of LBRs inhibited events
associated with both the initiation and promotion/progression stages of
carcinogenesis, which is promising considering the limited number of chemopreventives
with this potential.
Cancer Res 2001 Aug 15;61(16):6112-9
Bioorg Med Chem Lett 1998 Jan 6;8(1):97-100
DNA gyrase inhibitory activity of ellagic acid derivatives.
Weinder-Wells MA, Altom J, Fernandez J, Fraga-Spano SA, Hilliard J, Ohemeng
K, Barrett JF.
R.W. Johnson Pharmaceutical Research Institute, Raritan, NJ 08869, USA.
Ellagic acid was found to inhibit E. coli DNA gyrase supercoiling with
approximately the same potency as nalidixic acid. Tricyclic analogs of
ellagic acid, which vary in the number and position of the hydroxy groups
as well as their replacement with halogens, have been synthesized. The
biological activity of these analogs is discussed
Eksp Klin Farmakol 2001 Mar-Apr;64(2):55-9
[Antioxidant properties of novel preparations--bioflavonoid derivatives
and tannins.]
[Article in Russian]
Iakovleva LV, Gerasimova OA, Karbusheva IV, Ivakhnenko AK, Buniatian ND,
Sakharova TS.
Central Research Laboratory, Ukrainian Pharmaceutical Academy, ul. Pushkinskaya
53, Kharkov, 310002 Ukraine.
New medicinal plant preparations of polyphenol nature, representing the
derivatives of bioflavonoids (piflamin) and ellagotannins (altan and ellagic
acid) were experimentally studied. The drugs exhibited antioxidant properties,
which were manifested by inhibition of a pathological lipid peroxidation,
restoration of the functional activity of the antioxidant system components,
and stabilization of the hepatocyte membranes.
Antimicrob Agents Chemother 1998 Sep;42(9):2245-53
Human immunodeficiency virus type 1 cDNA integration: new aromatic
hydroxylated inhibitors and studies of the inhibition mechanism.
Farnet CM, Wang B, Hansen M, Lipford JR, Zalkow L, Robinson WE Jr, Siegel
J, Bushman F.
Salk Institute for Biological Studies, La Jolla, California, USA.
Integration of the human immunodeficiency virus type 1 (HIV-1) cDNA is
a required step for viral replication. Integrase, the virus-encoded enzyme
important for integration, has not yet been exploited as a target for
clinically useful inhibitors. Here we report on the identification of
new polyhydroxylated aromatic inhibitors of integrase including ellagic
acid, purpurogallin, 4,8, 12-trioxatricornan, and hypericin, the last
of which is known to inhibit viral replication. These compounds and others
were characterized in assays with subviral preintegration complexes (PICs)
isolated from HIV-1-infected cells. Hypericin was found to inhibit PIC
assays, while the other compounds tested were inactive. Counterscreening
of these and other integrase inhibitors against additional DNA-modifying
enzymes revealed that none of the polyhydroxylated aromatic compounds
are active against enzymes that do not require metals (methylases, a pox
virus topoisomerase). However, all were cross-reactive with metal-requiring
enzymes (restriction enzymes, a reverse transcriptase), implicating metal
atoms in the inhibitory mechanism. In mechanistic studies, we localized
binding of some inhibitors to the catalytic domain of integrase by assaying
competition of binding by labeled nucleotides. These findings help elucidate
the mechanism of action of the polyhydroxylated aromatic inhibitors and
provide practical guidance for further inhibitor development.
Microbios 1998;93(375):115-27
Inhibitory actions of ellagic acid on growth and arylamine N-acetyltransferase
activity in strains of Helicobacter pylori from peptic ulcer patients.
Chung JG.
Department of Medicine, China Medical College, Taiwan, Republic of China.
Arylamine N-acetyltransferase (NAT) activity in Helicobacter pylori was
inhibited by ellagic acid, a possible chemopreventive drug. The NAT activity
was determined using an acetyl CoA recycling assay and high pressure liquid
chromatography. Inhibition of growth studies using H. pylori demonstrated
that ellagic acid elicited a dose-dependent bactericidal effect in H.
pylori cultures, i.e. the greater the concentration of ellagic acid, the
greater the inhibition of growth of H. pylori. The IC50 value was 1 mM
for inhibition of growth of H. pylori. Cytosols or suspensions of H. pylori
with and without selected concentrations of ellagic acid co-treatment
showed different percentages of 2-aminofluorene and p-aminobenzoic acid
acetylation. The data indicated that there was decreased NAT activity
associated with increased ellagic acid in H. pylori cytosols and intact
cells. For the cytosol and intact bacteria examinations, the apparent
values of K(m) and Vmax decreased after co-treatment with 1 mM ellagic
acid. This report is the first demonstration of ellagic acid inhibition
of arylamine NAT activity and ellagic acid inhibition of growth in the
bacterium H. pylori.
Indian J Physiol Pharmacol 1996 Oct;40(4):363-6
Inhibition of liver fibrosis by ellagic acid.
Thresiamma KC, Kuttan R.
Amala Cancer Research Centre, Amala Nagar, Trichur, Kerala.
Chronic administration of carbon tetrachloride in liquid paraffin (1.7)
ip; 0.15 ml, (20 doses) has been found to produce severe hepatotoxicity,
as seen from the elevated levels of serum and liver glutamate-pyruvate
transaminase, alkaline phosphatase and lipid peroxides. The chronic administration
of carbon tetrachloride was also found to produce liver fibrosis as seen
from pathological analysis as well as elevated liver-hydroxy proline.
Oral administration of ellagic acid was found to significantly reduce
the elevated levels of enzymes, lipid peroxide and liver hydroxy proline
in these animals and rectified liver pathology. These results indicate
that ellagic acid administration orally can circumvent the carbon tetrachloride
toxicity and subsequent fibrosis
Eksp Klin Farmakol 1998 May-Jun;61(3):32-4
[The protective action of ellagic acid in experimental myocarditis]
[Article in Russian]
Iakovleva LV, Ivakhnenko AK, Buniatian ND.
Central Research Laboratory, Ukranian Pharmaceutical Academy, Kharkov,
Ukraine.
The article presents the material on the study of the cardioprotective
effect of ellagic acid on a model of neoepinephrine myocarditis in rats.
In doses of 0.5-1 mg/kg ellagic acid causes a marked antioxidant effect.
Restores the disturbed myocardial functions. The reference-agent vitamin
E (50 mg/kg) yields to ellagic acid as a cardioprotector. The effect of
0.5 mg/kg of ellagic acid was more stable than that of a 1 mg/kg dose.
The cardioprotective activity of the drugs under study was determined
according to the POL parameters in a myocardial homogenate and blood serum
and according to the EEG parameters and the degree of cardiomyocyte cytolysis.
J Nat Prod 2001 Aug;64(8):1010-4
Ellagitannins and hexahydroxydiphenoyl esters as inhibitors of
vertebrate squalene epoxidase.
Abe I, Kashiwagi Y, Noguchi H, Tanaka T, Ikeshiro Y, Kashiwada Y.
School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka 422-8526,
Japan. abei@ys7.u-shizuoka-ken.ac.jp
Ellagitannins isolated from various plant sources as well as newly synthesized
n-alkyl (C(1)-C(18)) esters of hexahydroxydiphenyl (HHDP) dicarboxylic
acid were evaluated as enzyme inhibitors of recombinant rat squalene epoxidase,
a rate-limiting enzyme of cholesterol biosynthesis. Among the ellagitannins
tested, pedunculagin (IC(50) = 2.0 microM) and eugeniin (IC(50) = 1.6
microM), both containing (S)-HHDP ester group(s), showed remarkable inhibition,
which was more potent than those of previously reported substrate analogue
inhibitors. Furthermore, ellagic acid (IC(50) = 2.0 microM), a bislactone
formed by hydrolytic release of a HHDP group from ellagitannins, was also
a good inhibitor of the enzyme. On the other hand, the synthetic HHDP
esters with C(6) (IC(50) = 0.93 microM) and C(8) alkyl side chains (IC(50)
= 0.83 microM) showed potent enzyme inhibition at the submicromolar concentration
range, while esters with shorter chain lengths (C(1)-C(4)) and a C(18)
ester exhibited moderate inhibition (IC(50) = 8-47 microM).
Planta Med 2001 Dec;67(9):825-32
Antileishmanial activity of hydrolyzable tannins and their modulatory
effects on nitric oxide and tumour necrosis factor-alpha release in macrophages
in vitro.
Kolodziej H, Kayser O, Kiderlen AF, Ito H, Hatano T, Yoshida T, Foo LY.
Institut fur Pharmazie, Pharmazeutische Biologie, Freie Universitat Berlin,
Berlin, Germany. kolpharm@zedat-fu-berlin.de
A series of 27 hydrolyzable tannins and related compounds was tested for
antiparasitic effects against both extracellular promastigote and intracellular
amastigote Leishmania donovani organisms. In parallel, the compounds were
evaluated for their immunomodulatory effects on macrophage functions,
including release of nitric oxide (NO), tumour necrosis factor-alpha (TNF-alpha)
and interferon (IFN)-like properties using several functional assays.
Of the series of polyphenols tested, only gallic acid (54 microM NO) and
its methyl ester (32 microM NO) induced murine macrophage-like RAW 264.7
cells to release NO in appreciable amounts (IFN-gamma/LPS 119 microM NO).
The in vitro TNF-inducing potential of the polyphenols examined increased
in the order of oligomeric ellagitannins (EC(50) > 25 microg/ml) <
monomeric ellagitannins, gallotannins (EC(50) 8.5 to > 25 microg/ml)
< C-glucosidic ellagitannins, dehydroellagitannins (EC(50) 0.6 - 2.8
microg/ml) at the host cell subtoxic concentration of 50 microg/ml. Furthermore,
promastigotes of Leishmania donovani were assayed in the presence of these
polyphenols and the results showed that none of the compounds was significantly
toxic (EC(50) > 25 microg/ml) to the extracellular forms. In contrast,
all polyphenols showed pronounced antileishmanial activities (EC(50) <
0.4 - 12.5 versus 7.9 microg/ml for Pentostam) against intracellular amastigotes
of L. donovani residing within RAW cells. Noteworthy, most compounds exhibited
low cytotoxicity against the murine host cells (EC(50) >25 microg/ml).
Furthermore, some ellagitannins and the majority of dehydroellagitannins
induced potent interferon-like activities as reflected by inhibition of
the cytopathic effect of encephalomyocarditis virus on fibroblast L929
cells. This is the first report on hydrolyzable tannins as a new class
of natural products with leishmanicidal activity including their potential
for inducing the release of NO, TNF and IFN-like activity in macrophage-like
RAW cells.
Antioxid Redox Signal 2001 Dec;3(6):995-1008
Chemical studies of proanthocyanidins and hydrolyzable tannins.
Bors W, Foo LY, Hertkorn N, Michel C, Stettmaier K.
Institut fur Strahlenbiologie, GSF Forschungszentrum fur Umwelt und Gesundheit,
Neuherberg, Germany. bors@gsf.de
We investigated a number of natural polyphenols representing flavan-3-ols,
gallotannins, and ellagitannins with regard to their antioxidant potential.
For this purpose we used pulse radiolysis to determine scavenging rate
constants with hydroxyl radicals and decay rates of the respective aroxyl
radicals and EPR spectroscopy to identify the radicals after in situ oxidation.
Using NMR spectroscopy, we could confirm phenolic coupling reactions of
epigallocatechin gallate and pentagalloyl glucose after radical-induced
oxidation.
Planta Med 2002 Feb;68(2):173-5
Ellagitannins from Lagerstroemia speciosa as Activators of Glucose
Transport in Fat Cells.
Hayashi T, Maruyama H, Kasai R, Hattori K, Takasuga S, Hazeki O, Yamasaki
K, Tanaka T.
Institute of Pharmaceutical Sciences, Faculty of Medicine, Hiroshima University,
Hiroshima, Japan.
Abstract.Glucose transport enhancers were searched for in Lagerstroemia
speciosa, a Philippine local herbal medicine used for diabetes mellitus.
Bioassay-guided fractionation of the aqueous acetone extract of the leaves
afforded three active ellagitannins, lagerstroemin, flosin B and reginin
A, identified by NMR and optical rotation. These compounds increased glucose
uptake of rat adipocytes, and could be responsible for lowering the blood
glucose level.
Nutr 2001 Nov;131(11):2837-42
Walnut polyphenolics inhibit in vitro human plasma and LDL oxidation.
Anderson KJ, Teuber SS, Gobeille A, Cremin P, Waterhouse AL, Steinberg
FM.
Department of Internal Medicine, Division of Rheumatology, Allergy and
Clinical Immunology, School of Medicine, University of California, Davis,
CA, USA.
Recent epidemiologic studies have associated nut consumption with a reduced
incidence of cardiovascular mortality. However, little is known about
the contribution of nut polyphenols to antioxidant and cardiovascular
protection. In this investigation, polyphenol-rich extracts from English
walnuts (Juglans regia) were studied and compared with ellagic acid for
their ability to inhibit in vitro plasma and LDL oxidation, as well as
their effects on LDL alpha-tocopherol during oxidative stress. In addition,
the Trolox equivalent antioxidant activity (TEAC) was determined and liquid
chromatography electrospray detection mass spectrometry (LC-ELSD/MS) analyses
of the walnut extracts were performed. 2,2'-Azobis'(2-amidino
propane) hydrochloride (AAPH)-induced LDL oxidation was significantly
inhibited by 87 and 38% with the highest concentration (1.0 micromol/L)
of ellagic acid and walnut extract, respectively. In addition, copper-mediated
LDL oxidation was inhibited by 14 and 84% in the presence of ellagic acid
and walnut extract, respectively, with a modest, significant LDL alpha-tocopherol
sparing effect observed. Plasma thiobarbituric acid reacting substance
(TBARS) formation was significantly inhibited by walnut extracts and ellagic
acid in a dose-dependent manner, and the extracts exhibited a TEAC value
greater than that of alpha-tocopherol. LC-ELSD/MS analysis of the walnut
extracts identified ellagic acid monomers, polymeric ellagitannins and
other phenolics, principally nonflavonoid compounds. These results demonstrate
that walnut polyphenolics are effective inhibitors of in vitro plasma
and LDL oxidation. The polyphenolic content of walnuts should be considered
when evaluating their antiatherogenic potential.
Anticancer Res 2001 Jan-Feb;21(1A):359-64
IGF-II down regulation associated cell cycle arrest in colon cancer
cells exposed to phenolic antioxidant ellagic acid.
Narayanan BA, Re GG.
American Health Foundation, 1, Dana Road Valhalla, NY 10595, USA. bhagavat@earthlink.net
Altered cell and tissue differentiation is characteristic of premalignant
lesions long before they become invasive and metastatic. One approach
to controlling preneoplastic lesions is to block their expansion with
non-toxic agents that suppress cell proliferation and induce apoptosis.
Here, we show that ellagic acid, a natural, dietary phenolic antioxidant
when given at 10(-5) M for 48 hours to colon cancer cells (SW 480), induced
down regulation of insulin like growth factor IGF-II, activated p21(waf1/Cip1),
mediated a cumulative effect on G1/S transition phase and caused apoptotic
cell death. SW480 colon cancer cells expressed significant mRNA levels
for the mitogenic insulin like growth factor (IGF-II). Collectively, these
observations suggest that growth inhibition by ellagic acid is mediated
by signaling pathways that mediate DNA damage, triggers p53, which in
turn activates p21 and at the same time alters the growth factor expression,
resulting in the down regulation of IGF-II.
Cancer Lett 1997 Mar 19;114(1-2):11-7 Related Articles, Books, LinkOut
Experimental evidence for cancer preventive elements in foods.
Wargovich MJ.
Department of Gastrointestinal Medical Oncology and Digestive Diseases,
The University of Texas M.D. Anderson Cancer Center, Houston, USA.
The last decade has witnessed an incredible advance in our understanding
of how fruits and vegetables work to prevent cancer. Epidemiological studies
have suggested that a diet rich in fruits and vegetables is associated
with reduced risk for a number of common cancers. Food chemists and natural
product scientists have identified hundreds of 'phytochemicals'
that are being evaluated for the prevention of cancer. Food components
can modify carcinogenesis in one of five different ways. They may: (1)
modify carcinogen activation by inhibiting Phase 1 enzymes; (2) modify
how carcinogens are detoxified through Phase 2 pathways; (3) scavenge
DNA reactive agents; (4) suppress the abnormal proliferation of early,
preneoplastic lesions; and (5) inhibit certain properties of the cancer
cell.
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