Extract of Meeker Raspberry
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Code 550 - Ellagic Acid (from Meeker Raspberry Extract) 500 mg. x 120 Capsules | $14.95 (Availability) |
llagic
acid is one of the most exciting, promising, nutraceutical compounds to
hit the cancer care field in years. It is found throughout members of
the berry family, but is found to be particularly concentrated
in raspberries -- particularly of the "Meeker" variety. 
Our supplier of the raw
material has prepared an introductory document
(in MS-Word format) providing a synopsis of the benefits of
"EA." A word about our product:
Each tablet contains 500 mg. of Meeker Raspberry seed extract, which
is 38.5% ellagic acid by weight. Because of their light density and
mass, the recommended dosage is four (4) per day. Below, we provide a summary
of various studies that have been conducted on EA.
S T U D Y
A B S T R A C T
# 1
A B S T R A C T
# 1
Effect of chemopreventive agents on DNA adduction induced by the potent mammary carcinogen dibenzo[a,l]pyrene in the human breast cells MCF-7.
Taken from: Mutat Res 2001 Sep 1;480-481:97-108
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.
S T U D Y
A B S T R A C T
# 2
A B S T R A C T
# 2
Tannins, xenobiotic metabolism and cancer chemoprevention in experimental animals.
Taken from: Eur J Drug Metab Pharmacokinet 1999 Apr-Jun;24(2):183-9
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.
S T U D Y
A B S T R A C T
# 3
A B S T R A C T
# 3
The effects of dietary ellagic acid on rat hepatic and esophageal mucosal cytochromes P450 and phase II enzymes.
Taken from: Carcinogenesis 1996 Apr;17(4):821-8
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.
S T U D Y
A B S T R A C T
# 4
A B S T R A C T
# 4
p53/p21(WAF1/CIP1) expression and its possible role in G1 arrest and apoptosis in ellagic acid treated cancer cells.
Taken from: Cancer Lett 1999 Mar 1;136(2):215-21
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.
S T U D Y
A B S T R A C T
# 5
A B S T R A C T
# 5
Chemoprevention of esophageal tumorigenesis by dietary administration of lyophilized black raspberries.
Taken from: Cancer Res 2001 Aug 15;61(16):6112-9
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.
S T U D Y
A B S T R A C T
# 6
A B S T R A C T
# 6
DNA gyrase inhibitory activity of ellagic acid derivatives.
Taken from: Cancer Res 2001 Aug 15;61(16):6112-9
Bioorg Med Chem Lett 1998 Jan 6;8(1):97-100
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.
S T U D Y
A B S T R A C T
# 7
A B S T R A C T
# 7
Antioxidant properties of novel preparations--bioflavonoid derivatives and tannins. --- (This is translation. Article written in Russian)
Taken from: Eksp Klin Farmakol 2001 Mar-Apr;64(2):55-9
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.
S T U D Y
A B S T R A C T
# 8
A B S T R A C T
# 8
Human immunodeficiency virus type 1 cDNA integration: new aromatic hydroxylated inhibitors and studies of the inhibition mechanism.
Taken from: Antimicrob Agents Chemother 1998 Sep;42(9):2245-53
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.
S T U D Y
A B S T R A C T
# 9
A B S T R A C T
# 9
Inhibition of liver fibrosis by ellagic acid.
Taken from: Indian J Physiol Pharmacol 1996 Oct;40(4):363-6
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.
S T U D Y
A B S T R A C T
# 1 0
A B S T R A C T
# 1 0
The protective action of ellagic acid in experimental myocarditis --- [This is translation. Article written in Russian]
Taken from: Eksp Klin Farmakol 1998 May-Jun;61(3):32-4
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.
Editor: The above ten studies represents our
initial effort to collect the more compelling research done on
tannins and ellagic acid, as found in high concentrates in
Meeker raspberry extract. We will continue to update this
list as the academic community provides more related work
on this important nutraceutical area.
"EA" Properties:
In A Nutshell
The studies found in the left column
were compiled by Susan Thorpe-Vargas Ph.D. and represent a summation
of EA's known medical properties:
- EA is an anticancer agent - it protects DNA from mutation.
- EA shrinks tumors within 72 hours if the cancer is not caused by a mutation in the p53 or WAF 1/p21 genes.
- EA is a natural phenolic antioxidant.
- EA exerts actions that are both anti-bacterial and an anti-viral.
- EA appears to inhibit liver fibrosis.
- EA is cardioprotective and may prove useful in the treatment of myocarditis.
|
To U.S. Users: The research
material presented on this page is for educational purposes only.
Ellagic acid has not been evaluated by the U.S. Food & Drug Administration.
This product is not intended to diagnose, treat, cure, or prevent any disease. |
A Testimonial
Of Note:
Of Note:
I was diagnosed with
lung cancer. As I was to begin the traditional
treatment, doctors discovered I also had kidney cancer.
In a stunning lack of bedside manner the doctor told me,
"Not to worry about the kidney cancer -- the lung cancer
will kill you first." I began chemo. My good friend
told me about raspberry seed. Her son gave me the
information and told me to take the raspberry seed
in addition to my chemo: "It is simply a food that
will help the body to heal itself." I began taking
4 tablets a day. I didn't tell my doctor about the
raspberries - I knew she felt my only hope was through
her treatment. After a few weeks I began to feel better.
My doctor noticed
I was doing better than anyone my age going through chemo
"had a right to." I still didn't tell her about the
raspberries. My doc was so pleased with her treatment
and my progress that my chemo was shortened by almost half!
My lung tumors stopped growing and the kidneys tumors began to shrink.Finally I was pronounced to be in remission!!
During a follow-up
visit I finally got the courage up to tell my doctor I
was taking raspberry seeds. I gave her a stack of
documents and studies on raspberries and cancer. She was
contemptuous. "Stop taking that -- it isn't doing you
any good. All they are doing is taking your money." I told her my
friend and her son were providing me with the tablets
out of their own pockets. She harrumphed and insisted
I stop taking "that unproven stuff." I stopped.
Within a month I began to experience all the side effects of
chemo I had been warned about. Loss of energy, pain.
My friend insisted I get back on the raspberries, but I
refused. After six months of feeling bad I finally
listened to my friend and started again. Within two
weeks my symptoms disappeared. Life felt good again!
I finally got
the courage to tell my doctor that I went ahead and started
the raspberries again and was feeling so much better.
I asked the doctor if she had read any of the info I had
given her months earlier ... She (finally) kept her
word and a couple weeks later she called me and asked for
more info. She told me she was talking to her boss at
the medical college about going after a $4 million
research grant to study the effects of raspberry seeds
as a nutritional supplement during chemo!
Betty A.- Georgia --- (USA)