From: healerstouch1 <healerstouch1@a...> 
Date: Wed Apr 5, 2000 6:58pm 
Subject: Re: ELLAGIC ACID SOURCES -but not for dogs? 

Arnold Gore
Consumers Health Freedom Coalition


Mr. Gore,

The clinical studies up until 1999 were mostly done on lab animals.
I am confident enough to give my two children (a yorkie and a silkie)
the product. the only ingredient is extracted from the red Meeger
raspberry seeds. Here are some of the many clinical studies on
the product. Also, if someone questions the product for their 
animal, they can have the product muscle tested by a clinical
kinesiologist.

Sincerely,

Steve

Protective Effect of Curcumin, Ellagic Acid and Bixin on Radiation Induced 
Genotoxicity
K.C. Thresiamma, J. George and R. Kuttan Amala Cancer Research Centre, Amala 
Nagar, Trichur, India

Induction of micronuclei and chromosomal aberrations produced by whole body 
exposure of r-radiation (1.5-3.0 Gy) in mice was found to be significantly 
inhibited by oral administration of natural antioxidants, curcumin (400 µ 
moles), ellagic acid (200 µ moles)
and bixin (200 µ moles) per kilogram body weight. These antioxidants induced 
inhibition of micronucleated polychromatic and normochromatic erythrocytes, 
was comparable with a-tocopherol (200 µ moles) administration. Curcumin and 
ellagic acid were also found to significantly reduce the number of bone 
marrow cells with chromosomal aberrations and chromosomal fragments as 
effectively as a-tocopherol. Moreover, administration of antioxidants 
inhibited the DNA strand breaks produced in rat lymphocytes upon radiation as 
seen from the DNA unwinding studies. These results indicated that antioxidant 
curcumin, ellagic acid and bixin provide protection against chromosome damage 
produced by radiation.

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Inhibitory effects of ellagic acid on the direct-acting mutagenicity of 
aflatoxin B1 in the Salmonella microsuspension assay.
Loarca-Pina G, Kuzmicky PA, de Mejia EG, Kado NY

Departamento de Investigacion y Posgrado, Facultad de Quimica, Universidad 
Autonoma de Queretaro, Qro., Mexico. Ellagic acid (EA) is a phenolic compound 
that exhibits both antimutagenic and anticarcinogenic activity in a wide 
range of assays in vitro and in vivo. It occurs naturally in some foods such 
as strawberries, raspberries, and grapes. In the previous work, we used the 
Salmonella microsuspension assay to examine the antimutagenicity of EA 
against the potent mutagen aflatoxin B1 (AFB1) using tester strains TA98 and 
TA100. Briefly, the microsuspension assay was approximately 10 times more 
sensitive than the standard Salmonella/microsome (Ames) test in detecting 
AFB1 mutagenicity, and EA significantly inhibited mutagenicity of all AFB1 
doses in both tester strains with the addition of S9. The greatest inhibitory 
effect of EA on AFB1 mutagenicity occurred when EA and AFB1 were incubated 
together (with metabolic enzymes). Lower inhibition was apparent when the 
cells were first incubated with EA followed by a second incubation with AFB1, 
or when the cells were first incubated with AFB1 followed by a second 
incubation with EA alone, all with metabolic enzymes. The result of these 
sequential incubation studies indicates that one mechanism of inhibition 
could involve the formation of an AFB1-EA chemical complex. In the present 
study, we further examine the effect of EA on AFB1 mutagenicity, but without 
the addition of exogenous metabolic enzymes. We report the mutagenicity of 
AFB1 in the microsuspension assay using TA98 and TA100 without the addition 
of S9. Neither the concentrations of AFB1 (0.6, 1.2, and 2.4 microg/tube) nor 
the concentrations of EA (0.3, 1.5, 3, 10, and 20 microg/tube) were toxic to 
the bacteria. The results indicate that AFB1 is a direct-acting mutagen, and 
that EA inhibits AFB1 direct-acting mutagenicity. PMID: 9626978

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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@m... 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. PMID: 10355751

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Regression of atherosclerosis: role of nitric oxide and apoptosis.
Wang BY, Ho HK, Lin PS, Schwarzacher SP, Pollman MJ, Gibbons GH, Tsao PS, 
Cooke JP

Section of Vascular Medicine, Division of Cardiovascular Medicine, Stanford 
University School of Medicine, Stanford, Calif, USA. <0.01). In subsequent 
studies, aortas were harvested for ex vivo studies. Aortic segments were 
incubated in cell culture medium for 4 to 24 hours with
modulators of the NO synthase pathway. The tissues were then collected for 
histological studies and the conditioned medium collected for measurement of 
nitrogen oxides by chemiluminescence. Addition of sodium nitroprusside 
(10(-5) mol/L) to the medium caused a time-dependent increase in apoptosis of 
vascular cells (largely macrophages) in the intimal lesion. L-Arginine 
(10(-3) mol/L) had an identical effect on apoptosis, which was associated 
with an increase in nitrogen oxides released into the medium. These effects 
were not mimicked by D-arginine, and they were antagonized by the NO synthase 
inhibitor L-nitro-arginine (10(-4) mol/L). The effect of L-arginine was not 
influenced by an antagonist of cGMP-dependent protein kinase, nor was the 
effect mimicked by the agonist of protein kinase G or 8-BR cGMP. CONCLUSIONS: 
These results indicate that supplemental L-arginine induces apoptosis of 
macrophages in intimal lesions by its metabolism to NO, which acts through a 
GMP-independent pathway. These studies are consistent with our previous 
observation that supplementation of dietary arginine induces regression of 
atheroma in this animal model. These studies provide a rationale for further 
investigation of the therapeutic potential of manipulating the NO synthase 
pathway in atherosclerosis. PMID: 10069793

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Epidemic of gastroenteritis of viral origin associated with eating imported 
raspberries.
Gaulin CD, Ramsay D, Cardinal P, D'Halevyn MA

Centre de sante publique de Quebec, Beauport. Several episodes of food 
poisoning affected the region of Quebec City in July and August 1997. In the 
first two episodes, the analysis of two cohorts (A and B) demonstrated that 
the consumption of a raspberry mousse with raspberry sauce increased the risk 
of contracting gastroenteritis (A, RR = 2.6 p = 0.001; B, RR = 4.7 p = 0.02). 
More than 200 people were sick after eating a raspberry dessert. The common 
ingredient of all those desserts was raspberries imported from Bosnia. Viral 
studies on the raspberry sauce (2) and stool samples (5) using the genome 
amplification method by PCR indicated the presence of genomic material 
compatible with a virus of the Caliciviruses family. Southern hybridization 
and sequence analysis showed that the nucleotide sequences found in the 
raspberry sauce and in the stool samples were identical. It is important to 
maintain active surveillance to detect and limit the spread of this kind of 
outbreak. PMID: 10189738

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Protective effects of antioxidants on experimental liver injuries.
Suzuki M, Kumazawa N, Ohta S, Kamogawa A, Shinoda M

Faculty of Pharmaceutical Science, Hoshi University, Tokyo, Japan. Protective 
effects of 14 kinds of antioxidant on liver injury induced by carbon 
tetrachloride (CCl4) were investigated in terms of serum enzyme activities 
and bilirubin concentration. Consequently, the significant protective effects 
were found in sesamol, ellagic acid, cysteamine and cysteine. These 
antioxidants clearly decreased the lipid peroxide in the liver tissue. The 
protective effects on CCl4-induced liver injury in vivo were independent of 
the inhibitory activities on lipid peroxidation in hepatic mitochondria 
fraction in vitro. PMID: 2262882

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Polyphenols as cancer chemopreventive agents.
Stoner GD, Mukhtar H

Department of Preventive Medicine, Ohio State University, Columbus 43210, 
USA. This article summarizes available data on the chemopreventive efficacies 
of tea polyphenols, curcumin and ellagic acid in various model systems. 
Emphasis is placed upon the anticarcinogenic activity of these polyphenols 
and their proposed mechanism(s) of action. Tea is grown in about 30 countries 
and, next to water, is the most widely consumed beverage in the world. Tea is 
manufactured as either green, black, or oolong; black tea represents 
approximately 80% of tea products. Epidemiological studies, though 
inconclusive, suggest a protective effect of tea consumption on human cancer. 
Experimental studies of the antimutagenic and anticarcinogenic effects of tea 
have been conducted principally with green tea polyphenols (GTPs). GTPs 
exhibit antimutagenic activity in vitro, and they inhibit carcinogen-induced 
skin, lung, forestomach, esophagus, duodenum and colon tumors in rodents. In 
addition, GTPs inhibit TPA-induced skin tumor promotion in mice. Although 
several GTPs possess anticarcinogenic activity, the most active is 
(-)-epigallocatechin-3-gallate (EGCG), the major constituent in the GTP 
fraction. Several mechanisms appear to be responsible for the 
tumor-inhibitory properties of GTPs, including enhancement of antioxidant 
(glutathione peroxidase, catalase and quinone reductase) and phase II 
(glutathione-S-transferase) enzyme activities; inhibition of chemically 
induced lipid peroxidation; inhibition of irradiation- and TPA-induced 
epidermal ornithine decarboxylase (ODC) and cyclooxygenase activities; 
inhibition of protein kinase C and cellular proliferation; 
antiinflammatory activity; and enhancement of gap junction intercellular 
communication. Curcumin is the yellow coloring agent in the spice tumeric. It 
exhibits antimutagenic activity in the Ames Salmonella test and has 
anticarcinogenic activity, inhibiting chemically induced preneoplastic 
lesions in the breast and colon and neoplastic lesions in the skin, 
forestomach, duodenum and colon of rodents. In addition, curcumin inhibits 
TPA-induced skin tumor promotion in mice. The mechanisms for the 
anticarcinogenic effects of curcumin are similar to those of the GTPs. 
Curcumin enhances glutathione content and glutathione-S-transferase activity 
in liver; and it inhibits lipid peroxidation and arachidonic acid metabolism 
in mouse skin, protein kinase C activity in TPA-treated NIH 3T3 cells, 
chemically induced ODC and tyrosine protein kinase activities in rat colon, 
and 8-hydroxyguanosine formation in mouse fibroblasts. Ellagic acid is a 
polyphenol found abundantly in various fruits, nuts and vegetables. Ellagic 
acid is active in antimutagenesis assays, and has been shown to inhibit 
chemically induced cancer in the lung, liver, skin and esophagus of rodents, 
and TPA-induced tumor promotion in mouse skin. PMID: 8538195

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Ellagic acid induces NAD(P)H:quinone reductase through activation of the 
antioxidant responsive element of the rat NAD(P)H:quinone reductase gene.
Barch DH, Rundhaugen LM

Department of Medicine, Lakeside Veterans Affairs Medical Center, Chicago, 
IL. Induction of cellular detoxification enzymes can increase detoxification 
of carcinogens and reduce carcinogen-induced mutagenesis and tumorigenesis. 
To determine if the dietary anticarcinogen ellagic acid induced enzymes which 
detoxify xenobiotics and carcinogens, we examined the effect of ellagic acid 
on the expression of the phase II detoxification enzyme NAD(P)H:quinone 
reductase (QR). QR is induced by xenobiotics and antioxidants interacting 
with the xenobiotic responsive and antioxidant responsive elements of the 5' 
regulatory region of the QR gene. Ellagic acid is structurally related to the 
antioxidants which induce QR and we proposed that ellagic acid would induce 
QR expression through activation of the antioxidant responsive element of the 
QR gene. Rats fed ellagic acid demonstrated a 9-fold increase in hepatic and 
a 2-fold increase in pulmonary QR activity, associated with an 8-fold 
increase in hepatic QR mRNA. To determine if this increase in QR mRNA was due 
to activation of the antioxidant responsive element, transient transfection 
studies were performed with plasmid constructs containing various portions of 
the 5' regulatory region of the rat QR gene. These transfection studies 
confirmed that ellagic acid induces transcription of the QR gene and 
demonstrated that this induction is mediated through the antioxidant 
responsive element of the QR gene. PMID: 7522986

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Pulmonary carcinogenesis and its prevention by dietary polyphenolic compounds.
Castonguay A

Laboratory of Cancer Etiology and Chemoprevention, School of Pharmacy, Laval 
University, Quebec City, Canada. The aims of this study were to define the 
cumulative exposure of Canadian smokers to NNK and to characterize the 
efficacy of ellagic acid to inhibit lung tumorigenesis induced by NNK. The 
sales-weighted average of NNK deliveries from Canadian cigarettes was 73.2 
ng/cigarette. NNK deliveries were highly correlated to declared tar values 
and were linear with puff volumes between 20 and 50 ml. Ellagic acid 
inhibited lung tumorigenesis induced by NNK in A/J mice. This inhibition was 
related to the logarithm of the dose of ellagic acid added to the diet. The 
biodistribution of ellagic acid was studied in mice gavaged with ellagic 
acid. Pulmonary levels of ellagic acid were directly proportional to the dose 
of ellagic acid between 0.2 and 2.0 mmol/kg b.w. PMID: 8512246

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Lung tumors in strain A mice: application for studies in cancer 
chemoprevention.
Stoner GD, Adam-Rodwell G, Morse MA

Ohio State University, Department of Preventive Medicine, Arthur G. James 
Cancer Hospital and Research Institute, Columbus 43210. Strain A mice develop 
a high incidence of spontaneous lung tumors during their lifetime. These 
tumors may be found in some animals as early as 3 to 4 weeks of age, 
increasing to nearly 100% by 24 months of age. The strain A mouse is also 
highly susceptible to the induction of lung tumors by several classes of 
chemical carcinogens and has been used extensively as a mouse lung tumor 
bioassay for assessing the carcinogenic activity of a variety of chemicals. 
In addition to its use in carcinogen detection, the strain A mouse lung tumor 
model has been employed extensively for the identification of inhibitors of 
chemical carcinogenesis. A number of chemopreventive agents including 
beta-naphthoflavone, butylated hydroxyanisole, ellagic acid, phenethyl 
isothiocyanate, phenylpropyl isothiocyanate, phenylbutyl isothiocyanate, 
phenylhexyl isothiocyanate, indole-3-carbinol, etc., have been shown to 
inhibit chemically induced lung tumors in strain A mice. In most instances, 
inhibition of lung tumorigenesis has been correlated with effects of the 
chemopreventive agent on the metabolic activation and/or detoxification of 
carcinogens. To date, no chemopreventive agent has been shown to inhibit lung 
tumorigenesis in strain A mice when administered after the carcinogen, i.e., 
during the promotion/progression stages of tumor development. Efforts should 
be made to develop a standardized protocol in strain A mice for evaluating 
chemopreventive agents as inhibitors of both the initiation and progression 
stages of lung tumor development. PMID: 8412213

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Medical research confirms eating red raspberries may be one of the most 
potent ways to fight cancer.
Dr. Daniel Nixon, Medical University of South Carolina

(JANUARY-1999) -- One of the most popular and flavorful fruits on the market 
now has an entirely new reason for becoming a part of a healthy diet. Recent 
medical tests have shown that the red raspberry is one of the most effective 
all-natural ways to fight certain forms of cancer. 

Red raspberries have the highest content of ellagic acid, a phenolic compound 
that is a proven anti-carcinogen, anti-mutagen and anti-cancer initiator. 
Tests conducted at the Hollings Cancer Center at the Medical University of 
South Carolina have revealed that the ellagic acid from red raspberries is 
readily absorbed by the human body. This ellagic acid has been clinically 
shown to cause apoptosis (cell death) in cancer cells. 

Additional tests have revealed that the ellagic acid in red raspberries 
retains its potency after heating, freezing and concentration processing. So 
whether consumed fresh, in juices, fruit spreads, preserves or sorbets, the 
red raspberry should become a part of any healthy diet.