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PubMed2006

Effects of cultivar, fruit number and reflected photosynthetically active radiation on Fragaria x ananassa productivity and fruit ellagic acid and ascorbic acid concentrations.

BACKGROUND AND AIMS: A number of strawberry varieties were surveyed for their total ellagic acid concentration, and attempts were made to determine if ellagic acid and ascorbic acid concentrations of two strawberry cultivars could be increased by polythene reflective mulches. METHODS: After adjusting crop yields and cultivation using polythene mulches with two different PAR reflective capacities, field- and polytunnel-grown strawberries were analysed for ellagic acid and ascorbic acid concentrations by HPLC. Comparative measurements of yield and fruit quality were determined along with plant developmental changes. KEY RESULTS: Ellagic acid concentration varied widely with strawberry cultivar (60-341 microg g(-1) frozen weight), as did the ratio of conjugated ellagic acid : free ellagic acid. Also, there was significant year-to-year variation in total ellagic acid concentration with some cultivars. Mulches with different reflective capacities impacted on strawberry production; highly reflective mulches significantly increased growth and yield, the latter due to increases in fruit size and number. CONCLUSIONS: Highly reflective mulches significantly increased total concentrations of ellagic acid and ascorbic acid relative to control in fruit of different cultivars. The potential of agronomic practices to enhance the concentration and amounts of these important dietary bioactive compounds is discussed.

Ascorbic Acid↗
PubMed2005

Evaluation of estrogenic/antiestrogenic activity of ellagic acid via the estrogen receptor subtypes ERalpha and ERbeta.

Ellagic acid is a plant-derived polyphenol, possessing antioxidant, antiproliferative, and antiatherogenic properties. Whether this compound has estrogenic/antiestrogenic activity, however, remains largely unknown. To answer this question, we first investigated the ability of ellagic acid to influence the activity of the estrogen receptor subtypes ERalpha and ERbeta in HeLa cells. Cells co-transfected with an estrogen response element (ERE)-driven luciferase (Luc) reporter gene and an ERalpha- or ERbeta-expression vector were exposed to graded concentrations of ellagic acid. At low concentrations (10(-7) to 10(-9) M), this compound displayed a small but significant estrogenic activity via ERalpha, whereas it was a complete estrogen antagonist via ERbeta. Further evaluation revealed that ellagic acid was a potent antiestrogen in MCF-7 breast cancer-derived cells, increasing, like the pure estrogen antagonist ICI182780, IGFBP-3 levels. Moreover, ellagic acid induced nodule mineralization in an osteoblastic cell line (KS483), an effect that was abolished by the estrogen antagonist. Endometrium-derived epithelial cells (Ishikawa) showed no response to the natural compound by using a cell viability assay (MTT). These findings suggest that ellagic acid may be a natural selective estrogen receptor modulator (SERM).

Breast Neoplasms↗
PubMed2001

Effect of processing and storage on the antioxidant ellagic acid derivatives and flavonoids of red raspberry (Rubus idaeus) jams.

From red raspberries, ellagic acid, its 4-arabinoside, its 4' (4' '-acetyl) arabinoside, and its 4' (4' '-acetyl)xyloside, as well as quercetin and kaempferol 3-glucosides, were identified. In addition, two unidentified ellagic acid derivatives were detected. The free radical scavenging activity of the ellagic acid derivatives was evaluated by using the DPPH method and compared to that of Trolox. All of the isolated compounds showed antioxidant activity. The effect of processing to obtain jams on raspberry phenolics was evaluated. The flavonol content decreased slightly with processing and more markedly during storage of the jams. The ellagic acid derivatives, with the exception of ellagic acid itself, remained quite stable with processing and during 6 months of jam storage. The content of free ellagic acid increased 3-fold during the storage period. The initial content (10 mg/kg of fresh weight of raspberries) increased 2-fold with processing, and it continued increasing up to 35 mg/kg after 1 month of storage of the jam. Then a slight decrease was observed until 6 months of storage had elapsed. The increase observed in ellagic acid could be explained by a release of ellagic acid from ellagitannins with the thermal treatment.

Chromatography, High Pressure Liquid↗
PubMed2006

Beware of pomegranates bearing 40% ellagic Acid.

A recent profusion of pomegranate nutraceutical products, "standardized to 40% ellagic acid," has appeared in the marketplace. This Perspective reviews the chemical and functional studies of pomegranate as well as the virtues and dangers of ellagic acid, and concludes that synergy among the various pomegranate fractions and phytochemicals is the most important factor for assessing strength of pomegranate nutraceutical preparations, and not simply the concentration of ellagic acid. Ellagic acid concentration in final products is likely to have an optimal therapeutic range, which very likely is less than 40%. The wisdom of designing and engineering pomegranate nutraceutical products to maximize therapeutic or chemopreventive synergy is suggested, as opposed to preparations that are designed and engineered simply to maximize the concentration of a single phytochemical. The implications of this strategy may be generalized for the optimization of nutraceutical preparations from other medicinal plants as well.

Anticarcinogenic Agents↗
PubMed2001

Application of Eudragit P-4135F for the delivery of ellagic acid to the rat lower small intestine.

Based on the assumption that the delivery of ellagic acid to its site of action would show an antiinflammatory activity in inflammatory bowel disease (IBD), we have prepared microspheres using a new pH-sensitive polymer, Eudragit P-4135F (P-4135F), to deliver ellagic acid to the lower small intestine in rats. The microspheres were spherical in shape and the mean diameters were approximately 100-150 microm. The amount of ellagic acid released from the microspheres decreased by increasing the formulated amount of P-4135F. The release characteristics of ellagic acid were pH-dependent. By considering the factors loading efficiency and microsphere particle size distribution, ellagic acid-2 microspheres (P-4135F/ellagic acid = 1.65) were selected for further investigation. In a dissolution study, more than 95% ellagic acid was released within 0.5 h in pH 7.4 and 8.0 buffers. The release percent of ellagic acid was less than 40% in pH 6.8 and 7.0 and was less than 10% in pH 5.6 and 5.9. To observe the dissolution sites of the microspheres in the rat small intestine fluorescein was formulated in the microspheres as a tracer drug along with ellagic acid (50 mg kg(-1)). After intraduodenal administration of fluorescein-labelled microspheres to rats, the plasma fluorescein level started to increase at 0.5 h, by which time the microspheres had reached the middle part of the ileum. Microspheres started to dissolve within 1.0 h and the peak plasma fluorescein concentration was observed at 3.0 h, when the majority of the administered microspheres were dissolved in the terminal ileum. These results suggested that P-4135F microspheres could deliver ellagic acid to the lower part of the small intestine, and that the released ellagic acid would be distributed into the caecum and the ascending colon.

Administration, Oral↗
PubMed1980

The metabolism of ellagic acid in the rat.

1. Following oral administration of ellagic acid to the rat, 10% of the dose was excreted as 3,8-dihydroxy-6H-dibenzo[b,d]pyran-6-one in urine and faeces. A second metabolite was detected in urine and faeces but not identified. Both metabolites were of microfloral origin, as their formation was not observed in germ-free rats but was demonstrated when ellagic acid was incubated in vitro with micro-organisms from rat gastro-intestinal tract. 2. Following intraperitoneal, but not oral, administration of ellagic acid, a third metabolite was detected in urine. 3. Unchanged ellagic acid was not detected in faeces or urine of any normal rat examined, but small amounts were detected in the faeces of germ-free animals. 4. Following oral administration of ellagic acid, two conjugates of 3,8-dihydroxy-6H-dibenzo[b,d]pyran-6-one were detected in bile, whereas intraperitoneal administration resulted in the biliary excretion of three conjugates of an unidentified metabolite.

Administration, Oral↗
PubMed1988

Inhibition of N-nitrosobenzylmethylamine metabolism and DNA binding in cultured rat esophagus by ellagic acid.

The effect of ellagic acid (EA), a naturally occurring plant phenol, on the metabolism, DNA binding and DNA adduct formation of N-nitrosobenzylmethylamine (NBMA) in cultured explants of rat esophagus was investigated. Explants were incubated in medium containing EA at non-toxic concentrations of 10, 50 and 100 microM for 16 h, followed by the addition of 1 microM [3H]NBMA and EA for 12 h. Explant DNA was isolated by phenol extraction and hydroxylapatite chromatography, and benzaldehyde formation was determined by HPLC analysis of the culture medium. EA produced a significant inhibition in the total covalent binding of NBMA metabolites to DNA and in the production of benzaldehyde in the medium. After acid hydrolysis of the isolated DNA, the NBMA--DNA adducts were separated by HPLC. EA caused a dose-dependent decrease in the formation of N7-methylguanine and O6-methylguanine adducts. These results suggest that EA inhibits both the metabolism of NBMA and the binding of NBMA metabolites to DNA in cultured rat esophagus.

Animals↗
PubMed1998

Biodistribution of, antimutagenic efficacies in Salmonella typhimurium of, and inhibition of P450 activities by ellagic acid and one analogue.

Ellagic acid (EA) is generated by hydrolysis of ellagitannins present in fruit berries and edible nuts and grapes. Large doses of EA prevent lung tumorigenesis induced by the tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in A/J mice. In this study, we document the efficacies of the EA structural analogue (3,4,7,8-tetrahydroxy-6H-benzo[b,d]pyran-6-one) (analogue 1) to inhibit specific P450 activities, pulmonary metabolism of NNK in A/J mice, and NNK-induced mutations in Salmonella typhimurium. Mouse lung microsomes metabolized benzyloxyresorufin, a marker of cytochrome P450 2B1 activity, more extensively than methoxyresorufin or ethoxyresorufin. The EA analogue was more effective than EA in inhibiting dealkylation of the three alkoxyresorufins, suggesting that it is a nonspecific inhibitor of P450s. Mouse lung microsomes hydroxylate testosterone in the 7alpha and 6beta positions, suggesting contributions of P450 2A1 and P450 3A2 isozymes, respectively. Inhibition of both pathways was more effective with the EA analogue than with EA. Mouse lung explants metabolized NNK by alpha-carbon hydroxylation (activation) and pyridine N-oxidation (deactivation). Both pathways were inhibited when 100 microM EA was added to the culture medium. The EA analogue was a better inhibitor of the activation of NNK to electrophilic species than EA. Mouse lung microsomes activate NNK to intermediates mutagenic to S. typhimurium. Inhibition of NNK mutagenicity by EA or the EA analogue was 20 or 65%, respectively. The distribution of the EA analogue in lung and liver was determined following gavage with 1.7 mmol of the EA analogue. In the lung, a maximal level of EA analogue corresponding to 105 nmol was observed 30 min after administration of the analogue. The level in liver tissues was 4-fold lower than in the lung. Results of this study demonstrate that the EA analogue is more effective than EA in inhibiting the pulmonary activation of NNK and suggest that the EA analogue could be effective in preventing lung tumorigenesis.

Animals↗
PubMed1995

The dietary anticancer agent ellagic acid is a potent inhibitor of DNA topoisomerases in vitro.

Ellagic acid and 12 related agents have been tested for their ability to inhibit the activities of human DNA topoisomerase (topo) I and II. Using specific in vitro assays, we found ellagic acid and flavellagic acid to be potent inhibitors of the catalytic activities of the two topoisomerases. The minimum concentration required to inhibit > or = 50% of catalytic activity (IC50) of ellagic acid was determined at 0.6 and 0.7 micrograms/ml for topo I and topo II, respectively. Flavellagic acid's IC50 was determined at 3.0 and 3.6 micrograms/ml for topo I and topo II, respectively. Unlike topoisomerase poisons, these two plant phenols did not trap the enzyme-DNA reaction intermediate, known as the cleavable complex. In contrast, ellagic acid prevented other topo I and topo II poisons from stabilizing the cleavable complex, suggesting that the mode of its action is that of an antagonist. Structure-activity studies identified the 3,3'-hydroxyl groups and the lactone groups as the most essential elements for the topoisomerase inhibitory actions of plant phenols. On the basis of these findings and other properties of ellagic acid, a mechanistic model for the documented anticarcinogenic effects of the agent is proposed.

Anticarcinogenic Agents↗
PubMed1988

Disposition of the plant phenol ellagic acid in the mouse following oral administration by gavage.

1. The absorption, distribution and elimination of 3H-ellagic acid, a putative antimutagen and anticarcinogen, was studied in male Swiss-Webster mice following oral administration. 2. Levels of 3H-ellagic acid were highest in blood 30 min after administration, in urine and bile 120 min post-administration, and in liver, lung and kidney 15 min after administration [corrected]. 3. Free ellagic acid and its conjugates were present in urine, bile and blood. H.p.l.c. analysis of the organic solvent extracts of urine, bile and blood indicated the presence of four metabolites in urine, two in blood and one in bile. 4. Sulphate ester, glucuronide and glutathione conjugates of ellagic acid were present in urine, bile and blood. H.p.l.c. analysis of organic solvent extracts after aryl sulphatase or beta-glucuronidase treatment showed that ellagic acid was the major component present. 5. Absorption of 3H-ellagic acid occurred mostly within two hours after oral administration. Levels in blood, bile and tissues were low and almost all of the absorbed dose was excreted in urine. 6. More than 53% of the orally administered 3H-ellagic acid remained in the gastrointestinal tract at 24 h. Approximately 19% was excreted in faeces and 22% in urine at 24 h. 7. Of the 24 h faecal radioactivity 93% was extractable into organic solvents and more than 80% of this fraction was free ellagic acid. Only one metabolite was found in faeces.

Administration, Oral↗
PubMed1994

Dietary ellagic acid inhibits the enzymatic activity of CYP1A1 without altering hepatic concentrations of CYP1A1 or CYP1A1 mRNA.

The anticarcinogen ellagic acid significantly reduces the incidence of polycyclic aromatic hydrocarbon induced carcinomas, in association with significant reductions in benzo[a]pyrene hydroxylase activity and CO reducible hepatic cytochrome P450. This suggested that ellagic acid reduced hepatic concentrations of CYP1A1, but these changes occurred without any alteration in CYP1A1 mRNA or in immunoreactive CYP1A1. Dietary ellagic acid results in muMolar concentrations of ellagic acid in hepatic tissue. Addition of similar concentrations of ellagic acid in vitro directly inhibited the measurement of benzo[a]pyrene hydroxylase activity and CO reducible cytochrome P450. Thus dietary ellagic acid does not alter the hepatic concentration of CYP1A1, but the dietary ellagic acid remaining in hepatic tissue appears to directly inhibit the measurement of benzo[a]pyrene hydroxylase activity and CO reducible cytochrome P450.

Animals↗
PubMed2003

Pharmacokinetic study of ellagic acid in rat after oral administration of pomegranate leaf extract.

Quantification of ellagic acid, the principal bioactive component of pomegranate leaf extract, in rats plasma following oral administration of pomegranate leaf extract was achieved by using a high-performance liquid chromatographic method. The calibration curve for ellagic acid was linear (r2=0.9998) ver the concentration range 0.026-1.3 microg/ml. The intra- and inter-day assays of ellagic acid from rat plasma were less than 6.52% at concentration range from 26 to 1300 ng/ml and good overall recoveries (94.5-102.4%) were found on same concentrations. The concentration-time profile was fitted with an open two-compartment system with lag time and its max concentration of ellagic acid in plasma was 213 ng/ml only 0.55 h after oral administration extract 0.8 g/kg. The pharmacokinetic profile indicates that ellagic acid has poor absorption and rapid elimination after oral administration pomegranate leaf extract, and part of it was absorbed from stomach.

Administration, Oral↗
PubMed1987

Mechanism of the congestion of lymph nodes induced by ellagic acid in rats.

Intravenous injection of ellagic acid (EA, 30 mg/Kg), an activator of the Hageman factor, induced congestion of lymph nodes and dilatation of the spleen in rats. The dilatation of the spleen was inhibited by heparin, thrombin, defibrase, clocoumarol, lambda carrageenan, SBTI, PCR 4099 and CCI 17810. The congestion of lymph nodes was inhibited by heparin, thrombin, defibrase, clocoumarol, SBTI, lambda carrageenan, aspirin, indomethacin and ketoprofen, phentolamine and hexamethonium. Thrombin, defibrase, lambda carrageenan did not induce any congestion of the lymphoid tissues. These results suggest the the dilatation of the spleen induced by ellagic acid would result from blood coagulation, platelet stimulation and kinin formation. The congestion of lymph nodes would depend on kinins, blood coagulation and prostaglandin;s. The activation of Hageman factor in acute inflammatory reactions could mediate the early congestion of lymph nodes.

Animals↗
PubMed1986

Effect of ellagic acid and 3-O-decylellagic acid on the formation of benzo[a]pyrene-derived DNA adducts in vivo and on the tumorigenicity of 3-methylcholanthrene in mice.

The effect of ellagic acid and its more lipophilic derivative, 3-O-decylellagic acid, on the amount of DNA-bound adducts in the epidermis or lung of CD-1 mice treated with [3H]benzo-[a]pyrene ([3H]B[a]P) was evaluated using several different treatment protocols. The i.v. administration of 50 mumol/kg of ellagic acid or 3-O-decylellagic acid either together with or 5 min before a 0.2 mumol/kg i.v. dose of [3H]B[a]P did not inhibit the formation of pulmonary DNA-bound adducts. Feeding mice a diet that contained 1% ellagic acid for 10 days or the i.p. administration of 120 mumol/kg of ellagic acid 30 min before the i.v. administration of 0.2 mumol/kg of [3H]B[a]P did not inhibit the formation of DNA-bound adducts in the lung. The application of 2,500 nmol of ellagic acid or 3-O-decylellagic acid to mouse skin 5 min before the application of 2, 10 or 50 nmol of [3H]B[a]P had little or no effect on the covalent binding of [3H]B[a]P metabolites to epidermal DNA. Feeding mice a diet containing 1% ellagic acid for 10 days did not inhibit the formation of epidermal DNA-bound adducts after a topical dose of 2 nmol of [3H]B[a]P. Similarly, the topical application of 2,500 nmol of ellagic acid at 2 h, 1 h and 5 min before and at 10 min after the application of 2 nmol of [3H]B[a]P did not inhibit the formation of DNA-bound adducts, but the same dosing regimen of 3-O-decylellagic acid (total dose of 10,000 nmol) resulted in a modest inhibition in the formation of DNA-bound adducts. The topical application of 1,500 nmol of ellagic acid 1 h before the application of 1,500 nmol of 3-methylcholanthrene (3-MC) to CD-1 or BALB/c mice twice weekly did not inhibit the development of skin tumors. Our results indicate that ellagic acid and 3-O-decylellagic acid are not effective in inhibiting [3H]B[a]P DNA adduct formation in mouse skin and lung and that ellagic acid does not inhibit 3-MC-induced skin tumorigenesis in BALB/c or CD-1 mice.

Animals↗
PubMedDate not supplied

Determination of ellagic acid in pseudofruits of some species of roses.

Ellagic acid (EA) is known as a naturally occurring dietary antimutagen and anticarcinogen with strong antioxidant and anti-inflammatory activities. An SPE RP HPLC method was optimized and applied for identification and determination of ellagic acid in hips of fourteen species of roses, wildly growing in Poland. A large amount of total EA, ranged from 487.2 to 1065.2 microg/g of dry material was found. The results suggest that studied materials are good sources of dietary ellagic acid and could be used as a natural antioxidant and functional food.

Calibration↗
PubMed2000

[Studies on procedure for sample preparation of ellagic acid in several kinds of foodstuffs].

A sample preparation for ellagic acid in several kinds of foodstuffs, which is included in the List of Existing Food Additives as natural antioxidants in Japan, functioning as an antioxidant, was studied. The solid samples were refluxed with methanol, and then the extract was refined using a solid-phase cartridge. The liquid samples were directly pretreated by solid-phase extraction. On the other hand, test solutions for cooking oils and fats were inapplicable to solid-phase extraction in this work, because the recovery tests from samples spiked with ellagic acid gave low recoveries. Consequently, they were prepared by modified frozen method using methanol or acetonitrile-2-propanol-ethanol (2:1:1). The recoveries from tested foodstuffs spiked with ellagic acid (50 micrograms/g) were 75.2-96.9%. The limits of quantification for ellagic acid were 0.05 microgram/g by the proposed method.

Antioxidants↗
PubMed1992

Antimutagenicity of ellagic acid towards the food mutagen IQ: investigation into possible mechanisms of action.

The ability of the plant phenol ellagic acid to inhibit the mutagenicity of the food mutagen IQ was evaluated using Salmonella typhimurium strain TA98 in the Ames mutagenicity test. Ellagic acid caused a concentration-dependent decrease in the S-9- and microsome-mediated mutagenicity of IQ. The plant phenol did not interact directly with the IQ-derived mutagenic species and did not modify the cytosol-mediated activation of the promutagen. At the concentrations used in the mutagenicity studies, ellagic acid failed to inhibit microsomal mixed-function oxidase activity, including that mediated by the P450I family responsible for the bioactivation of IQ, despite being an essentially planar molecule as indicated by computer-graphic analysis. The inhibitory effect of ellagic acid was independent of its ability to chelate Mg2+. However, pre-incubation of ellagic acid with the bacteria, followed by removal of the plant phenol, did not completely prevent the inhibitory effect of the phenol on the mutagenicity of IQ. Intraperitoneal administration of ellagic acid to rats caused a decrease in total cytochrome P-450 levels and related activities as well as in cytosolic glutathione S-transferase activity. Finally, the possibility that the reported anticarcinogenic action of ellagic acid reflects nothing more than non-selective destruction of hepatic cytochromes P-450, and thus reduced chemical activation, is considered.

Animals↗
PubMed1992

Ellagic acid protects rat embryos in culture from the embryotoxic effects of N-methyl-N-nitrosourea.

Ellagic acid is a naturally occurring plant phenol that has demonstrated anticarcinogenic and antimutagenic activity in several test systems. Given the common proposed etiopathogenic processes of mutagenesis, carcinogenesis, and teratogenesis induced by genotoxic chemicals, the present study was initiated to determine whether ellagic acid would protect rat embryos in culture from the teratogenic effects of N-methyl-N-nitrosourea (MNU). Ellagic acid alone (as used in these experiments; 50 microM in DMSO) was not embryotoxic. Ellagic acid (50 microM) significantly (P less than 0.01) prevented MNU (75 microM)-induced effects including mortality (absence of heart beat), abnormal formation of the cephalic neural tube derivatives, and delayed differentiation as assessed by a morphological scoring system. These embryoprotective effects were dose responsive. Sequential treatment of embryos with ellagic acid followed by MNU in fresh media also was embryoprotective with no diminution of effect. The site at which ellagic acid interrupts the critical teratogenic events induced by MNU is apparently within the embryo and/or placenta. This model of chemical embryoprotection may be useful in determining the role of cell death and/or mutation in the teratogenic mechanism of action of methylating agents.

Abnormalities, Drug-Induced↗