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PubMed1994

Screening for agents inhibiting the mutagenicity of extracts and constituents of tobacco products.

The aim of this study was to screen for potential agents affecting the mutagenicity of tobacco products. The influence of a number of compounds which have been suggested to be antimutagenic some of which are present in tobacco products, was investigated on the mutagenicity of a cigarette smoke condensate (CSC) and, in some cases, an extract of oral Swedish moist snuff (SNUS), using a screening procedure of the Ames Salmonella/microsome assay (STY). For some of the compounds the V79/hprt mutagenicity assay with benzo[a]pyrene metabolites as mutagens was used to obtain complementary and confirmatory information on mammalian cells. The antimutagens used included two selenium compounds, sodium selenite and ebselen; the flavonoids and polyphenols, ellagic acid, (+)-catechin hydrate, scopoletin, chlorogenic acid and rutin trihydrate; the porphyrin derivatives, bovine hemin, biliverdine dihydrochloride, chlorophyllin and a plant extract containing chlorophyll; the terpenoids, beta-carotene, retinol and a mixture of the two epimers (4R) and (4S) of (1S,2E,6R,7E,11E)-cembra-2,7,11-triene-4,6-diols (CBD); and cyclohexanol and ubiquinone. Screening of antimutagenic activities using the STY involves problems with toxicity. In several cases in this study mutagenicity was decreased below the control level without signs of toxicity in the background growth of bacteria. Since the survival of mutants and slight bacteriostatic effects on the background growth cannot be determined accurately in the STY, a reduction in mutagenicity may simply be due to toxicity. Only in cases where a dose-response curve declines to a level at or above the background and then levels off, can toxicity be excluded. An antimutagenic effect determined using this test system is therefore often not sufficient for classifying a compound as antimutagenic until these findings are confirmed in other test systems and, preferably, the mechanism behind this effect is clarified. The results obtained with the selenium compounds were considered to be inconclusive since the reduction in the mutation rate declined below the background level and might only reflect the toxic effects of these compounds. For ellagic acid an almost complete inhibition of the mutagenicity of CSC and SNUS in STY was indicated. This indication of antimutagenicity was confirmed in V79 cells using two metabolites of the CSC constituent benzo[a]pyrene, i.e., trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene and (+)-7 beta, 8 alpha-dihydroxy-9 alpha, 10 alpha-oxy-7,8,9,10- tetrahydrobenzo[a]pyrene (BPDE). Chlorogenic acid and (+)--catechin reduced the mutagenicity of CSC and chlorogenic acid also strongly inhibited SNUS mutagenicity. Scopoletin and rutin trihydrate inhibited the mutagenicity of CSC, but showed confounding effects with SNUS.(ABSTRACT TRUNCATED AT 400 WORDS)

Antimutagenic Agents↗

PubMed1990

The production of reactive oxygen species by dietary flavonols.

Flavonols are a group of naturally occurring compounds which are widely distributed in nature where they are found glycosylated primarily in vegetables and fruits. A number of studies have found both anti- and prooxidant effects for many of these compounds. The most widely studied because of their ubiquitous nature have been quercetin, a B-dihydroxylated and myricetin, a B-trihydroxylated flavonol. Some of their prooxidant properties have been attributed to the fact that they can undergo autooxidation when dissolved in aqueous buffer. Studying a number of factors affecting autooxidation, we found the rate of autooxidation for both quercetin and myricetin to be highly pH dependent with no autooxidation detected for quercetin at physiologic pH. Both the addition of iron for the two flavonols and the addition of iron followed by SOD for quercetin at physiologic pH. Both the addistantially. Neither kaempferol, a monohydroxylated flavonol nor rutin, a glycosylated quercetin showed any ability to autooxidize. The results with rutin differ from what we expected based on the B-ring structural similarity to quercetin. The autooxidation of quercetin and myricetin was further studied by electron spin resonance spectroscopy (ESR). Whereas quercetin produced a characteristic DMPO-OH radical, it was not detected below a pH of 9. However, the addition of iron allowed the signal to be detected at a pH as low as 8.0. On the other hand, myricetin autooxidation yielded a semiquinone signal which upon the addition of iron, converted to a DMPO-OH signal detected at a pH of 7.5. In a microsome-NADPH system, quercetin produced an increase in oxygen utilization and with ESR, an ethanol-derived radical signal which could be completely suppressed by catalase indicating the dependence of the signal on hydrogen peroxide. These studies demonstrate that the extracellular production of active oxygen species by dietary flavonols is not likely to occur in vivo but the potential for intracellular redox cycling may have toxicologic significance.

Animals↗

PubMed2006

Differential effects of flavonols on inactivation of alpha1-antitrypsin induced by hypohalous acids and the myeloperoxidase-hydrogen peroxide-halide system.

Alpha1-antitrypsin is well known for its ability to inhibit human neutrophil elastase. Pretreatment of alpha1-antitrypsin with hypohalous acids HOCl and HOBr as well as with the myeloperoxidase-hydrogen peroxide-chloride (or bromide) system inactivated this proteinase. The flavonols rutin, quercetin, myricetin, and kaempferol inhibited the inactivation of alpha1-antitrypsin by HOCl and HOBr with rutin having the most pronounced effect. In contrast, these flavonols did not remove the proteinase inactivation by the myeloperoxidase-hydrogen peroxide-halide system. Taurine did not protect against the inactivation of alpha1-antitrypsin by HOCl, HOBr, or the myeloperoxidase-hydrogen peroxide-halide system, while methionine was efficient in all systems. A close association between myeloperoxidase and alpha1-antitrypsin was revealed by native gel electrophoresis and in-gel peroxidase staining. In addition, alpha1-antitrypsin binds to the myeloperoxidase components transferred after SDS-PAGE on a blotting membrane. With this complex formation, myeloperoxidase overcomes the natural antioxidative protective system of plasma and prevents the inactivation of alpha1-antitrypsin.

Bromates↗

PubMed2004

Effect of change in cellular GSH levels on mitochondrial damage and cell viability loss due to mitomycin c in small cell lung cancer cells.

The effect of GSH depletion on mitochondrial damage and cell death due to mitomycin c (MMC) was assessed in small cell lung cancer (SCLC) cells. Cytotoxicity of MMC was attenuated by Tempol and dicumarol, inhibitors of the enzymatic reduction, and increased by xanthine oxidase. The MMC-induced cell death and decrease in the GSH contents in SCLC cells were inhibited by caspase inhibitors (z-DQMD.fmk, z-IETD.fmk and z-LEHD.fmk) and antioxidants (N-acetylcysteine, dithiothreitol and N-(2-mercaptopropionyl)glycine, melatonin, rutin and carboxy-PTIO). Thiol compounds, melatonin and rutin attenuated the MMC-induced nuclear damage, decrease in mitochondrial transmembrane potential, release of cytochrome c and activation of caspase-3. Treatment of MMC caused a significant decrease in GSH contents in SCLC cells, which was followed by increase in the formation of reactive oxygen species. Depletion of GSH due to L-buthionine sulfoximine enhanced the MMC-induced activation of caspase-3 and cell death in SCLC cells. Antioxidants, including N-acetylcysteine, depressed formations of nitric oxide, malondialdehyde and carbonyls due to MMC in SCLC cells. The results show that the reductive activation of MMC may cause cell death in SCLC cells by inducing mitochondrial dysfunction, leading to caspase-3 activation, and by activation of caspase-8. The MMC-induced change in the mitochondrial membrane permeability, followed by cell death, in SCLC cells may be significantly enhanced by decrease in the intracellular GSH contents due to oxidative attack of free radicals.

Antibiotics, Antineoplastic↗

PubMed2004

Comparative vasodilating actions among terpenoids and flavonoids contained in Ginkgo biloba extract.

BACKGROUND: Comparative vasodilating actions of the constituents of Ginkgo biloba extract (GBE), terpenoids (bilobalide, ginkgolides A, B and C) and flavonoids (quercetin and rutin), were examined using rat aorta ring strips. METHODS: Cumulative administrations of GBE and its constituents were followed with the pretreatment of 5 micromol/l NE. RESULTS: GBE at 0.03 to 3 mg/ml had a potent concentration-dependent relaxation; by 70 +/- 4.5% (n = 6, P < 0.001) at 3 mg/ml. Terpenoids and flavonoids at 0.1 to 100 micromol/l had potent concentration-dependent relaxation. At 100 micromol/l, bilobalide dilated by 17.6 +/- 3.9% (n = 7, P < 0.05), and ginkgolides A, B and C also caused it to the almost same extent. Quercetin (100 micromol/l) caused a potent vasorelaxation by 49.9 +/- 4.8% (n = 10, P < 0.001). Rutin at 100 micromol/l had weaker vasorelaxation; by 13.7 +/- 3.2% (n = 6, P < 0.01). CONCLUSIONS: All constituents of GBE have the concentration-dependent vasorelaxtant effect. The potency of GBE's action was not made simply by addition of those of the constituents. Each constituent itself would contribute to the GBE-induced vasodilation, although the constituents have the complicated interactions with each other.

Animals↗

PubMed2004

Assay of phenolic compounds in red wine by on-line combination of capillary isotachophoresis with capillary zone electrophoresis.

The on-line combination of capillary zone electrophoresis (CZE) with capillary isotachophoresis (ITP) increases significantly the separation capability and sensitivity of capillary electrophoresis. This technique was used for separation and quantification of fourteen selected natural constituents in red wine belonging to flavonoids and phenolic acids. The leading electrolyte (LE) in the ITP pre-separation step was 10 mM HCl of pH* 7.2 with Tris as counterion, the terminating electrolyte (TE) was 50 mM boric acid of pH* 8.2 (adjusted with barium hydroxide). The background electrolyte in the electrophoretic step contained 25 mM beta-hydroxy-4-morpholinopropanesulfonic acid (MOPSO), 50 mM Tris, 15 mM boric acid and 5 mM beta-cyclodextrin of pH* 8.5. The content of methanol in all electrolytes was 20% (v/v). For exact timing of the transfer of isotachophoretically stacked analyte zones into the CZE column and for the control of the residual amount of leading and terminating ITP electrolytes picric acid was used as coloured marker. The R.S.D. values (n = 6) ranged between approximately 0.1% (for 0.25 microg ml(-1) rutin) and approximately 11% (for 0.25 microg ml(-1) of quercitrin). Detection limits were 30 ng mi(-1) for phenolic acids, quercitrin and rutin, 100 ng ml(-1) for quercetin, kaempferol and epicatechin and 250 ng ml(-1) for catechin. A single analysis took 45 min.

Electrophoresis↗

PubMed2005

Modulation of drug transport by selected flavonoids: Involvement of P-gp and OCT?

Flavonoids, as a common component of daily nutrition, are a possible source of interference with absorption processes, due to modulation of transporting proteins. In this study, the influence of selected flavonoids (quercetin, isoquercitrin, spiraeoside, rutin, kaempferol, naringenin, naringin, and kaempferol) on the transport of the P-gp substrate [3H]talinolol across Caco-2 cell monolayers was investigated. To elucidate the mechanism behind the interaction observed in this system the potency of the flavonoids to replace [3H]talinolol from its P-gp binding site as well as their activity to inhibit OCT2-mediated [14C]TEA uptake into LLC-PK(1) cells were measured, as P-gp and OCT have been shown to be present in Caco-2 cells. Six of the investigated flavonoids reduced the secretory flux of talinolol across Caco-2 cells (IC50-values: hesperetin<quercetin<kaempferol<<spiraeoside<isoquercitrin<naringin). But none of the selected flavonoids was able to replace [3H]talinolol from its binding to P-gp. However, the investigated flavonoids did show potency to inhibit OCT-mediated transport (IC50-values: quercetin<kaempferol<<naringenin<isoquercitrin<spiraeoside<<rutin<hesperetin<naringin). The present in vitro results demonstrate that flavonoids bear the ability to interfere with secretory intestinal transport processes. This might be due to an interaction with P-gp, but apparently not via competition at the talinolol binding site of P-gp. Another mode of interaction may be the inhibition of members of the OCT-family, which is located at the basolateral membrane of intestinal epithelial cells.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2004

Colonic metabolism of dietary polyphenols: influence of structure on microbial fermentation products.

The metabolism of chlorogenic acid, naringin, and rutin, representative members of three common families of dietary polyphenols, the hydroxycinnamates, the flavanones, and the flavonols, respectively, was studied in an in vitro mixed culture model of the human colonic microflora. Time- and concentration-dependent degradation of all three compounds was observed, which was associated with the following metabolic events after cleavage of the ester or glycosidic bond: reduction of the aliphatic double bond of the resulting hydroxycinnamate caffeic acid residue; dehydroxylation and ring fission of the heterocyclic C-ring of the resulting deglycosylated flavanone, naringenin, and of the deglycosylated flavonol, quercetin (which differed depending on the substitution). The metabolic events, their sequences, and major phenolic end products, as identified by GC-MS or LC-MS/MS, were elucidated from the structural characteristics of the investigated compounds. The major phenolic end products identified were 3-(3-hydroxyphenyl)-propionic acid for chlorogenic acid, 3-(4-hydroxyphenyl)-propionic acid and 3-phenylpropionic acid for naringin, and 3-hydroxyphenylacetic acid and 3-(3-hydroxyphenyl)-propionic acid for rutin. The degree of degradation of the compounds studied was significantly influenced by the substrate concentration as well as individual variations in the composition of the fecal flora. The results support extensive metabolism of dietary polyphenols in the colon, depending on substrate concentration and residence time, with resultant formation of simple phenolics, which can be considered biomarkers of colonic metabolism if subsequently absorbed. It is also apparent that a relatively small number of phenolic degradation products are formed in the colon from the diverse group of natural polyphenols.

Chromatography, High Pressure Liquid↗

PubMed2006

Acute and chronic toxicological studies of Dimorphandra mollis in experimental animals.

Dimorphandra mollis Benth. (Caesalpiniaceae), known as "faveira" or "fava d'anta" is a common plant in central Brazilian cerrado that is used mainly as a vasoprotector. Its main marker is rutin. The present study aimed to evaluate the security of Dimorphandra mollis dry extract in rodents. The extract presented a rutin content of 76+/-3%. Acute and chronic (180 days) toxicity was evaluated after per os administration. In acute toxicity, 3500 and 5000 mg/kg doses presented reversible effects. In chronic toxicity, 1000 and 2000 mg/kg doses did not provoke significant changes in body weight of the animals and in water and food consumption. Behavioral reversible changes and in blood count parameters (hemoglobin, hematocrit and red cells decrease and platelets increase in male in rats) were observed only in 2000 mg/kg dose. In biochemical evaluation, the results varied a lot considering doses and sex, without a linear profile. Some parameters showed a significant difference but without a clinical correlation. In histopathological examination, lung hemorrhage was observed in 2000 mg/kg dose. In conclusion, the study suggest that the extract is safe in a 1000 mg/kg dose, whereas for 2000 mg/kg dose further studies are needed. In long-term use, caution is required.

Animals↗

PubMed2006

In vivo anti-inflammatory and anti-nociceptive activities of Cheilanthes farinosa.

In Ethiopia inflammatory skin diseases are among the most common health problems treated with traditional remedies which mainly comprise medicinal plants. In the present work, the anti-inflammatory and anti-nociceptive activities of Cheilanthes farinosa (Forsk.) Kaulf (Adianthaceae), a fern used in many parts of Ethiopia to treat inflammatory skin disorders, were studied using in vivo models of inflammation and pain. The results of the study showed that the fronds Cheilanthes farinosa possess strong anti-inflammatory and anti-nociceptive properties. It was further demonstrated that the active ingredients of the fern reside mainly in the methanol fraction from which three compounds viz. the flavonol glycoside rutin, and the natural cinnamic acids, caffeic acid and its quinic acid derivative chlorogenic acid have been isolated. The methanol extract was also shown to potentiate the anti-inflammatory activity of acetyl salicylic acid. At the tested concentrations, the methanol extract displayed a better anti-nociceptive activity than that of ASA in both the early and late phases of formalin induced nociception in mice. However, the activity of the extract was more pronounced in the late phase, which is commonly associated with inflammatory pain. Evaluation of the pharmacological properties of the compounds isolated from the active fractions pointed out that chlorogenic acid possesses strong anti-inflammatory and anti-nociceptive activities while caffeic acid and rutin were inactive. Moreover, on molar basis chlorogenic acid was proved to be superior in its anti-inflammatory action to acetyl salicylic acid. It was therefore concluded that chlorogenic acid contributes, in full or in part, to the anti-inflammatory and anti-nociceptive activities of Cheilanthes farinosa. Both the methanolic extract and pure chlorogenic acid failed to display anti-nociceptive activity when tested by the tail-flick test indicating that the plant is not a centrally acting analgesic but instead exerts its analgesic activity by way of its antinflammtory action.

Administration, Oral↗

PubMed2005

Quercetin decreases the expression of ErbB2 and ErbB3 proteins in HT-29 human colon cancer cells.

Quercetin has chemoprotective properties in experimental colon cancer models, and in vitro studies have demonstrated that quercetin inhibits HT-29 colon cancer cell growth. ErbB2 and ErbB3 receptor tyrosine kinases have been associated with the development of human colon cancer, and the expressions of both receptors are high in HT-29 cells. In this study, we assessed quercetin regulation of HT-29 and SW480 cell apoptosis and the influence of quercetin on the protein expression of ErbB2, ErbB3, Akt, Bax and Bcl-2. We cultured HT-29 cells in the presence of various concentrations (0, 25, 50, or 100 micromol/L) of quercetin or rutin. Quercetin inhibited HT-29 cell growth in a dose-dependent manner, whereas rutin had no effect on the cell growth. DNA that was isolated from cells treated with 50 micromol/L of quercetin exhibited an oliogonucleosomal laddering pattern characteristic of apoptotic cell death. Western blot analysis of cell lysates revealed that Bcl-2 levels decreased dose-dependently in cells treated with quercetin, but Bax remained unchanged. Quercetin increased levels of cleaved caspase-3 and the 89-kDa fragment of poly (ADP-ribose) polymerase. In addition, phosphorylated Akt levels were markedly lower in cells treated with 25 micromol/L quercetin, but total Akt levels decreased only at 100 micromol/L quercetin. Furthermore, a dose-dependent decrease in ErbB2 and ErbB3 levels was detected in quercetin-treated cells. The results obtained using SW480 cells were similar to those obtained with HT-29 cells. In conclusion, we have shown that quercetin inhibits cell growth and induces apoptosis in colon cancer cells, and that this may be mediated by its ability to down-regulate ErbB2/ErbB3 signaling and the Akt pathway.

Apoptosis↗

PubMed2004

The protozoan Tetrahymena as a bioindicator to screen bioactive substances.

Tetrahymena thermophila has been used as a "swimming receptor" to study its chemotaxis in the presence of various bioactive substances from herbal plants. Chemotaxis of this ciliated protozoan is, in part, controlled by a cyclic GMP-dependent protein kinase (PKG), which can adjust ciliary beating. In this paper, the effects of Ginkgo biloba extract (GBE) and its main functional constituents, terpene lactones, flavonol glycosides and aglycones, on the chemotaxis and PKG activity of ciliates, were systematically investigated. GBE and its constituents exerted significant inhibition of chemotaxis and PKG activity in cells of T. thermophila. The minimal concentrations to completely inhibit chemotaxis of T. thermophila were 12, 25, 50, 100, 300, 400, 400, 500 microM, 2 mg/ml for isorhamnetin, kaempferol, quercetin, myricetin, isoquercitrin, quercetin-3-beta-d-galactoside, rutin, quercitrin, and GBE, respectively. The IC(50) values for PKG were 14, 17, 20, 25, 186, 78 microM, 0.157 mg/ml for isorhamnetin, kaempferol, quercetin, myricetin, isoquercitrin, rutin and GBE, respectively. The results indicate that the chemotaxis inhibition by GBE and its constituents and their effects on PKG are similar. This suggests that T. thermophila may be a potential experimental organism for screening other bioactive substances.

Animals↗

PubMed2005

Inhibition of human cytochrome CYP 1 enzymes by flavonoids of St. John's wort.

CYP 1B1 is involved in metabolizing both polycyclic aromatic hydrocarbons and estradiol to potentially carcinogenic intermediates, and it is also over-expressed in human cancer cells. In order to investigate whether flavonoids could specifically inhibit CYP 1B1, seven flavonoids in St. John's wort and apigenin were screened for their inhibition of recombinant human CYP 1B1 and CYP 1A1. While seven flavonoids (myricetin, apigenin, kaempferol, quercetin, amentoflavone, quercitrin and rutin) were slightly more selective for CYP 1B1 EROD inhibition (K(i)s 0.06-5.96 microM) compared to CYP 1A1 (K(i)s 0.20-1.6 microM) the difference in K(i)s for the P450s were not significantly different. Rutin did not inhibit CYP 1A1 at concentrations up to 10 microM. Kinetic analyses determined that apigenin and amentoflavone were competitive inhibitors of CYP 1B1, while quercetin showed mixed type inhibition. To characterize the inhibition potential of these flavonoids, five were studied further for their ability to inhibit TCDD-induced EROD activity in 22Rv1 human prostate cancer cells. 22Rv1 cells express constitutive and TCDD-inducible CYP 1A1 and CYP 1B1 mRNA. In the cells, the IC(50)s were similar to those measured for the recombinant CYP 1A1 except for amentoflavone. Quercetin (IC(50): 4.1 microM), kaempferol (3.8 microM), myricetin (3.0 microM) and apigenin (3.1 microM) caused significant inhibition of EROD activity whereas amentoflavone did not cause inhibition. Depending on their bioavailability, flavonoids that can selectively inhibit CYP1 enzymes may be useful as chemoprotective agents in prostate cancer prevention.

Aryl Hydrocarbon Hydroxylases↗

PubMed1999

Determination of polyphenols by high-performance liquid chromatography with inhibited chemiluminescence detection.

A chemiluminescence reaction detector was developed for the detection of polyphenols separated by HPLC based on the inhibition of chemiluminescence from the luminol-potassium hexacyanoferrate(III) reaction by polyphenols. The separation was carried out on a RP-C18 column at 37 degrees C by using stepwise gradient elutions. The detection limits are in the range of 6.8 x 10(-7)-2.0 x 10(-9) g/ml for catechol, protocatechuic acid, chlorogenic acid, rutin, resorcinol, hydroquinone and p-tert.butylpyrocatechol. The method is sensitive, selective, fast and simple. It has been successfully applied to the determination of chlorogenic acid and rutin in real tobacco samples.

Chromatography, High Pressure Liquid↗

PubMed2003

Ability of antioxidants to prevent oxidative mutations in Salmonella typhimurium TA102.

An assay for the ability of antioxidants to prevent mutations induced by various oxidants in Salmonella typhimurium TA102 cells was developed. Protection against hydrogen-peroxide-induced mutagenicity was observed for quercetin, caffeic acid, ascorbic acid and dimethyl sulfoxide (used as a solvent for water-insoluble antioxidants). No protective effect was observed for green tea extract (weakly pro-oxidative), catechin, rutin, sinigrin, ferulic acid and alpha-tocopherol. Mutagenicity caused by tert-butyl hydroperoxide (tBOOH) was prevented most effectively by quercetin and ascorbic acid, whereas weaker effects were observed for green tea extract and for rutin, and no effect being observed for the other antioxidants tested. The results for hydrogen peroxide indicate iron chelation to be the most important protective mechanism. Radical scavenging appeared to be effective only with dimethyl sulfoxide and ascorbic acid, which are effective scavengers of hydroxyl radicals and were used here in high concentrations. It is proposed that the hydrogen-peroxide-induced mutations in the Salmonella cells are caused by hydroxyl radicals generated by iron ions closely associated with DNA. Protection against mutagenicity caused by tert-butyl hydroperoxide appears to occur mainly through the scavenging of alkoxyl and possibly of alkyl radicals.

Antimutagenic Agents↗

PubMed1999

Anti-oxidant effect of flavonoids on hemoglobin glycosylation.

A high glucose concentration has been found to lead to the glycosylation of amino groups of lysine residue in proteins. The addition of reducing agent not only prevents this reaction but also reverses it. On the other hand, flavonoids which found in plant sources have antioxidant properties. Since the glycosylation of protein is an oxidation reaction, therefore, antioxidants should be able to prevent this reaction. In this study, the best concentration and time to incubate glucose with hemoglobin was investigated. Then the glycosylation degree of hemoglobin in the presence of flavonoids and their absence was measured by means of a colorimetric method. Different concentration of flavonoids (Quercetin, Rutin, Kaempferol) were used. The preventing effect on hemoglobin glycosylation by the three concentrations; 0.5, 5, 10 micrograms/ml was estimated as follows: for Rutin; 11%, 27%, 42%, Quercetin; 3%, 37%, 52%, Kaempferol; 10%, 12%, 15% respectively. So, the in vivo effect should be investigated and then plants that containing flavonoids can be utilized to prevent or treat complication of diabetes.

Antioxidants↗

PubMed2001

Degradation of natural polyphenols by methanogenic consortia enriched from digested municipal sludge.

Using digested municipal sludge as the inoculum and either rutin, quercetin or hesperidin as the sole external carbon source. methanogenic consortia were enriched which converted various flavonoids at initial concentration of 0.5 3.0mM during stationary incubation at 37 degrees C in serum bottles with specific rates ranging from 0.025 to 0.073 micromol min(-1) (mg protein)(-1). In the culture fluid, several hydroxyaromatic metabolites as well as VFA (acetate, propionate, n-butyrate) were detected and biogas was formed in the headspace of the test bottles. Most of these metabolites were identified. Based on their sequential appearance/disappearance in the test cultures it was concluded that following initial hydrolysis of the glycosidic bond by cellular enzymes, ring C of the flavane skeleton was hydrolytically cleaved yielding an A- and B-ring fission product. In case of the flavonol quercetin, phloroglucinol (A-ring) and 3,4-dihydroxyphenylacetate (B-ring) were identified as the fission products whereas the flavanone hesperetin was cleaved with formation of phloroglucinol (A-ring) and 3,4-dihydroxyphenylpropionate (B-ring). In pre-adapted subcultures amended with either hesperidin or hesperetin, all of the formed hydroxyaromatic metabolites disappeared within 100 h of incubation whereas in the culture medium of rutin and quercetin degrading consortia m-cresol (3-methylphenol) was formed as the ultimate hydroxyaromatic metabolite being detectable in considerable amounts even after prolonged incubation.

Acetates↗

PubMedDate not supplied

Phenolics: blocking agents for heterocyclic amine-induced carcinogenesis.

Chemopreventive effects of synthetic and naturally occurring antioxidants on heterocyclic amine (HCA)-induced rat carcinogenesis and mechanisms of inhibition were assessed. In a medium-term liver bioassay, combined treatment with 0.03% 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) and synthetic antioxidants such as 1-O-hexyl-2,3,5-trimethylhydroquinone (HTHQ), butylated hydroxyanisole (BHA), butylated hydroxutoluene (BHT), tert-butylhydroquinone (TBHQ) or propyl gallate, each at a dose of 0.25%, inhibited development of preneoplastic glutathione S-transferase placental form (GST-P) positive foci as compared with MeIQx alone, after initiation with diethylnitrosamine (DEN). Of these antioxidants, HTHQ showed the greatest activity. 8-Hydroxydeoxyguanosine (8-OHdG), a marker for DNA damage induced by active oxygen species, and malonedialdehyde and 4-hydroxynonenal levels were not largely influenced by the treatment with MeIQx or antioxidants, either alone or in combination. In the same medium-term liver bioassay, effects of some naturally occurring antioxidants, such as green tea catechins (GTC), hesperidin, chlorogenic acid, quercetin, rutin, curcumin, daidzin, ferulic acid and genistein were also examined. Of these antioxidants, only GTC tended to inhibit GST-P positive foci development, while quercetin, rutin, curcumin, daidzin, ferulic acid and genistein all exerted significant enhancing effects. Examination of HTHQ influence in a medium term liver bioassay with HCA Glu-P-1, in which the experimental period was extended for up to 26 weeks, also demonstrated a significant decrease in the incidence of liver tumours to 40% in the group treated with 0.5% HTHQ and 0.03% 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1) as compared with the Glu-P-1 alone value of 89%. Effects of HTHQ on colon carcinogenesis induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) were evaluated in a two-stage colon carcinogenesis model using 1,2-dimethylhydrazine (DMH) as an initiator. At week 36, the multiplicity of colon tumours induced by 0.02% PhIP after DMH initiation (9.1+/-6.2/rat) was dose-dependently decreased by the combined treatment with 0.5% HTHQ (3.6+/-1.8, P < 0.001) and 0.125% HTHQ (6.2+/-3.2, not significant). Similarly, the incidence of mammary carcinomas in female F344 rats induced by oral administration of 0.02% PhIP (40%) for 52 weeks was significantly decreased by simultaneous treatment with 0.5% HTHQ (5%). Alpha-tocopherol and chlorophyllin only reduced the multiplicity of carcinomas. Analysis of the influence of HTHQ on metabolic activation of Glu-P-1 or PhIP after incubation with rat S9 mixture and NADPH by HPLC, revealed that each major metabolite was strongly reduced by the addition of HTHQ. Immunohistochemically detected PhIP-DNA adduct positive nuclei in the colon induced by continuous oral treatment with 0.02% PhIP for 2 weeks decreased by the combined treatment with 0.5 or 0.125% HTHQ. These results indicate that synthetic antioxidant HTHQ is a very strong chemopreventor of heterocyclic amine (HCA)-induced carcinogenesis and that depressed metabolic activation rather than antioxidant activity is responsible for the observed effect.

Animals↗