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PubMed2006

Immunomodulating effects of flavonoids on acute and chronic inflammatory responses caused by tumor necrosis factor alpha.

Flavonoids have beneficial activities which modulate oxidative stress, allergy, tumor growth and viral infection, and which stimulate apoptosis of tumor cells. In addition to these activities, dietary flavonoids are able to regulate acute and chronic inflammatory responses. Here we describe new aspects of regulatory mechanisms by which flavonoids suppress production of tumor necrosis factor-alpha (TNF-alpha) by macrophages, microglial cells and mast cells stimulated with lipopolysaccharide (LPS) and others via toll-like receptors (TLRs), and TNF-alpha-mediated acute and chronic inflammatory responses. Treatment with flavonoids such as luteolin, apigenin, quercetin, genistein, (-)-epigallocatechin gallate, and anthocyanidin resulted in significant downregulation of LPS-elicited TNF-alpha and nitric oxide (NO) production and diminished lethal shock. In chronic diseases, pathogenesis of collagen-induced arthritis (CIA), a mouse model of rheumatoid arthritis which is triggered by TNF-alpha, was improved by the oral administration of flavonoids after the onset of CIA. Here, we discuss that inhibitory effects of flavonoids on acute and chronic inflammation are due to regulation of signaling pathways, including the nuclear factor kappaB (NF-kappaB) activation and mitogen-activated protein (MAP) kinase family phosphorylation. FcetaRI expression by NF-kappaB activation was also reduced by flavonoids; while accumulation of lipid rafts, which is the critical step for signaling, was blocked by flavonoids. The intake of dietary flavonoids reduces acute and chronic inflammation due to blocking receptor accumulation and signaling cascades, and would assist individuals at high-risk from life-style related diseases.

Animals↗
PubMedDate not supplied

[Flavonoids: antithrombotic agents or nutrients?].

Flavonoids are a vast group of natural substances, but their pharmacological properties have not all been explored. The term flavonoid is used at large to designate a series of more than 4,000 molecules, which in fact can have very heterogenous molecular structures. We have shown that some flavonoids are good inhibitors of cyclic nucleotide phosphodiesterase (PDE). The most active PDE inhibitors among the flavonoids were also good inhibitors of the aggregation of human platelets in vitro. This suggests that flavonoids could serve as a template for the development of new anti-platelet drugs. However, a direct extrapolation of our experimental results to possible therapeutical use of flavonoid-containing medicinal plant extracts is not possible. The metabolic fate of these plant flavonoids is poorly understood, and their absence of toxicity has not always been clearly demonstrated. Flavonoids are also present in a regular diet in significant amounts. The role of these dietary flavonoids in the prevention of thrombotic diseases or atherosclerosis should also be investigated.

Fibrinolytic Agents↗
PubMed2026

Progressive salinity drives flavonoid branch reprogramming in Anoectochilus roxburghii.

Flavonoids play critical roles in plant adaptation to abiotic stress; however, how salt stress modulates metabolic flux distribution within flavonoid branches remains poorly understood, particularly in non-model medicinal plants. Here, we integrated targeted metabolomics, transcriptomics, and proteomics to examine flavonoid regulation in Anoectochilus roxburghii under 0, 50, 100, and 200 mmol·L- 1 NaCl. Metabolite profiling showed that salinity reshaped flavonoid composition rather than uniformly increasing flavonoid abundance. A metabolite-derived branch bias index (MI), representing the balance between reductive branch metabolites and flavonol products, increased under salt treatment, peaked at 100 mmol·L- 1 NaCl, and declined at 200 mmol·L- 1, indicating maximal branch bias under moderate stress followed by partial rebalancing under severe stress. Transcriptomic analysis showed induction of upstream phenylpropanoid and flavonoid entry genes, including PAL, 4CL, and CHS, whereas F3H was suppressed and FLS showed no induction. Furthermore, several short-chain dehydrogenase/reductase homologs (IFR-like SDR homologs) were upregulated, and the transcript-derived reductive branch index (EI) increased progressively across the salt gradient. EI was positively associated with MI, although the relationship was not strictly proportional under severe stress (200 mmol·L- 1 NaCl). Proteomic profiling further provided supportive evidence for sustained activation of upstream flavonoid biosynthesis, such as salt-induced accumulation of chalcone synthase (CHS) protein, complementing the transcriptomic and metabolomic datasets. Together, these results indicate that salt stress reorganizes flavonoid metabolism in A. roxburghii through persistent upstream activation and branch-specific regulation, favoring the reductive branch under moderate salinity.

Orchidaceae↗
PubMed1999

Distribution pattern of a flavonoid extract in the gastrointestinal lumen and wall of rats.

Purified flavonoid extract from illuminated parsley (Petroselinum crispum (Mill.) Nym.) cell culture was administered by gavage to Wistar rats. The dose corresponded to 6.9 mg flavonoids on aglycone base/kg body mass. Segments of the gastrointestinal wall from stomach to colon, their luminal contents, and liver and kidneys were collected at time intervals between 1 and 12 h and investigated by HPLC of the respective extracts for flavonoids. The spreading of the flavonoids was accompanied by partial deglycosylation that began already in the stomach where at first quercetin and later apigenin, chrysoeriol and isorhamnetin aglycones were detected. We got evidence of flavonoid absorption by the stomach that does not require the liberation of aglycones. Due to obvious differences in metabolization and absorption rates the composition and the content of flavonoids changes in the gastrointestinal segments and their contents with time. Flavonoids could be detected neither within the gastrointestinal lumen after 12 h nor in the kidneys at any time. But traces of flavonoids were found in the livers at 1.5 and 12 h.

Animals↗
PubMed2003

Flavonoids and thyroid disease.

UNLABELLED: The most potent natural plant-derived compounds that can affect thyroid function, thyroid hormone secretion and availability to tissues is the group of flavonoids, i.e. plant pigments. They are present in our daily food, such as vegetables, fruits, grains, nuts, wine, and tea. Epidemiological studies suggest beneficial effects on health of flavonoids, which are commonly attributed to their activity as antioxidants. Experimental studies in vitro, however, showed inhibition of organification in thyroid cells and follicles by several flavonoids. Studies in vivo and vitro with synthetic and natural flavonoids showed displacement of T4 from transthyretin leading to disturbances in thyroid hormone availability in tissues. Radioactive labeled flavonoids appeared to be eliminated rapidly from the body mainly through excretion in the feces. In pregnant rats synthetic flavonoids cross the placenta and accumulate in the fetal compartment, including the fetal brain. Therefore, a high intake of flavonoids is contraindicated. IN CONCLUSION: flavonoids show strong interference with many aspects of thyroid hormone synthesis and availability.

Animals↗
PubMed2001

Influence of metal ions on flavonoid protection against asbestos-induced cell injury.

Influence of metal ions (Fe2+, Fe3+, Cu2+, Zn2+) on the protective effect of rutin, dihydroquercetin, and green tea epicatechins against in vitro asbestos-induced cell injury was studied. Metals have been found to increase the capacity of rutin and dihydroquercetin to protect peritoneal macrophages against chrysotile asbestos-induced injury. The data presented here show that this effect is due to the formation of flavonoid metal complexes, which turned out to be more effective radical scavengers than uncomplexed flavonoids. At the same time epicatechins and their metal complexes have similar antiradical properties and protective capacities against the asbestos induced injury of macrophages. Metal complexes of all flavonoids were found to be considerably more potent than parent flavonoids in protecting red blood cells against asbestos-induced injury. It was also found that the metal complexes of all flavonoids were absorbed by chrysotile asbestos fibers considerably better than uncomplexed compounds and probably for this reason flavonoid metal complexes have better protective properties against asbestos induced hemolysis. Thus, the results of the present study show that flavonoid metal complexes may be effective therapy for the inflammatory response associated with the inhalation of asbestos fiber. The advantage of their application could be the strong increase in ROS scavenging by flavonoids and finally a better cell protection under the conditions of cellular oxidative stress.

Adsorption↗
PubMed1995

Heterogenous effects of natural flavonoids on monooxygenase activities in human and rat liver microsomes.

The in vitro effects of nine flavonoids on different monooxygenase activities from human and rat liver were investigated. Flavonoids belonging to different chemical classes [flavones (chrysin, tangeretin, flavone, 5,6-benzoflavone, 7,8-benzoflavone), flavonols (quercetin), and flavanones (pinocembrin, eriodictyol, flavanone)] were chosen. Ethoxyresorufin O-deethylase (EROD) and benzyloxyresorufin O-debenzylase (BROD) were selected as marker activities of P450 isoenzymes involved in carcinogen activation. Human EROD activity was inhibited by all flavonoids. Flavonoids without hydroxyl groups were more effective than those with hydroxyl groups. Flavonoids with an unsaturated flavone nucleus were more inhibitory than the corresponding saturated analogues. Similar structure-activity relationships were found in microsomes from methylcholanthrene-treated rats. The effects of flavonoids on human BROD activity were quite different from those observed on EROD activity. Nonhydroxylated flavones were effective activators. Hydroxylated flavonoids showed a biphasic effect, being activators at low concentrations and inhibitors at higher concentrations. The effects of flavonoids on BROD activity were rather similar in man and control rats.

Adult↗
PubMed1998

Dietary flavonoids interact with trace metals and affect metallothionein level in human intestinal cells.

Flavonoids are natural compounds found in food items of plant origin. The study examined systematically the interaction of structurally diverse dietary flavonoids with trace metal ions and the potential impact of dietary flavonoids on the function of intestinal cells. Spectrum analysis was first performed to determine flavonoid-metal interaction in the buffer. Among the flavonoids tested, genistein, biochanin-A, naringin, and naringenin did not interact with any metal ions tested. Members of the flavonol family, quercetin, rutin, kaempferol, flavanol, and catechin, were found to interact with Cu(II) and Fe(III). On prolonged exposure, quercetin also interacted with Mn(II). Quercetin at 1:1 ratio to Cu(II) completely blocked the Cu-dependent color formation from hematoxylin. When quercetin was added to the growth medium of cultured human intestinal cells, Caco-2, the level of metal binding antioxidant protein, metallothionein, decreased. The effect of quercetin on metallothionein was dose- and time-dependent. Genistein and biochanin A, on the contrary, increased the level of metallothionein. The interaction between dietary flavonoids and trace minerals and the effect of flavonoids on metallothionein level imply that flavonoids may affect metal homeostasis and cellular oxidative status in a structure-specific fashion.

Cadmium↗
PubMed2006

Modulation of activator protein-1 (AP-1) and MAPK pathway by flavonoids in human prostate cancer PC3 cells.

In last couple of decades the use of natural compounds like flavonoids as chemopreventive agents has gained much attention. Our current study focuses on identifying chemopreventive flavonoids and their mechanism of action on human prostate cancer cells. Human prostate cancer cells (PC3), stably transfected with activator protein 1 (AP-1) luciferase reporter gene were treated with four main classes of flavonoids namely flavonols, flavones, flavonones, and isoflavones. The maximum AP-1 luciferase induction of about 3 fold over control was observed with 20 microM concentrations of quercetin, chrysin and genistein and 50 microM concentration of kaempferol. At higher concentrations, most of the flavonoids demonstrated inhibition of AP-1 activity. The MTS assay for cell viability at 24 h showed that even at a very high concentration (500 microM), cell death was minimal for most of the flavonoids. To determine the role of MAPK pathway in the induction of AP-1 by flavonoids, Western blot of phospho MAPK proteins was performed. Four out of the eight flavonoids namely kaempferol, apigenin, genistein and naringenin were used for the Western Blot analysis. Induction of phospho-JNK and phospho-ERK activity was observed after two hour incubation of PC3-AP1 cells with flavonoids. However no induction of phospho-p38 activity was observed. Furthermore, pretreating the cells with specific inhibitors of JNK reduced the AP-1 luciferase activity that was induced by genistein while pretreatment with MEK inhibitor reduced the AP-1 luciferase activity induced by kaempferol. The pharmacological inhibitors did not affect the AP-1 luciferase activity induced by apigenin and naringenin. These results suggest the possible involvement of JNK pathway in genistein induced AP-1 activity while the ERK pathway seems to play an important role in kaempferol induced AP-1 activity.

Anticarcinogenic Agents↗
PubMed2004

Modulation of suppressive activity of lipopolysaccharide-induced nitric oxide production by glycosidation of flavonoids.

Flavonoids have been demonstrated to exhibit a wide range of biological activities including anti-inflammatory and neuroprotective actions. Although a significant amount of flavonoids has been identified to be present as glycosides in medicinal plants, determinations of the biological activities of flavonoids were mainly carried out with aglycones of flavonoids. Therefore, the exact role of the glycosidation of flavonoid aglycones needs to be established. In an attempt to understand the possible role of glycosidation on the modulation of the biological activities of flavonoids, diverse glycosides of kaempferol, quercetin, and aromadendrin were examined in terms of their anti-inflammatory activity determined with the suppression of lipopolysaccharide (LPS)-induced nitric oxide (NO) production in BV2 microglial cells. The results indicated that glycosidation of aglycones attenuated the suppressive activity of aglycones on LPS-induced NO production. Although attenuated, some of glycosides, depending on the position and degree of glycosidation, maintained the inhibitory capability of LPS-induced NO production. These findings suggest that glycosidation of flavonoid aglycones should be considered as an important modulator of the biological activities of flavonoids.

Animals↗
PubMed1999

Comparative analysis of the effects of flavonoids on proliferation, cytotoxicity, and apoptosis in human colon cancer cell lines.

Flavonoids are polyphenolic compounds that occur ubiquitously in foods of plant origin. Their proposed protective role in tumor development may prevail especially in the intestinal tract due to direct exposure of intestinal epithelia to these dietary ingredients. We have screened more than 30 flavonoids for their effects on cell proliferation and potential cytotoxicity in the human colon cancer cell lines Caco-2, displaying features of small intestinal epithelial cells, and HT-29, resembling colonic crypt cells. In addition, for selected compounds we assessed whether they induce apoptosis by determining caspase-3 activation. Studies on the dose dependent effects of the flavonoids showed antiproliferative activity of all compounds with EC50 values ranging between 39.7 +/- 2.3 microM (baicalein) and 203.6 +/- 15.5 microM (diosmin). In almost all cases, growth inhibition by the flavonoids occurred in the absence of cytotoxicity. There was no obvious structure-activity relationship in the antiproliferative effects either on basis of the subclasses (i.e., isoflavones, flavones, flavonols, flavonones) or with respect to kind or position of substituents within a class. In a subset of experiments we examined the antiproliferative activities of the most potent compound of each flavonoid subgroup in addition in LLC-PK1, a renal tubular cell line, and the human breast cancer cell line MCF-7. Out of four flavonols tested, three displayed almost equal antiproliferative activities in all cell lines but fisetin was less potent in MCF-7 cells. The flavanones bavachinin and flavanone inhibited growth of Caco-2 and HT-29 cells with lower EC50 values than that obtained in LLC-PK1 and MCF-7 cells. The lower susceptibility of LLC-PK1 and MCF-7 cells towards growth arrest was even more pronounced in the case of the flavone baicalein. Half maximal growth-inhibition in LLC-PK1 and MCF-7 required 2.5 and 6.6 fold higher concentrations than that needed in the intestinal cell lines. The flavonoids failed to affect apoptosis in LLC-PK1 and MCF-7, whereas baicalein and myricetin were able to induce apoptosis in HT-29 and Caco-2 cells. In conclusion, flavonoids of the flavone, flavonol, flavanone, and isoflavone classes possess antiproliferative effects in different cancer cell lines. The capability of flavonoids for growth inhibition and induction of apoptosis can not be predicted on the basis of their chemical composition and structure.

Apoptosis↗
PubMed1993

Dietary antioxidant flavonoids and risk of coronary heart disease: the Zutphen Elderly Study.

Flavonoids are polyphenolic antioxidants naturally present in vegetables, fruits, and beverages such as tea and wine. In vitro, flavonoids inhibit oxidation of low-density lipoprotein and reduce thrombotic tendency, but their effects on atherosclerotic complications in human beings are unknown. We measured the content in various foods of the flavonoids quercetin, kaempferol, myricetin, apigenin, and luteolin. We then assessed the flavonoid intake of 805 men aged 65-84 years in 1985 by a cross-check dietary history; the men were then followed up for 5 years. Mean baseline flavonoid intake was 25.9 mg daily. The major sources of intake were tea (61%), onions (13%), and apples (10%). Between 1985 and 1990, 43 men died of coronary heart disease. Fatal or non-fatal myocardial infarction occurred in 38 of 693 men with no history of myocardial infarction at baseline. Flavonoid intake (analysed in tertiles) was significantly inversely associated with mortality from coronary heart disease (p for trend = 0.015) and showed an inverse relation with incidence of myocardial infarction, which was of borderline significance (p for trend = 0.08). The relative risk of coronary heart disease mortality in the highest versus the lowest tertile of flavonoid intake was 0.42 (95% CI 0.20-0.88). After adjustment for age, body-mass index, smoking, serum total and high-density-lipoprotein cholesterol, blood pressure, physical activity, coffee consumption, and intake of energy, vitamin C, vitamin E, beta-carotene, and dietary fibre, the risk was still significant (0.32 [0.15-0.71]). Intakes of tea, onions, and apples were also inversely related to coronary heart disease mortality, but these associations were weaker. Flavonoids in regularly consumed foods may reduce the risk of death from coronary heart disease in elderly men.

Aged↗
PubMed1984

Comparison of the effects of quercetin with those of other flavonoids on the generation and effector function of cytotoxic T lymphocytes.

In previous studies (Schwartz et al., 1982) we showed that the naturally occurring plant flavonoid quercetin can inhibit both the in vitro generation and effector function of alloantigen specific cytotoxic T lymphocytes (CTL). In the present studies, several additional flavonoids of different chemical classes were tested similarly to determine whether structure-function relationships exist. We have found that some other flavonoids, e.g. apigenin , fisetin , hesperetin and chalcone also can inhibit both CTL generation and effector function, with the effective concentration varying with the specific flavonoid tested. On the other hand, flavonoids such as rutin, naringin and catechin were inactive in both systems. Taxifolin ( dihydroquercetin ) differed from all the other flavonoids in that it was a relatively active inhibitor of CTL generation, but was essentially unable to inhibit CTL effector function. The presence of a double bond at position C-2-3 in the flavone and flavonol aglycones, a keto group at C-4, B ring hydroxylation and/or a free hydroxyl group at C-3 may be associated with activity. We also show that the effects of some, but not all, of the flavonoids active in our systems can be blocked by Cu2+ ions. Therefore, chelation of divalent cations such as Cu2+ cannot explain the function of all flavonoids in these systems.

Animals↗
PubMed2006

Flavonoids suppresses the enhancing effect of beta-carotene on DNA damage induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in A549 cells.

This study investigated the individual and combined effects of beta-carotene with a common flavonoid (naringin, quercetin or rutin) on DNA damage induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a potent tobacco-related carcinogen in human. A human lung cancer cell line, A549, was pre-incubated with beta-carotene, a flavonoid, or both for 1h followed by incubation with NNK for 4 h. Then, we determined DNA strand breaks and the level of 7-methylguanine (7-mGua), a product of NNK metabolism by cytochrome P450 (CYP). We showed that beta-carotene at 20 microM significantly enhanced NNK-induced DNA strand breaks and 7-mGua levels by 90% (p < 0.05) and 70% (p < 0.05), respectively, and that the effect of beta-carotene was associated with an increased metabolism of NNK by CYP because the concomitant addition of 1-aminobenzotriazole, a CYP inhibitor, with beta-carotene to cells strongly inhibited NNK-induced DNA strand breaks. In contrast to beta-carotene, incubation of cells with naringin, quercetin or rutin added at 23 microM led to significant inhibition of NNK-induced DNA strand breaks, and the effect was in the order of quercetin > naringin > rutin. However, these flavonoids did not significantly affect the level of 7-mGua induced by NNK. Co-incubation of beta-carotene with any of these flavonoids significantly inhibited the enhancing effect of beta-carotene on NNK-induced DNA strand breaks; the effects of flavonoids were dose-dependent and were also in the order of quercetin > naringin > rutin. Co-incubation of beta-carotene with any of these flavonoids also significantly inhibited the loss of beta-carotene incorporated into the cells, and the effects of the flavonoids were also in the order of quercetin > naringin > rutin. The protective effects of these flavonoids may be attributed to their antioxidant activities because they significantly decreased intracellular ROS, and the effects were also in the order of quercetin > naringin > rutin. These in vitro results suggest that a combination of beta-carotene with naringin, rutin, or quercetin may increase the safety of beta-carotene.

DNA Damage↗
PubMed2005

Quantitative determination of the group of flavonoids and saponins from the extracts of the seeds of Glinus lotoides and tablet formulation thereof by high-performance liquid chromatography.

The total flavonoids and saponins of the seeds of Glinus lotoides in the crude extracts and tablet formulation thereof were quantified by reversed-phase high-performance liquid chromatographic (RP-HPLC) methods with UV detection. The saponins were analyzed after acid hydrolysis in 3 M HCI at 100 degrees C for 1 h. Vicenin-2 and mollugogenol B were isolated and used as reference substances for the quantification of total flavonoids and saponins, respectively. The identity and purity (> 97%) of the standards were confirmed by spectroscopic (UV, MS, and NMR) and chromatographic (HPLC) methods. The flavonoids and saponins of the crude extract of the seeds and tablet formulation were separated by RP-HPLC (Nucleosil RP-18 column, 250 mm x 4.6 mm) using linear gradient elution systems of acetonitrile-water-0.1 M H3PO4 for flavonoids and methanol-water for saponins. Satisfactory separation of the compounds was obtained in less than 30 and 25 min, for the flavonoids and saponins, respectively. The methods were validated for linearity, repeatability, limits of detection (LOD) and limits of quantification (LOQ). Repeatability (inter- and intra-day, n = 6 and 9, respectively) showed less than 2% relative standard deviation (RSD). The LOD and LOQ were found to be 0.075 and 0.225 mg/mL, respectively, for vicenin-2 and 0.027 and 0.082 mg/100 mL, respectively, for mollugogenol B. The content of flavonoids and saponins of six single tablets was between 95 and 103% for flavonoids and 94-98% for saponins. The validated HPLC methods were employed to standardize a fingerprint of a laboratory produced purified extract, which could be used as a secondary standard for the routine quality control. Accordingly, the purified extract was found to contain 21.3% flavonoids (vicenin-2, 10%) and 25.4% saponins (glinuside G, 14.2%).

Apigenin↗
PubMed2005

Protection against nuclear DNA damage offered by flavonoids in cells exposed to hydrogen peroxide: the role of iron chelation.

The ability of a number of flavonoids belonging to the flavone, flavonol, flavanone, and flavan-3-ol subclasses to protect cellular DNA from H2O2-induced single-strand breaks and the underlying molecular mechanisms were investigated in this work. Formation of single-strand breaks on nuclear DNA, after exposure of Jurkat cells to continuously generated H2O2 in the presence or absence of the flavonoid compounds, was evaluated by the comet assay (single-cell gel electrophoresis). The results indicate the following structural requirements of flavonoids for effective DNA protection: (a) the ortho-dihydroxy structure in either ring A or ring B, (b) the hydroxyl moiety on position 3 in combination with the oxo group at position 4, and (c) the presence of a C2, C3 double bond in ring C. In contrast to free flavonoids, the ability of complexes of [Fe2+]/[flavonoid] to protect nuclear DNA was decreased as the ratio increased, and the complex was completely inactive when the ratio reached a certain value. Moreover, it was observed that several of the flavonoids tested were able to remove iron from calcein loaded into cells and that this property was in excellent correlation with their ability to protect DNA (Spearman's correlation coefficient, rho = 0.9, p = 0.005). The antioxidant (electron donating) capacities of the same flavonoids were also evaluated by a conventional method, but no relation with their DNA-protective ability could be established even when their membrane-penetrating abilities were taken into account (p = 0.64). In conclusion, the results presented in this work strongly support the notion that intracellular binding of iron is responsible for the protection offered by flavonoids against H2O2-induced DNA damage.

Cell Nucleus↗
PubMed2005

Antimicrobial activity of flavonoids.

Flavonoids are ubiquitous in photosynthesising cells and are commonly found in fruit, vegetables, nuts, seeds, stems, flowers, tea, wine, propolis and honey. For centuries, preparations containing these compounds as the principal physiologically active constituents have been used to treat human diseases. Increasingly, this class of natural products is becoming the subject of anti-infective research, and many groups have isolated and identified the structures of flavonoids possessing antifungal, antiviral and antibacterial activity. Moreover, several groups have demonstrated synergy between active flavonoids as well as between flavonoids and existing chemotherapeutics. Reports of activity in the field of antibacterial flavonoid research are widely conflicting, probably owing to inter- and intra-assay variation in susceptibility testing. However, several high-quality investigations have examined the relationship between flavonoid structure and antibacterial activity and these are in close agreement. In addition, numerous research groups have sought to elucidate the antibacterial mechanisms of action of selected flavonoids. The activity of quercetin, for example, has been at least partially attributed to inhibition of DNA gyrase. It has also been proposed that sophoraflavone G and (-)-epigallocatechin gallate inhibit cytoplasmic membrane function, and that licochalcones A and C inhibit energy metabolism. Other flavonoids whose mechanisms of action have been investigated include robinetin, myricetin, apigenin, rutin, galangin, 2,4,2'-trihydroxy-5'-methylchalcone and lonchocarpol A. These compounds represent novel leads, and future studies may allow the development of a pharmacologically acceptable antimicrobial agent or class of agents.

Anti-Bacterial Agents↗
PubMed2005

Arbuscular mycorrhizal colonization of tomato by Gigaspora and Glomus species in the presence of root flavonoids.

The effect of flavonoids isolated from arbuscular mycorrhizal (AM) colonized and noncolonized clover roots on the number of entry points and percentage of root colonization of tomato (Lycopersicum esculentum L.) by Gigaspora rosea, Gi margarita, Glomus mosseae and G. intrarradices symbionts was determined. With fungi of both genera, a correlation between the number of entry points and the percentage of root colonization was found in the presence of some of the tested flavonoids. The flavonoids acacetin and rhamnetin, present in AM clover roots, inhibited the formation of AM penetration structures and the AM colonization of tomato roots, whereas the flavonoid 5,6,7,8,9-hydroxy chalcone, which could not be detected in AM clover root, inhibited both parameters. The flavonoid quercetin, which was present in AM clover roots, stimulated the penetration and root colonization of tomato by Gigaspora. However, the flavonoids 5,6,7,8-hydroxy-4'-methoxy flavone and 3,5,6,7,4'-hydroxy flavone, which was not found in AM clover root, increased the number of entry points and the AM colonization of tomato roots by Gigaspora. These results indicated that flavonoids could be imnplicated in the process of regulation of AM colonization in plant root, but its role is highly complex and depend not only on flavonoids, but also on AM fungal genus or even species.

Flavonoids↗