Myricetin

Last updated
Myricetin
Myricetin.png
Myricetin-3D-balls.png
Names
IUPAC name
3,3′,4′,5,5′,7-Hexahydroxyflavone
Systematic IUPAC name
3,5,7-Trihydroxy-2-(3,4,5-trihydroxyphenyl)-4H-1-benzopyran-4-one
Other names
Cannabiscetin
Myricetol
Myricitin
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
DrugBank
ECHA InfoCard 100.007.695 OOjs UI icon edit-ltr-progressive.svg
EC Number
  • 208-463-2
KEGG
PubChem CID
UNII
  • InChI=1S/C15H10O8/c16-6-3-7(17)11-10(4-6)23-15(14(22)13(11)21)5-1-8(18)12(20)9(19)2-5/h1-4,16-20,22H Yes check.svgY
    Key: IKMDFBPHZNJCSN-UHFFFAOYSA-N Yes check.svgY
  • Oc1cc(O)c2c(=O)c(O)c(oc2c1)c3cc(O)c(O)c(O)c3
Properties
C15H10O8
Molar mass 318.237 g·mol−1
Density 1.912 g/mL
Hazards
GHS labelling:
GHS-pictogram-exclam.svg
Warning
H315, H319, H335
P261, P264, P271, P280, P302+P352, P304+P340, P305+P351+P338, P312, P321, P332+P313, P337+P313, P362, P403+P233, P405, P501
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
X mark.svgN  verify  (what is  Yes check.svgYX mark.svgN ?)

Myricetin is a member of the flavonoid class of polyphenolic compounds, with antioxidant properties. [1] Common dietary sources [2] include vegetables (including tomatoes), fruits (including oranges), nuts, berries, tea, [3] and red wine. [4]

Contents

Myricetin is structurally similar to fisetin, luteolin, and quercetin and is reported to have many of the same functions as these other members of the flavonol class of flavonoids. [3] Reported average intake of myricetin per day varies depending on diet, but has been shown in the Netherlands to average 23 mg/day. [5]

Myricetin is produced from the parent compound taxifolin through the (+)-dihydromyricetin intermediate and can be further processed to form laricitrin and then syringetin, both members of the flavonol class of flavonoids. [6] Dihydromyricetin is frequently sold as a supplement and has controversial function as a partial GABAA receptor potentiator and treatment in Alcohol Use Disorder (AUD). Myricetin can alternatively be produced directly from kaempferol, which is another flavonol. [6]

Sources

FoodsMyricetin

(mg/100g)

carob fiber48 [7]
fennel leaves, raw20 [7]
parsley, fresh15 [7]
goji berry, dried11 [7]
bog blueberry, frozen7 [7]
carob flour7 [7]
cranberry 7 [7]
dock, raw6 [7]
European black currant, raw6 [7]
crowberry 5 [7]
rabbit-eye blueberry, raw5 [7]
sweet potato leaves, raw4 [7]

Oxidative Properties

Antioxidant

Antioxidants are molecules present in fruits and vegetables that have been demonstrated to protect against some forms of cancer and cardiovascular disease. Biomolecules and cell structures can experience oxidative stress due to the presence and activity of reactive oxygen species (ROS). ROS like •OH, •O2−, and H2O2 are produced during cellular metabolism processes (aerobic respiration). ROS can damage lipids, DNA, and proteins.

Gradual but steady accretion of such damage can lead to the development of many diseases and conditions including thrombosis, diabetes, persistent inflammation, cancer, and atherosclerosis. Flavonoids including myricetin are able to scavenge for ROS and can chelate intracellular transition metal ions that ultimately produce ROS. [3]

Myricetin also enhances the effects of other antioxidants. Myricetin can induce the enzyme glutathione S-transferase (GST). GST has been suggested to protect cells against oxidative stress by protecting cells against free-radicals. In vitro studies have shown that myricetin significantly increased GST activity. [3]

Pro-oxidant

Multiple studies have demonstrated that myricetin also has the potential to act as a pro-oxidant due to its tendency to undergo autoxidation depending upon its environment [ citation needed ]. It has been seen that when in the presence of cyanide, autoxidation is favored, resulting in superoxide, a byproduct characteristic of causing cellular damage [ citation needed ]. However, sodium azide, superoxide dismutase, and catalase have been seen to inhibit the autoxidation of myricetin. [1]

Myricetin may also act as a pro-oxidant in its ability to increase the production of hydroxy radicals through reactions with Fe2+ or Fe3+−EDTA and hydrogen peroxide [ citation needed ]. The resulting hydroxy radicals are often linked to DNA degradation, however, there are doubts as to whether or not this damage would be significant when analyzed in vivo since in vitro studies with both bovine and human serum albumin exhibited extensive protection against it. [1]

Myricetin's pro-oxidative capabilities can also be seen in its ability to act as an inhibitory agent against glutathione reductase, which is responsible for regenerating glutathione, a scavenger of free radicals and peroxides. [1]

Potential health effects

Anticarcinogen

Myricetin is also effective in protecting cells from carcinogenic mutation. Myricetin reduces the risk of skin tumorigenicity that is caused by polycyclic aromatic hydrocarbons like benzo(a)pyrene, a highly carcinogenic compound. Myricetin provided protection against the formation of skin tumors in mice models after tumor initiating and tumor promoter agents were applied to the skin. On a more biochemical level, it was shown that topical application of myricetin to mice inhibited the binding of benzo(a)pyrenes to DNA and protein native to epidermal skin cells. [1]

Myricetin also has been shown to inhibit the act of genetic mutation as exhibited by the Ames test. This test showed that myricetin was more effective in preventing mutagenesis initiated by certain carcinogenic polycyclic aromatic hydrocarbons (benzo(a)pyrene, dibenzo(a,h)pyrene, and dibenzo(a,i)pyrene) as compared to others in which it was less effective in preventing against mutagenesis (benzo(a)pyrene 4, 5-oxide and the bay-region diol-epoxides of benzo(a)anthracene, chrysene, and benzo(c)phenathrene). [1] This data shows that myricetin is not unilaterally able to reduce the carcinogenic activity of all polycyclic aromatic hydrocarbons or even the more specific subclass of benzo(a)pyrenes. Myricetin’s exact biochemical activity is still not fully understood. Clearly there is a multifaceted, complex system involved in the anticarcinogenic activity displayed by myricetin that does not apply equally to all carcinogens of the same subfamily.

Mutagen

It has also been shown that myricetin can itself act as an agent of mutagenicity. Myricetin can produce frameshift mutations in the genomes of particular strains of Salmonella typhimurium. [1] In general, biochemical structural studies have shown that flavonoid structures can tautomerize in biological systems to become active mutagens. [1]

Interactions with DNA

Myricetin can act as a pro-oxidant compound when it interacts with DNA. Studies involving in vitro models have shown that myricetin causes the degradation of DNA. Additionally, myricetin, in the presence of Fe3+ and Cu2+, intensified this DNA degradation. The antioxidants catalase, superoxide dismutase, mannitol, and sodium azide in combination with Cu2+ increased the DNA degradation activity of myricetin. Myricetin was shown to create reactive oxygen species that caused the DNA damage. [1]

It has been demonstrated that myricetin, depending on its concentration, displays different oxidizing effects on DNA. Polyphenols like myricetin are able to reduce (donate electrons to) Fe3+. Thus, this reaction yields a less oxidized (more reduced) form of the iron cation: Fe2+ and a less reduced (more oxidized) form of myricetin. [1] This allows myricetin to form a complex with oxygen and biochemically target the DNA molecule. At higher and higher concentrations of myricetin, the rate of DNA damage has been shown to decrease. [1] A current hypothesis for why this occurs can be attributed to myricetin’s ability to chelate iron (Fe) (myricetin ligand forms two or more coordinate bonds to iron). These in vitro studies cannot be correlated directly to human models and should not be extrapolated.

Myricetin also impacts the biochemical efficacy and binding ability of large intracellular biomolecules. Myricetin has been shown to inhibit viral reverse transcriptase, cellular DNA polymerase, and cellular RNA polymerase. [1] Inhibition of cellular DNA polymerases could have dangerous effects on the cell’s ability to replicate its genome and its progression through the cell cycle. Inhibition of cellular RNA polymerase could have deleterious effects on the cell’s capacity to transcribe and translate DNA and RNA to produce vital proteins for the cell. Researchers have found that myricetin has the ability to interfere in the RNA polymerase pathway in two different ways. In E. coli myricetin competitively inhibited GTP substrate binding to RNA polymerase. In T7 bacteriophages myricetin competitively inhibited DNA template binding to RNA polymerase. [1]

Antiviral

Myricetin has been seen to demonstrate antiviral activity against a number of viruses including Moloney murine leukemia virus, Rauscher murine leukemia virus, and the human immunodeficiency virus. Its effects against the proliferation of viruses is thought to be a consequence of myricetin’s ability to inhibit the proper functioning of reverse transcriptase. Myricetin was identified as a competitive inhibitor of the reverse transcriptase of Rauscher murine leukemia virus and a partial competitor with respect to the human immunodeficiency virus. [1] Investigations into the activity of the HIV-1 strain when introduced to myricetin suggest the antiviral effects are derived from the inhibition of HIV-1 integrase, however, there are suspicions that the inhibition is non-specific. [8] Structural analysis of myricetin and other flavonoids with observed antiviral effects indicate that the 3,4’ free hydroxyl groups likely are responsible for inhibition. [1]

Antithrombotic

Polyphenols such as myricetin may prevent oxidative stress-induced platelet activation/aggregation. Thus, consumption of antioxidants may serve an anti-thrombotic function. In addition to offering protection by neutralizing peroxide radicals and effecting thromboxane production via the PTGS1 pathway, polyphenols such as myricetin may target other platelet activation pathways, limiting fibrinogen’s ability to bind platelet surface receptors. [9]

Antidiabetic

Several in vitro and animal studies have indicated the antidiabetic capabilities of myricetin; however, the evidence in clinical trials is less convincing. The flavonoid has been demonstrated to have a hypoglycemic effect by increasing the ability of adipocytes, as well as cells of the soleus muscle and liver of rats, to uptake glucose. [1] [10] This insulinomimetic effect is hypothesized to be a consequence of myricetin's either direct or indirect interaction with GLUT4, however, no analysis has produced concrete conclusions detailing exactly from where this effect is derived. In the hepatocytes of rats suffering from diabetes, myricetin has been observed to increase the activity of glycogen synthase 1. In trials done on Xenopus laevis oocytes, myricetin is thought to regulate the transport of glucose and fructose through the function of glucose transporter 2 (GLUT2) in sugar absorption. In addition, daily injections of myricetin into rats has been seen to be correlated with increased sensitivity to insulin, indicating the possibility of using a myricetin as treatment or protection against insulin resistance, a frequent cause of diabetes mellitus. In the mouse myoblast cell line known as C2C12, treatment with myricetin not only increased glucose uptake, but also enhanced lipogenesis, a result not seen from any of the other bioflavonoids tested. [10]

Although myricetin has not been concluded to have more than a neutral effect on humans, it has been used as a form of traditional medicine for diabetes in Northern Brazil and is hypothesized by the Finnish Mobile Clinic Health Examination Survey to potentially be correlated to the lower risk of Type 2 diabetes in individuals whose diets included higher than average amounts of myricetin. However, since studies in the United States, such as the Women's Health Study, do not confirm these results, there is doubt of whether or not the difference is risk can actually be accredited to myricetin and is not the result of the inability to fully control other variables such as racial background or inconsistencies in diet between participants. [10]

There is also evidence indicating that other characteristics of myricetin, such as its effect against inflammation, oxidative stress, and hyperlipidemia, may be helpful to reduce or even prevent other clinical issues which arise from diabetes mellitus. [10]

Antiatherosclerotic

Antioxidants, including flavonoids such as myricetin, are often touted to reduce the risk of atherosclerosis, the hardening of arteries associated with high cholesterol. However, in vivo studies are lacking and in vitro studies are contradictory and do not support this claim. This claim is based on myricetin's proposed ability to increase LDL uptake by macrophages, which in theory would protect against atherosclerosis. This theoretical action of myricetin is not supported by experimental data. [11] It is also proposed that myricetin may have the ability as a potent flavonoid antioxidant to prevent LDL oxidation, thus slowing the body's local inflammatory response and delaying the appearance of the first fatty streak and onset of atherosclerosis. [12]

Although mechanisms relating to myricetin specifically have not been proven, a diet that is rich in fruits and vegetables, and therefore rich in antioxidants, correlates with a decreased risk of cardiovascular disease, including atherosclerosis. [13] [14]

Neuroprotectant

It has also been shown that myricetin is effective in protecting neurons against oxidative stressors. Researchers have shown that PC12 cells treated with hydrogen peroxide (H2O2) as an oxidative stressor experience cell death due to apoptosis. When treated with myricetin, these oxidatively stressed cells displayed statistically significant increased cell survival. [15] It has been suggested that myricetin not only has oxygen radical scavenging abilities, but also inherent, specific cell-survival capacities. Other molecules known for oxygen radical scavenging (vitamin E and boldine) did not successfully protect the cell models from oxidative stress and eventual cell death as effectively as myricetin and other biochemically related molecules. [15]

Anti-inflammatory

Myricetin, along with other lipoxygenase- and cyclooxygenase-blocker flavonoids are seen to have significant anti-inflammatory characteristics, demonstrated by their ability to reduce edemas caused by carrageenan and croton oil. [1] The anti-inflammatory nature of myricetin lies in its ability to inhibit the amplified production of cytokines that occurs during inflammation. Testing on various types of macrophage cells, including RAW264.7, as well as on human synovial sarcoma cells, demonstrated the inhibition of several kinds of cytokines, such as interleukin-12 and interleukin-1β, through down-regulation of transcription factors and mediators involved in their production. [10] Other studies suggest that myricetin's anti-inflammatory nature could also potentially be dependent upon interfering in inflammatory signal pathways by inhibiting various kinases and, consequently, the function of tumor necrosis factor alpha. [10] [16]

Anti-platelet aggregation activity

Exposure to myricetin caused inhibition of rabbit platelet aggregation, induced by adenosine diphosphate, arachidonic acid, collagen and platelet activating factor (PAF). It inhibited specific receptor binding of PAF in rabbit platelets. The compound was found to be active against thrombin and neutrophil elastase. In addition, A prostacyclin-stimulated rise in the levels of platelet adenosine 3',5'-cyclic monophosphate (cAMP) was stimulated by myricetin. [17]

Immunomodulatory activities

Myricetin's preclinical immunomodulatory properties are now becoming increasingly widely known. [18] It was discovered that myricetin may prevent T-lymphocyte stimulation in a mouse model by binding to anti-CD3 and anti-CD28 monoclonal antibodies immobilised on beads. The inhibitory effect of myricetin on T cells, which was described in this study, was explained as being mediated via extracellular H2O2 production. Through the inhibition of NF-B binding activity, these natural compounds were reported to significantly reduce the lipopolysaccharide (LPS)-induced interleukin (IL)-12 production in mouse main macrophages as well as the RAW264.7 monocytic cell-line. [19] Myricetin produced epithelial layer contractile reflexes in separate rat aortic rings at a concentration of 50 M. [20] This substance induces the synthesis of cytosolic unbound calcium in cultured bovine endothelial cells. Myricetin suppressed the release of IL-2 protein from mouse EL-4 T cells that had been stimulated with phorbol 12-myristate 13-acetate (PMA) and ionomycin in a daily dosage approach. [21]

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<span class="mw-page-title-main">Flavonoid</span> Class of plant and fungus secondary metabolites

Flavonoids are a class of polyphenolic secondary metabolites found in plants, and thus commonly consumed in the diets of humans.

<span class="mw-page-title-main">Polyphenol</span> Class of chemical compounds

Polyphenols are a large family of naturally occurring phenols. They are abundant in plants and structurally diverse. Polyphenols include flavonoids, tannic acid, and ellagitannin, some of which have been used historically as dyes and for tanning garments.

<span class="mw-page-title-main">Methylcholanthrene</span> Chemical compound

Methylcholanthrene is a highly carcinogenic polycyclic aromatic hydrocarbon produced by burning organic compounds at very high temperatures. Methylcholanthrene is also known as 3-methylcholanthrene, 20-methylcholanthrene or the IUPAC name 3-methyl-1,2-dyhydrobenzo[j]aceanthrylene. The short notation often used is 3-MC or MCA. This compound forms pale yellow solid crystals when crystallized from benzene and ether. It has a melting point around 180 °C and its boiling point is around 280 °C at a pressure of 80 mmHg. Methylcholanthrene is used in laboratory studies of chemical carcinogenesis. It is an alkylated derivative of benz[a]anthracene and has a similar UV spectrum. The most common isomer is 3-methylcholanthrene, although the methyl group can occur in other places.

Advanced glycation end products (AGEs) are proteins or lipids that become glycated as a result of exposure to sugars. They are a bio-marker implicated in aging and the development, or worsening, of many degenerative diseases, such as diabetes, atherosclerosis, chronic kidney disease, and Alzheimer's disease.

<span class="mw-page-title-main">Quercetin</span> Chemical compound

Quercetin is a plant flavonol from the flavonoid group of polyphenols. It is found in many fruits, vegetables, leaves, seeds, and grains; capers, red onions, and kale are common foods containing appreciable amounts of it. It has a bitter flavor and is used as an ingredient in dietary supplements, beverages, and foods.

<span class="mw-page-title-main">Oxidative stress</span> Free radical toxicity

Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. Disturbances in the normal redox state of cells can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell, including proteins, lipids, and DNA. Oxidative stress from oxidative metabolism causes base damage, as well as strand breaks in DNA. Base damage is mostly indirect and caused by the reactive oxygen species generated, e.g., O2− (superoxide radical), OH (hydroxyl radical) and H2O2 (hydrogen peroxide). Further, some reactive oxidative species act as cellular messengers in redox signaling. Thus, oxidative stress can cause disruptions in normal mechanisms of cellular signaling.

Oxygen radical absorbance capacity (ORAC) was a method of measuring antioxidant capacities in biological samples in vitro. Because no physiological proof in vivo existed in support of the free-radical theory or that ORAC provided information relevant to biological antioxidant potential, it was withdrawn in 2012.

<span class="mw-page-title-main">Genistein</span> Chemical compound

Genistein (C15H10O5) is a naturally occurring compound that structurally belongs to a class of compounds known as isoflavones. It is described as an angiogenesis inhibitor and a phytoestrogen.

<span class="mw-page-title-main">CYP1A1</span> Protein-coding gene in the species Homo sapiens

Cytochrome P450, family 1, subfamily A, polypeptide 1 is a protein that in humans is encoded by the CYP1A1 gene. The protein is a member of the cytochrome P450 superfamily of enzymes.

<span class="mw-page-title-main">Antioxidant effect of polyphenols and natural phenols</span>

A polyphenol antioxidant is a hypothetized type of antioxidant, in which each instance would contain a polyphenolic substructure; such instances which have been studied in vitro. Numbering over 4,000 distinct chemical structures, such polyphenols may have antioxidant activity {{{1}}} in vitro (although they are unlikely to be antioxidants in vivo). Hypothetically, they may affect cell-to-cell signaling, receptor sensitivity, inflammatory enzyme activity or gene regulation, although high-quality clinical research has not confirmed any of these possible effects in humans as of 2020.

<span class="mw-page-title-main">Flavonols</span> Class of plant and fungus secondary metabolites

Flavonols are a class of flavonoids that have the 3-hydroxyflavone backbone. Their diversity stems from the different positions of the phenolic –OH groups. They are distinct from flavanols such as catechin, another class of flavonoids.

Pro-oxidants are chemicals that induce oxidative stress, either by generating reactive oxygen species or by inhibiting antioxidant systems. The oxidative stress produced by these chemicals can damage cells and tissues, for example, an overdose of the analgesic paracetamol (acetaminophen) can fatally damage the liver, partly through its production of reactive oxygen species.

<span class="mw-page-title-main">Endothelial NOS</span> Protein and coding gene in humans

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<span class="mw-page-title-main">Phenolic content in wine</span> Wine chemistry

The phenolic content in wine refers to the phenolic compounds—natural phenol and polyphenols—in wine, which include a large group of several hundred chemical compounds that affect the taste, color and mouthfeel of wine. These compounds include phenolic acids, stilbenoids, flavonols, dihydroflavonols, anthocyanins, flavanol monomers (catechins) and flavanol polymers (proanthocyanidins). This large group of natural phenols can be broadly separated into two categories, flavonoids and non-flavonoids. Flavonoids include the anthocyanins and tannins which contribute to the color and mouthfeel of the wine. The non-flavonoids include the stilbenoids such as resveratrol and phenolic acids such as benzoic, caffeic and cinnamic acids.

<span class="mw-page-title-main">Fisetin</span> Chemical compound

Fisetin (7,3′,4′-flavon-3-ol) is a plant flavonol from the flavonoid group of polyphenols. It can be found in many plants, where it serves as a yellow/ochre colouring agent. It is also found in many fruits and vegetables, such as strawberries, apples, persimmons, onions and cucumbers. Its chemical formula was first described by Austrian chemist Josef Herzig in 1891.

<span class="mw-page-title-main">Phenolic content in tea</span> Natural plant compounds

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(+)-Benzo(<i>a</i>)pyrene-7,8-dihydrodiol-9,10-epoxide Cancer-causing agent derived from tobacco smoke

(+)-Benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide is an organic compound with molecular formula C20H14O3. It is a metabolite and derivative of benzo[a]pyrene (found in tobacco smoke) as a result of oxidation to include hydroxyl and epoxide functionalities. (+)-Benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide binds to the N2 atom of a guanine nucleobase in DNA, distorting the double helix structure by intercalation of the pyrene moiety between base pairs through π-stacking. The carcinogenic properties of tobacco smoking are attributed in part to this compound binding and inactivating the tumor suppression ability of certain genes, leading to genetic mutations and potentially to cancer.

<span class="mw-page-title-main">Tellimagrandin I</span> Chemical compound

Tellimagrandin I is an ellagitannin found in plants, such as Cornus canadensis, Eucalyptus globulus, Melaleuca styphelioides, Rosa rugosa, and walnut. It is composed of two galloyl and one hexahydroxydiphenyl groups bound to a glucose residue. It differs from Tellimagrandin II only by a hydroxyl group instead of a third galloyl group. It is also structurally similar to punigluconin and pedunculagin, two more ellagitannin monomers.

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 Ong KC, Khoo HE (August 1997). "Biological Effects of Myricetin". General Pharmacology. 29 (2): 121–126. doi:10.1016/S0306-3623(96)00421-1. PMID   9251891.
  2. ↑ Holland, Thomas M.; Agarwal, Puja; Wang, Yamin; Leurgans, Sue E.; Bennett, David A.; Booth, Sarah L.; Morris, Martha Clare (2020-01-29). "Dietary flavonols and risk of Alzheimer dementia". Neurology. 94 (16): e1749–e1756. doi:10.1212/WNL.0000000000008981. ISSN   0028-3878. PMC   7282875 . PMID   31996451.
  3. 1 2 3 4 Ross JA, Kasum CM (July 2002). "Dietary Flavonoids: Bioavailability, Metabolic Effects, and Safety". Annual Review of Nutrition. 22: 19–34. doi:10.1146/annurev.nutr.22.111401.144957. PMID   12055336.
  4. ↑ Basli A, Soulet S, Chaher N, Merillon JM, Chibane M, Monti JP, Richard T (July 2012). "Wine polyphenols: potential agents in neuroprotection". Oxidative Medicine and Cellular Longevity. 2012: 805762. doi: 10.1155/2012/805762 . PMC   3399511 . PMID   22829964.
  5. ↑ Hollman PC, Katan MB (Dec 1999). "Health effects and bioavailability of dietary flavonols". Free Radical Research. 31 Suppl: Suppl S75–80. doi:10.1080/10715769900301351. PMID   10694044.
  6. 1 2 Flamini R, Mattivi F, De Rosso M, Arapitas P, Bavaresco L (Sep 2013). "Advanced knowledge of three important classes of grape phenolics: anthocyanins, stilbenes and flavonols". International Journal of Molecular Sciences. 14 (10): 19651–69. doi: 10.3390/ijms141019651 . PMC   3821578 . PMID   24084717.
  7. 1 2 3 4 5 6 7 8 9 10 11 12 "USDA Database for the Flavonoid Content of Selected Foods, Release 3" (PDF). U.S. Department of Agriculture. 2011.
  8. ↑ Cushnie T, Lamb A (November 2005). "Antimicrobial activity of flavonoids". International Journal of Antimicrobial Agents. 26 (5): 343–356. doi:10.1016/j.ijantimicag.2005.09.002. PMC   7127073 . PMID   16323269.
  9. ↑ Santhakumar AB, Bulmer AC, Singh I (November 2013). "A review of the mechanisms and effectiveness of dietary polyphenols in reducing oxidative stress and thrombotic risk". Journal of Human Nutrition and Dietetics. 27 (1): 1–21. doi:10.1111/jhn.12177. hdl: 10018/1029016 . PMID   24205990.
  10. 1 2 3 4 5 6 Li Y, Ding Y (December 2012). "Minireview: Therapeutic potential of myricetin in diabetes mellitus". Food Science and Human Wellness. 1: 19–25. doi: 10.1016/j.fshw.2012.08.002 .
  11. ↑ Wedworth, SM (1995). "Dietary flavonoids in atherosclerosis prevention". Annals of Pharmacotherapy. 29 (6): 627–8. doi:10.1177/106002809502900614. PMID   7663037. S2CID   37311639.
  12. ↑ Berliner JA, Navab M, Fogelman AM (1995). "Atherosclerosis: basic mechanisms. Oxidation, inflammation, and genetics". Circulation. 91 (9): 2488–96. doi:10.1161/01.CIR.91.9.2488. PMID   7729036.
  13. ↑ Rice, BH (2014). "Dairy and Cardiovascular Disease: A Review of Recent Observational Research". Current Nutrition Reports. 3 (2): 130–138. doi:10.1007/s13668-014-0076-4. PMC   4006120 . PMID   24818071.
  14. ↑ Kratz, M; Baars, T; Guyenet, S (Feb 2013). "The relationship between high-fat dairy consumption and obesity, cardiovascular, and metabolic disease". European Journal of Nutrition. 52 (1): 1–24. doi:10.1007/s00394-012-0418-1. PMID   22810464. S2CID   1360916.
  15. 1 2 Dajas F, Rivera-Megret, F (December 2003). "Neuroprotection by Flavonoids". Brazilian Journal of Medical and Biological Research. 36 (12): 1613–1620. doi: 10.1590/S0100-879X2003001200002 . PMID   14666245.
  16. ↑ Gupta SC, Tyagi AK, Deshmukh-Tasker P, Hinojosa M, Prasad S, Aggarwal BB (October 2014). "Downregulation of tumor necrosis factor and other proinflammatory biomarkers by polyphenols". Archives of Biochemistry and Biophysics. 559: 91–99. doi:10.1016/j.abb.2014.06.006. PMID   24946050.
  17. ↑ Semwal, D. K.; Semwal, R. B.; Combrinck, S.; Viljoen, A. (2016). "Myricetin: A Dietary Molecule with Diverse Biological Activities". Nutrients. 8 (2): 90. doi: 10.3390/nu8020090 . PMC   4772053 . PMID   26891321.
  18. ↑ Ghassemi-Rad, Javad; Maleki, Mahdis; Knickle, Allison F.; Hoskin, David W. (2018-05-10). "Myricetin-induced oxidative stress suppresses murine T lymphocyte activation". Cell Biology International. 42 (8): 1069–1075. doi:10.1002/cbin.10977. ISSN   1065-6995. PMID   29745443. S2CID   13675528.
  19. ↑ Kang, Bok Yun; Kim, Seung Hyun; Cho, Daeho; Kim, Tae Sung (2005). "Inhibition of interleukin-12 production in mouse macrophagesvia decreased nuclear factor-κB DNA binding activity by myricetin, a naturally occurring flavonoid". Archives of Pharmacal Research. 28 (3): 274–279. doi:10.1007/bf02977791. ISSN   0253-6269. PMID   15832812. S2CID   30554297.
  20. ↑ Jiménez, Rosario; Andriambeloson, Emile; Duarte, Juan; Andriantsitohaina, Ramaroson; Jiménez, José; Pérez-Vizcaino, Francisco; Zarzuelo, Antonio; Tamargo, Juan (August 1999). "Involvement of thromboxane A2in the endothelium-dependent contractions induced by myricetin in rat isolated aorta". British Journal of Pharmacology. 127 (7): 1539–1544. doi: 10.1038/sj.bjp.0702694 . ISSN   0007-1188. PMC   1566141 . PMID   10455307.
  21. ↑ Cho, Young-Chang; Yoon, Goo; Lee, Kwang Youl; Choi, Hyun Jin; Kang, Bok Yun (September 2007). "Inhibition of Interleukin-2 Production by Myricetin in Mouse EL-4 T Cells". Archives of Pharmacal Research. 30 (9): 1075–1079. doi:10.1007/bf02980240. ISSN   0253-6269. PMID   17958323. S2CID   40028977.
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