Flavonoids are a large and diverse group of naturally occurring polyphenolic compounds, characterized by a basic 15-carbon skeleton consisting of two phenyl rings (A and B) connected by a three-carbon linking chain that forms a heterocyclic ring (C), and they are widely distributed in the plant kingdom.[1] These secondary metabolites, often hydroxylated and glycosylated, serve essential roles in plant physiology while offering potential health-promoting effects in humans through dietary consumption.[2]Flavonoids are classified into several subclasses based on variations in their chemical structure, with the six primary classes being flavones, flavonols, flavanones, flavan-3-ols, isoflavones, and anthocyanidins; additional subclasses include aurones, chalcones, and dihydrochalcones, bringing the total to over 12 recognized groups.[1] This structural diversity—exemplified by the double bond between carbons 2 and 3 in flavones and flavonols, or the absence thereof in flavanones—underlies their varied biological activities and occurrence in different plant tissues.[3]In plants, flavonoids function primarily as pigments, antioxidants, and signaling molecules, attracting pollinators through coloration in flowers and fruits, protecting against ultraviolet radiation, and defending against pathogens and herbivores via antimicrobial and anti-feedant properties.[4] They are synthesized through the phenylpropanoid pathway and accumulate in vacuoles, epidermis, and other tissues, contributing to plant stress tolerance and reproduction.[3]Dietary sources of flavonoids are abundant in everyday foods, including fruits (e.g., apples, berries, citrus), vegetables (e.g., onions, broccoli), grains, teas, red wine, and herbs, with average daily intake in Western diets estimated at 200–300 mg, though bioavailability varies due to glycosylation and gut metabolism.[5] Prominent examples include quercetin (a flavonol in onions and apples), catechins (flavan-3-ols in green tea), and anthocyanins (in berries and red grapes), which contribute to the sensory qualities and nutritional value of these plant-based foods.[6]In human health, flavonoids exhibit a range of bioactivities, including potent antioxidant and free radical-scavenging effects that mitigate oxidative stress, alongside anti-inflammatory, cardioprotective, and anticancer properties supported by epidemiological and in vitro studies.[4] Diets rich in flavonoids are associated with reduced risks of cardiovascular disease, improved endothelial function, and potential benefits in managing diabetes and neurodegeneration, though clinical evidence remains mixed due to factors like absorption and metabolism.[7] Ongoing research emphasizes their role as nutraceuticals, with over 10,000 identified compounds highlighting their significance in preventive nutrition.[8]
Overview
Definition and Biological Significance
Flavonoids constitute a diverse class of secondary metabolites characterized by polyphenolic structures, with more than 10,000 distinct compounds identified to date.[9] These compounds are predominantly synthesized by plants, where they accumulate in various tissues such as fruits, vegetables, flowers, and roots, but they have also been detected in certain fungi and bacteria through biosynthetic pathways.[10] As plant secondary metabolites, flavonoids play essential roles beyond primary metabolism, contributing to the adaptation and survival of producing organisms in their environments.[11]In plants, flavonoids exhibit multifaceted biological significance, including potent antioxidant activity that helps neutralize reactive oxygen species generated under stress conditions.[12] They serve as pigments, particularly through anthocyanins, imparting colors to flowers, fruits, and leaves to attract pollinators and seed dispersers, thereby facilitating reproduction and ecological interactions.[3] Additionally, flavonoids provide ultraviolet (UV) protection by absorbing harmful UV radiation, shielding plant tissues from photodamage, and act as signaling molecules in symbiotic relationships, such as nodulation with nitrogen-fixing bacteria.[13]From an evolutionary perspective, flavonoids are derived from the phenylpropanoid pathway, originating from the amino acidphenylalanine, which enables their production in response to environmental stresses like drought, pathogens, and herbivory.[14] This biosynthetic route underscores their role in plant defense and interspecies signaling, enhancing resilience and promoting beneficial microbial associations within ecosystems.[15]In human diets, flavonoids from plant sources contribute to health through their antioxidant properties, with higher intakes linked to improved vascular function and reduced risk of chronic conditions.[11]
Basic Chemical Structure
Flavonoids are characterized by a fundamental 15-carbon skeleton known as flavan, structured as C6–C3–C6, comprising two benzene rings labeled A and B linked by a three-carbon chain that cyclizes to form a central heterocyclic pyran ring designated as C.[3] Ring A is a benzene ring fused to the pyran ring C at positions 5–10, while ring B is attached to ring C at position 2, creating a diphenylpropane-derived framework that underpins all flavonoid variants.[16] This core architecture is visually represented in standard diagrams as a tricyclic system, with ring A positioned on the bottom left, the oxygen-containing ring C in the center featuring a pyrone ring motif, and ring B extending from the top right, often annotated with numbered carbon positions to indicate substitution sites.[11]A defining feature of the flavonoid structure involves multiple hydroxyl groups attached primarily to rings A and B, typically at positions such as 5, 7 on ring A and 3', 4' on ring B, which impart polarity, enhance watersolubility, and facilitate hydrogen bonding interactions central to their chemical reactivity.[3] These phenolic hydroxyls are prone to modifications, most notably glycosidation, where monosaccharide or oligosaccharide units (e.g., glucose or rhamnose) are esterified to the oxygen of a hydroxyl group, forming O-glycosides that predominate in plant tissues and boost compound stability against oxidation and enzymatic degradation.[7] Less commonly, C-glycosides occur via direct carbon-carbon bonding to the aglycone core, further diversifying solubility profiles.[17]Structural diversity within flavonoids stems from modifications to the central ring C, including the presence or absence of a ketone (carbonyl) group at carbon 4, which influences planarity and conjugation; a double bond between carbons 2 and 3, promoting aromaticity in the pyrone ring; and stereochemical arrangements at asymmetric carbons (e.g., C2 or C3 in partially saturated forms), which dictate molecular conformation and subclass affiliation without altering the overarching C6–C3–C6 motif.[11] These variations modulate electronic properties and hydrogen-bonding capacity while preserving the essential bicyclic aromatic system connected by the heterocyclic linker.[16]
History
Early Discovery
The early discovery of flavonoids traces back to the late 18th century, when plant extracts rich in these compounds were utilized as natural yellow dyes. Quercitron bark, derived from the black oak (Quercus velutina), was introduced as a commercial source of yellow pigment in 1775 by American physician Edward Bancroft, who recognized its dyeing potential for textiles. The active principle, quercetin—a flavonol—was first isolated in pure form in 1814 by French chemist Michel Eugène Chevreul from onion skins and other plant sources, though its structure remained undetermined for decades.[18][19]By the mid-19th century, chemists began systematically extracting and naming these yellow substances from various plants, often referring to them as "yellow dyes" or flavins due to their coloration. Quercetin, obtained from quercitron bark through acid hydrolysis, became a prototypical example, yielding a brilliant yellow hue valued in the dye industry. These compounds were initially studied for their practical applications in coloring rather than their chemical identity.[20]In the 1890s, structural elucidation advanced significantly through the work of Polish-Swiss chemist Stanisław Kostanecki and British chemist Arthur George Perkin. Kostanecki, collaborating with J. Tambor, first proposed the term "flavone" in 1895 to describe the core structure of these oxygen-containing heterocyclic compounds, based on degradative analyses of natural isolates like chrysin from bee propolis. This marked a pivotal shift from empirical dye extraction to understanding their polyphenolic backbone. Perkin, building on this, isolated and elucidated the structures of several flavones and flavonols from floral sources, such as apigenin from parsley, using methylation and oxidation techniques that confirmed the diphenylpyrone skeleton.[21][22][23]Flavonoids were soon recognized as key plant pigments contributing to flower colors, particularly yellows from flavones and flavonols, and reds/blues from anthocyanidins, while certain polymeric forms were identified as condensed tannins used in leather processing. This early appreciation highlighted their roles in pigmentation and astringency, predating deeper biosynthetic insights.[11][24]
Key Developments and Nomenclature
In the mid-20th century, significant breakthroughs in flavonoid research advanced the understanding of their chemical diversity and classification. A pivotal contribution was T.A. Geissman's 1962 edited volume, The Chemistry of Flavonoid Compounds, which compiled comprehensive reviews on the synthesis, structure, and reactions of flavonoids, establishing a foundational framework for their systematic classification based on structural variations.[25] Concurrently, the full elucidation of anthocyanin structures, key flavonoid pigments responsible for plant coloration, was achieved through detailed chemical analyses, confirming their flavylium cation backbone and glycosylated forms, which had been progressively refined since early proposals in the 1910s.[26]Nomenclature for flavonoids evolved to provide clarity amid growing structural complexity, with the International Union of Pure and Applied Chemistry (IUPAC) playing a central role in standardization during the 1970s and beyond. Early efforts distinguished flavonoids, characterized by the 2-phenylchromen-4-one core, from related classes like isoflavonoids (3-phenylchromen-4-one), using the diphenylpropane descriptor C6-C3-C6 to denote the basic 15-carbon skeleton linking two aromatic rings via a three-carbon bridge.[27] These IUPAC guidelines, building on semi-systematic naming conventions, facilitated precise identification of substituents and stereochemistry, addressing ambiguities in earlier trivial names and enabling consistent reporting across chemical literature.[28]In the 2000s, genomic approaches revolutionized the study of flavonoid biosynthesis, identifying key regulatory genes and enzymes through whole-genome sequencing of model plants like Arabidopsis thaliana. Milestones included the mapping of phenylpropanoid pathway genes, such as chalcone synthase and flavonoid hydroxylases, which revealed evolutionary conservation and tissue-specific expression patterns.[13] By the 2020s, advances in mass spectrometry, particularly high-resolution LC-MS/MS, enabled the identification of over 10,000 distinct flavonoid compounds across plant species, expanding the known chemical repertoire and linking structural diversity to ecological roles.[29]Modern taxonomy has addressed historical gaps by incorporating neoflavonoids (4-phenylcoumarin derivatives) and homoisoflavonoids (3-benzylidenechromanones) into the broader flavonoid superfamily, recognizing their biosynthetic origins from the same phenylpropanoid pathway despite structural deviations from the classic C6-C3-C6motif. This inclusion, formalized in IUPAC definitions, reflects phylogenetic evidence from genomic studies showing shared ancestry, while maintaining subclass distinctions to account for unique distributions in families like Fabaceae and Asparagaceae.[27][30]
Classification
Flavones and Flavonols
Flavones constitute a subclass of flavonoids characterized by a 2-phenylchromen-4-one backbone, featuring a double bond between carbons 2 and 3 and a ketone group at position 4. This core structure imparts stability and aromatic properties to flavones, which often appear as yellow pigments in various herbs and plants. Representative examples include apigenin, a 4',5,7-trihydroxyflavone abundant in parsley, celery, and chamomile, and luteolin, a 3',4',5,7-tetrahydroxyflavone found in thyme, oregano, and green peppers.[31][32][33]Flavonols, in contrast, are distinguished by the addition of a hydroxyl group at the 3-position of the flavone skeleton, resulting in a 3-hydroxyflavone core that enhances their polarity and reactivity.[34] These compounds are ubiquitous in fruits, vegetables, and leaves, contributing to pigmentation and sometimes bitterness in foods like apples and onions. Key examples are quercetin, a 3,3',4',5,7-pentahydroxyflavone prevalent in onions, berries, and capers, and kaempferol, a 3,4',5,7-tetrahydroxyflavone common in kale, tea, and broccoli.[11][35]The primary structural difference between flavones and flavonols lies in the presence of the 3-hydroxyl group in the latter, which influences hydroxylation patterns across the rings and thereby affects solubility and bioavailability. Flavones typically exhibit fewer hydroxyl substitutions, rendering them less polar, while flavonols' additional hydroxyls increase water solubility, particularly when combined with glycosylation—a prevalent modification where sugar moieties attach to hydroxyl groups, further enhancing solubility and stability in plant tissues.[36][37] Varying degrees of hydroxylation, such as in the B-ring (e.g., catechol moiety in luteolin and quercetin), modulate these properties, with more hydroxyl groups generally promoting greater aqueous solubility.[38]
Flavanones and Flavanonols
Flavanones represent a subclass of flavonoids defined as 2,3-dihydroflavones, distinguished by the saturation of the double bond between carbons 2 and 3 in the central heterocyclic C ring, which imparts a partially reduced structure compared to fully aromatic flavones.[11] This structural modification results in a single chiral center at C-2, enabling the existence of enantiomers that influence their biological interactions.[39] Flavanones commonly occur in both aglycone and glycoside forms, with glycosylation often enhancing their solubility and stability in plant tissues.[40]Prominent examples of flavanones include naringenin and hesperetin as aglycones, alongside their corresponding glycosides naringin and hesperidin, which are neohesperidosides prevalent in citrus species.[40] These compounds are particularly abundant in Citrus fruits, such as sweet oranges (Citrus sinensis), grapefruits (Citrus paradisi), and lemons (Citrus limon), where they contribute to the characteristic bitterness and astringency of the fruit.[11] For instance, hesperidin predominates in sweet oranges and mandarins, while naringin is a major constituent in grapefruits, often comprising the bulk of total flavonoid content in these sources.[41]Flavanonols, closely related to flavanones, are characterized as 3-hydroxyflavanones, featuring an additional hydroxyl group at C-3 alongside the saturated C2-C3 bond in the C ring.[42] This substitution introduces a second chiral center at C-3, yielding diastereomers with distinct stereochemical configurations that affect their reactivity and function in plants.[43] Like flavanones, flavanonols exist as aglycones or glycosides, though aglycone forms are more commonly studied for their roles in metabolic pathways.A key example of a flavanonol is taxifolin, also termed dihydroquercetin, which is widely distributed in plants including conifers like Taxus species, as well as in onions and certain citrus fruits.[44]Taxifolin acts as an important intermediate in flavonoid biosynthesis, serving as a precursor to flavan-3-ols such as catechins through subsequent enzymatic modifications.[45] Its presence in glycosylated forms further supports its incorporation into plant defense mechanisms and nutritional profiles.[46]
Flavan-3-ols and Anthocyanidins
Flavan-3-ols, also known as flavanols, represent a subclass of flavonoids characterized by a saturated C-ring with a hydroxyl group at the C-3 position, distinguishing them from other flavonoids by the absence of a double bond between C-2 and C-3.[47] These compounds are typically found as monomers such as (+)-catechin and (-)-epicatechin, which feature multiple hydroxyl groups on the A, B, and C rings, contributing to their reactivity and biological interactions.[48] The hydroxyl groups, particularly the ortho-dihydroxy configuration on the B-ring in catechins, enable strong binding to proteins, resulting in the sensory property of astringency observed in foods rich in these compounds.[49]Monomeric flavan-3-ols can undergo polymerization through carbon-carbon linkages, primarily between the C-4 position of one unit and the C-8 or C-6 position of another, forming oligomeric and polymeric structures known as proanthocyanidins or condensed tannins.[50] Proanthocyanidins, such as those composed of epicatechin units (procyanidins), exhibit increased astringency with higher degrees of polymerization due to enhanced protein-binding capacity, while bitterness tends to decrease as chain length grows.[51] In plants, these polymers play protective roles by deterring herbivores through their bitter and astringent taste and by contributing to structural integrity in tissues like seeds and bark.[52]Anthocyanidins, in contrast, form the colored subgroup of flavonoids, existing primarily as flavylium cations—a positively charged oxonium ion in the C-ring that imparts vibrant hues to plant tissues.[53] Key examples include cyanidin, with five hydroxyl groups at positions 3, 5, 7, 3', and 4', and delphinidin, which has an additional hydroxyl at 5' for a total of six, influencing their pigmentation intensity and stability.[26] The color of anthocyanidins is highly pH-dependent: at acidic pH (below 3), the flavylium cation dominates, producing red-orange shades, while at neutral to slightly alkaline pH (4-6), transformation to the quinonoidal base yields purple to blue colors, enabling dynamic visual signaling in flowers and fruits.[54]To enhance stability against degradation from light, heat, or pH shifts, anthocyanidins are commonly glycosylated at the 3-position or other hydroxyl sites, forming anthocyanins that benefit from intramolecular hydrogenbonding between sugar moieties and the chromophore.[55]Glycosylation not only improves solubility and resistance to oxidation but also modulates color expression, with acylated glycosides showing greater resilience in plant vacuoles where these pigments accumulate.[56] In ecological contexts, anthocyanidins serve visual functions by attracting pollinators and seed dispersers through vivid petal and fruit coloration, while also providing photoprotection against UV radiation.[57]
Isoflavonoids and Other Subclasses
Isoflavonoids represent a significant subclass of flavonoids characterized by a rearranged carbon skeleton, specifically a 3-phenylchromen-4-one backbone, which differs from the typical 2-phenylchromen-4-one structure of most flavonoids.[58] This structural isomerism arises biogenetically from the standard flavonoid framework through a 1,2-aryl migration, resulting in the attachment of the B-ring at the C-3 position of the central pyrone ring.[59] Predominantly found in leguminous plants, isoflavonoids serve as phytoalexins, contributing to defense against pathogens and herbivores.[60] Prominent examples include genistein and daidzein, which are aglycones abundant in soybeans and exhibit phytoestrogenic properties due to their ability to bind estrogen receptors, mimicking endogenous estrogens.[61] These compounds play roles in plant signaling and symbiosis, particularly with nitrogen-fixing bacteria in legumes.[58]Beyond isoflavonoids, other flavonoid subclasses feature distinct structural modifications, often involving reduced, open-chain, or alternatively rearranged skeletons. Flavan-3,4-diols, also known as leucoanthocyanidins, possess a flavan skeleton with hydroxyl groups at both the 3 and 4 positions, lacking the carbonyl at C-4 typical of many flavonoids; they serve as key intermediates in the formation of condensed tannins and proanthocyanidins.[62] Aurones, a less common group, exhibit a five-membered benzofuranone core with a 2-benzylidene substituent, making them structural isomers of flavones and responsible for yellow pigmentation in certain flowers and leaves.[63] Chalcones, considered acyclic precursors in the flavonoid biosynthetic pathway, feature an open-chain α,β-unsaturated ketone linking two aromatic rings, and they can cyclize to form flavanones or other cyclic flavonoids.[64] Dihydrochalcones, related to chalcones but with a saturated three-carbon bridge connecting two aromatic rings, represent another subclass; prominent examples include phloretin and its glycoside phloridzin, which are abundant in apples and contribute to the plant's defense and sensory properties like sweetness.[65] Neoflavonoids, another rearranged variant, are defined by a 4-phenylchromen backbone where the B-ring attaches at the C-4 position, distinguishing them from the standard C-2 attachment; they are rare and primarily occur in families such as Moraceae and Fabaceae, with examples like neoflavone demonstrating antimicrobial potential.[11]These subclasses highlight the diversity of flavonoid rearrangements, enabling specialized biological niches such as pigmentation, precursor roles, and defense mechanisms in plants.[66] In some cases, microbial associations influence the accumulation or modification of these compounds, enhancing their ecological functions.[60]
The biosynthesis of flavonoids in plants initiates within the phenylpropanoid pathway, starting from the aromatic amino acid phenylalanine. The first committed step is catalyzed by phenylalanine ammonia-lyase (PAL), which deaminates phenylalanine to form trans-cinnamic acid, releasing ammonia in the process.[67] This reaction represents the entry point into phenylpropanoid metabolism, shared with other phenolic compounds.[68]Trans-cinnamic acid is then hydroxylated at the 4-position by cinnamate 4-hydroxylase (C4H), a cytochrome P450-dependent monooxygenase, yielding p-coumaric acid.[67] Subsequently, 4-coumarate:CoA ligase (4CL) activates p-coumaric acid through adenylation and thioesterification with coenzyme A, producing 4-coumaroyl-CoA, the key intermediate for flavonoid assembly.[68] These early steps, involving PAL, C4H, and 4CL, are tightly coordinated in the endoplasmic reticulum and cytosol of plant cells.[69]The flavonoid-specific branch diverges from 4-coumaroyl-CoA via chalcone synthase (CHS), a polyketide synthase that performs three sequential condensations with malonyl-CoA (derived from acetyl-CoA via acetyl-CoA carboxylase), followed by a Claisen-type cyclization to generate naringenin chalcone.[67]Chalcone isomerase (CHI) then catalyzes the stereospecific cyclization of naringenin chalcone to the flavanone naringenin, establishing the central C6-C3-C6 scaffold of flavonoids.[68] This core sequence can be summarized as:Phenylalanine →PAL trans-Cinnamic acid →C4H p-Coumaric acid →4CL 4-Coumaroyl-CoA →CHS Naringenin chalcone →CHI Naringenin (flavanone).[69]Downstream from naringenin, the pathway branches to produce diverse flavonoid subgroups through specific enzymes. Flavones arise directly from flavanones via flavone synthases, which exist in two forms: FNS I (a 2-oxoglutarate-dependent dioxygenase) or FNS II (a cytochrome P450).[69] Flavonols are synthesized by sequential action of flavanone 3-hydroxylase (F3H), which introduces a hydroxyl group at the 3-position to form dihydroflavonols like dihydrokaempferol, followed by flavonol synthase (FLS), another 2-oxoglutarate-dependent dioxygenase that dehydrates and aromatizes the C-ring to yield flavonols such as kaempferol.[68] Additional branch points include isoflavonoid formation via isoflavone synthase (IFS) on naringenin or liquiritigenin, and proanthocyanidin/anthocyanin pathways via dihydroflavonol 4-reductase (DFR), enabling specialization across plant species and tissues.[67]
Regulation and Variations
The regulation of flavonoid biosynthesis in plants is primarily orchestrated by the MBW transcriptional complex, comprising R2R3-MYB, basic helix-loop-helix (bHLH), and WD40-repeat (WDR) proteins, which binds to promoters of structural genes to activate their expression. This complex plays a pivotal role in controlling the early steps of the pathway, particularly the upregulation of chalcone synthase (CHS), the first committed enzyme, thereby fine-tuning flavonoid production in response to developmental and stress cues. For instance, MYB factors often act as activators or repressors within the MBW assembly, with subgroup IIIf bHLHs providing specificity for anthocyanin and proanthocyanidin branches, while WD40 proteins stabilize the complex for efficient gene regulation.[70][71][72]Environmental triggers significantly modulate flavonoid biosynthesis through signaling cascades that intersect with the MBW complex. Ultraviolet (UV) light, particularly UV-B radiation, induces rapid accumulation of flavonoids by activating photoreceptors that enhance transcription of biosynthetic genes, serving as a protective response against oxidative damage. Similarly, pathogen attacks stimulate the pathway via jasmonic acid (JA) signaling, where JA acts as a hormone mediator to upregulate CHS and downstream enzymes, promoting flavonoid-derived phytoalexins for defense; this is evident in rice responses to fungal infections like Magnaporthe oryzae. These abiotic and biotic cues highlight the pathway's adaptability, with JA often synergizing with other hormones to amplify MBW activity under stress.[73][74][75]Species-specific variations in flavonoid regulation underscore evolutionary diversification, particularly in enzyme recruitment and tissue-specific accumulation. In legumes, isoflavone synthase (IFS), a cytochrome P450 enzyme unique to this family, catalyzes the conversion of flavanones to isoflavones, branching the pathway toward bioactive compounds essential for nodulation and defense; this specialization is absent in non-legumes, reflecting gene duplication events in Fabaceae. In legumes like red clover, CRISPR/Cas9-mediated deletion of the IFS1 gene has reduced isoflavone levels and altered nodulation, illustrating their role in symbiosis.[76][77] Anthocyanin accumulation in fruits, conversely, exhibits temporal and genotypic variations, often peaking during ripening due to MBW-mediated activation in vacuolar compartments, as seen in berries where altitude and developmental stage influence profiles through differential gene expression. These variations enable tailored ecological roles, such as UV protection in high-altitude fruits or microbial signaling in legumes.[69][78]Recent advances in CRISPR/Cas9-based pathway engineering have illuminated regulatory mechanisms and enabled precise modifications. Studies from the 2020s have targeted MBW components and structural genes, such as editing CHS2 in horticultural crops to redirect flux from flavonoids to stilbenoids, revealing competitive branch-point dynamics.[79] Multiplexed CRISPR activation has enhanced flavonol production in a cell-type-specific manner. These efforts demonstrate CRISPR's utility in dissecting variations and engineering resilient varieties without off-target effects.[80]
Natural Functions
Roles in Plants
Flavonoids play crucial physiological roles in plant pigmentation, primarily through subclasses like anthocyanins, which impart red, purple, and blue hues to flowers, fruits, and vegetative tissues. These pigments attract pollinators by providing visual cues that enhance reproductive success, as demonstrated in petunia where anthocyanin accumulation influences pollinator preference in field conditions.[81] Anthocyanins also contribute to seed dispersal by signaling to animals, though their primary internal function lies in modulating light absorption within plant cells. In contrast, flavonols such as quercetin and kaempferol accumulate in epidermal layers and act as UV-B screens, absorbing ultraviolet radiation to protect underlying photosynthetic tissues from damage and photoinhibition.[82] This screening function is particularly vital in high-altitude or open environments, where flavonol levels increase in response to UV exposure to maintain cellular integrity.[83]Beyond pigmentation, flavonoids function as key components of the plant's antioxidant defense system, scavenging reactive oxygen species (ROS) produced during abiotic stresses like drought, salinity, and excess light. Under such conditions, flavonoids such as flavonols and flavones neutralize ROS through their phenolic hydroxyl groups, which donate electrons or hydrogen atoms to stabilize free radicals and prevent oxidative damage to membranes and proteins.[84] This ROS-scavenging activity supplements enzymatic antioxidants like superoxide dismutase, forming a secondary line of defense when primary systems are overwhelmed.[85] Additionally, flavonoids chelate transition metals such as iron and copper, inhibiting Fenton-type reactions that generate highly reactive hydroxyl radicals and thereby mitigating metal-induced oxidative stress in plant cells.[86]Flavonoids also regulate plant development, notably by modulating auxin transport, which controls root architecture and tropisms. Flavonols, including quercetin glycosides, inhibit polar auxin efflux carriers like PIN proteins, leading to localized auxin accumulation that influences lateral root emergence and root gravitropism in species such as Arabidopsis.[87] This inhibition fine-tunes developmental responses to environmental cues, ensuring adaptive growth patterns. A specific example is quercetin's role in reproductive tissues, where it supports pollen viability and tube growth by maintaining ROS homeostasis and stabilizing cellular structures during germination.[88] In pollen tubes, quercetin modulates signaling pathways to sustain integrity and directed growth toward the ovule.[89]
Ecological and Protective Functions
Flavonoids serve as key defensive compounds in plants, particularly through their role as phytoalexins that combat fungal and bacterial pathogens. Isoflavonoids, a subclass of flavonoids, accumulate in response to infection and inhibit the growth of fungi such as Fusarium species by disrupting pathogen cell membranes and enzymatic activities. For instance, in wheat, novel isoflavone phytoalexins like triticein (5-hydroxy-2′,4′,7-trimethoxyisoflavone) are induced upon fungal challenge, providing broad-spectrum resistance. Similarly, in legumes, isoflavonoid phytoalexins such as medicarpin exhibit antifungal properties against root pathogens, enhancing plant survival in microbe-rich soils.[90][91][92]Beyond direct antimicrobial action, flavonoids contribute to allelopathy, where root exudates inhibit the growth of neighboring plants through chemical interference. Quercetin, a flavonol commonly exuded from roots of species like buckwheat (Fagopyrum esculentum), suppresses seedling elongation in competing weeds by interfering with cell division and nutrient uptake. In barley (Hordeum vulgare), flavonoids such as catechin and cyanidin in root exudates exhibit phytotoxic effects, reducing radicle growth in sensitive species and thus conferring a competitive advantage in crop fields. These exudate-mediated interactions highlight flavonoids' role in shaping plant community dynamics in natural and agricultural ecosystems.[93][94][95]In symbiotic relationships, flavonoids act as signaling molecules that facilitate beneficial interactions with soil microbes, particularly in nitrogen-fixing symbioses. Legume roots exude specific flavonoids like luteolin, a flavone, which binds to the NodD receptor protein in rhizobial bacteria, triggering the expression of nodulation (nod) genes essential for nodule formation. This induction enables Rhizobium species to produce Nod factors, lipo-chitooligosaccharides that promote root cortical cell division and infection thread development in hosts like alfalfa (Medicago sativa). Such flavonoid-rhizobia crosstalk ensures efficient nitrogen fixation, enhancing legume productivity in nitrogen-poor soils.[96][97][98]Flavonoids also provide protection against herbivory by imparting bitterness and astringency, sensory properties that deter feeding by insects and mammals. Condensed tannins, polymeric flavonoids abundant in leaves and bark, bind to proteins in the herbivore's mouth, causing a dry, puckering sensation that discourages consumption; for example, in forage crops like birdsfoot trefoil (Lotus corniculatus), high tannin levels reduce palatability to grazing animals. Certain monomeric flavonoids, such as quercetin glycosides, contribute to bitter taste via activation of taste receptors, signaling toxicity and thereby reducing herbivore damage in species like tea (Camellia sinensis). These deterrent effects are amplified under herbivore attack, where flavonoid biosynthesis is upregulated.[99][100][101]Conversely, flavonoids play a protective role in reproduction by serving as visual cues for pollinators through flower pigmentation. Anthocyanins and flavonols absorb UV and visible light, producing colors from red to blue that attract insects and birds; in bee-pollinated flowers like those of snapdragon (Antirrhinum majus), pelargonidin-derived anthocyanins enhance visibility against green foliage, increasing visitation rates. These pigments not only guide pollinators but also protect reproductive tissues from UV damage during anthesis, ensuring successful pollination in exposed environments.[102][103][104]Under abiotic stresses like drought and UV radiation, plants upregulate flavonol production as an adaptive response to mitigate oxidative damage. In grapevines (Vitis vinifera), moderate drought induces the transcription factor VviMYB24, boosting flavonol synthase activity and accumulating kaempferol and quercetin glycosides that scavenge reactive oxygen species (ROS) in leaves. Recent studies on tea (Camellia sinensis) show UV-B pre-exposure elevates flavonol levels via CsHY5-mediated pathways, improving membrane stability and photosynthetic efficiency during subsequent water deficits. In desert shrubs like Artemisia species, combined drought and UV stress correlate with 2-3-fold increases in flavonol content, enhancing tolerance through antioxidant reinforcement and osmotic adjustment. These adaptations underscore flavonoids' contributions to climate resilience in vascular plants.[105][106][107]
Occurrence and Dietary Sources
Plant Sources and Distribution
Flavonoids are ubiquitous secondary metabolites found in a wide array of plant species, with over 6,000 distinct structures identified across vascular plants, contributing to pigmentation, flavor, and defense mechanisms.[11] Common sources include fruits such as berries (e.g., blueberries, strawberries) and citrus (e.g., oranges, lemons), vegetables like onions and kale, beverages derived from tea leaves and grapes (wine), and herbs such as parsley.[1] These compounds are particularly abundant in edible plant parts, including grains, bark, roots, stems, flowers, and seeds, reflecting their role in plant physiology.[3]Within plants, flavonoids exhibit tissue-specific accumulation patterns, often concentrating in protective outer layers. High levels are typically observed in fruit skins and seeds, where they serve as barriers against environmental stressors; for instance, proanthocyanidins accumulate in grape skins and seeds.[108] Anthocyanins, responsible for red, purple, and blue hues, are predominantly found in the skins and flesh of colored produce like berries, red grapes, and purple cabbage. In contrast, flavonols such as quercetin and kaempferol are more prevalent in leaves and outer tissues of vegetables, including kale leaves and onion skins, as well as in apples and tea leaves.[109] This distribution varies by plant organ, with shoots and external structures like glandular hairs showing higher concentrations compared to roots in many species.[110]Global variations highlight subclass-specific sources, with isoflavonoids like genistein and daidzein concentrated in legumes, particularly soybeans, which are a primary source in Asian flora. Flavan-3-ols, including catechins and epicatechins, are notably abundant in cocoa beans from Theobroma cacao trees native to tropical regions. Flavonoids have been documented in over 9,000 plant species worldwide, underscoring their evolutionary conservation across angiosperms, gymnosperms, and even some ferns.[111] Emerging research in the 2020s has revealed flavonoids in marine algae, such as brown seaweeds (e.g., Sargassum species) and green seaweeds (e.g., Ulva lactuca), expanding their known distribution beyond terrestrial plants to aquatic environments.[112][113]
Human Dietary Intake Patterns
Human dietary intake of flavonoids typically ranges from 200 to 500 mg per day in Western populations, with studies reporting means such as 176 mg/day in a large cohort analysis and 225 mg/day in U.S. adults.[114][115] In Asian diets, intake is often higher, averaging around 318 mg/day in Korean adults, largely due to soy-based isoflavone sources.[116] Mediterranean diets show similar levels, approximately 370 mg/day, supported by consumption of fruits, vegetables, and moderate wine intake.[117]Major contributors to flavonoid intake include tea, which provides the bulk of flavan-3-ols at about 157 mg/day on average, followed by citrus fruit juices (8 mg/day, primarily flavanones like hesperidin), wine (4 mg/day), and citrus fruits (3 mg/day).[118]Flavonols such as quercetin are predominantly sourced from onions and apples, while berries and soy products contribute anthocyanidins and isoflavones, respectively.[119] These sources account for over 50% of total intake in most diets, with fruits and vegetables comprising 54% and tea adding another 33%.[116]Intake patterns have shown a decline in diets high in ultra-processed foods, where total flavonoid consumption decreases by 50-70% compared to minimally processed diets.[120] Concurrently, the use of flavonoid-containing supplements has risen in the 2020s, driven by concerns over declining nutrient density in modern food supplies.[121] Global surveys reveal variations by region, with the European Prospective Investigation into Cancer and Nutrition (EPIC) study showing differences between Mediterranean and non-Mediterranean European countries and no significant gender differences.[117] U.S. surveys indicate higher intakes among non-Hispanic Asian adults compared to other groups.[122] Recent cohort analyses as of 2025 suggest median intakes up to 792 mg/day in diverse, flavonoid-rich diets.[123] Intake tends to be lower in the elderly, potentially due to reduced fruit and vegetable consumption.[124]
Metabolism and Bioavailability
Absorption and Metabolism in Humans
Flavonoids in the diet are predominantly present as glycosides, which exhibit limited direct absorption in their conjugated form. Upon ingestion, these compounds reach the small intestine, where absorption primarily occurs via passive diffusion of the aglycone moiety after deglycosylation. The enzyme lactase-phlorizin hydrolase (LPH), located in the brush border of enterocytes, can hydrolyze β-glycosides such as quercetin-4'-glucoside, facilitating uptake into epithelial cells. However, the majority of flavonoid glycosides, especially those with more complex sugar attachments, resist small intestinal hydrolysis and proceed to the colon, where gut microbiota play a crucial role in deconjugation through microbial β-glucosidases, releasing free aglycones for potential absorption across the colonic epithelium.[125][126]Once absorbed, flavonoids undergo extensive phase I and phase II metabolism, primarily in the enterocytes and liver, transforming them into more polar conjugates for efficient transport and elimination. Phase I metabolism involves cytochrome P450 (CYP450) enzymes, such as CYP1A2 and CYP3A4, which perform oxidation reactions on certain flavonoids like quercetin, generating hydroxylated derivatives. Phase II conjugation follows, mediated by uridine 5'-diphospho-glucuronosyltransferases (UGTs), sulfotransferases (SULTs), and catechol-O-methyltransferases (COMT), producing glucuronides, sulfates, and methylated metabolites, respectively. A major circulating metabolite of quercetin, for instance, is quercetin-3-glucuronide, which predominates in plasma after dietary intake. This glucuronidation process can be represented as:\text{Aglycone} + \text{UDPGA} \xrightarrow{\text{UGT}} \text{[Glucuronide](/page/Glucuronide) conjugate} + \text{[UDP](/page/UDP)}where UDPGA denotes uridine 5'-diphosphoglucuronic acid. These modifications enhance water solubility, reducing the bioavailability of the parent aglycone but enabling distribution to tissues.[126][127][128]Following metabolism, flavonoid conjugates are distributed systemically, with some undergoing enterohepatic recirculation, whereby they are secreted into bile, re-enter the intestine, and are partially reabsorbed. Excretion occurs mainly through the urine as phase II conjugates, accounting for up to 80-90% of ingested flavonoids in human studies, while fecal elimination handles unabsorbed portions and microbial degradation products like phenolic acids. This recirculation and renal clearance contribute to the prolonged plasma half-life of metabolites, often ranging from 10-30 hours for quercetin derivatives, influencing their potential physiological roles. Gut microbiota further metabolize unabsorbed flavonoids into bioactive catabolites, such as 3-hydroxyphenylacetic acid from quercetin, which may also enter circulation.[125][129][130]
Factors Affecting Bioavailability
The bioavailability of flavonoids is notably low, typically resulting in plasma concentrations below 1 μM following dietary intake, with elimination half-lives ranging from 4 to 24 hours depending on the specific compound and individual factors.[131][125]The food matrix plays a critical role in modulating flavonoid absorption, where co-ingested macronutrients can either enhance or inhibit bioavailability. Lipids, for instance, improve the solubility and uptake of flavonoids by facilitating micelle formation in the gut, leading to higher plasma levels of compounds like quercetin when consumed with fatty meals.[132] In contrast, dietary fiber binds to flavonoids, reducing their bioaccessibility and absorption in the small intestine, as demonstrated by studies showing decreased recovery of flavonols in high-fiber diets.[133] Cooking methods further influence bioavailability; boiling and frying often lead to losses of flavonoid glycosides (up to 30% for quercetin glycosides in onions), as heat and water extraction degrade or leach these conjugates, while steaming preserves more intact forms.[134]Individual physiological factors contribute significantly to inter-person variability in flavonoid bioavailability. Gut microbiome diversity is a key determinant, with higher microbial richness promoting the biotransformation of flavonoids into more absorbable metabolites via enzymatic cleavage of glycosides, whereas low diversity limits this process and reduces overall uptake.[135] Age-related changes, such as altered gut permeability and reduced metabolic enzyme activity, can diminish bioavailability in older adults, potentially exacerbating low plasma levels compared to younger individuals.[136] Genetic polymorphisms, particularly in the COMT gene (e.g., Val158Met variant), affect phase II methylation of flavonoids, resulting in up to fourfold differences in enzyme activity and thus variable plasma metabolite profiles among individuals.[137]Recent advances in formulation strategies have addressed these limitations by enhancing delivery and stability. Nanoparticles and liposomes encapsulate flavonoids, protecting them from degradation and improving intestinal absorption; for example, quercetin-loaded liposomes increased bioavailability by 5-10 fold in rodent models, with sustained release profiles observed in 2023 studies.[138] Solid lipid nanoparticles have similarly boosted the solubility of hydrophobic flavonoids, achieving higher plasma concentrations and prolonged circulation in preclinical studies, as reviewed in 2023.[139][140] As of 2025, glycosylation techniques have emerged as a promising chemical modification to further improve flavonoid solubility and bioavailability.[141]
Health Research
Antioxidant and Anti-inflammatory Effects
Flavonoids demonstrate potent antioxidant activity primarily through direct free radical scavenging, where their phenolic hydroxyl (OH) groups donate hydrogen atoms or electrons to neutralize reactive oxygen species (ROS), including superoxide, peroxyl, hydroxyl, and alkoxyl radicals. This mechanism prevents oxidative damage to cellular components such as lipids, proteins, and DNA. In addition, flavonoids indirectly enhance antioxidant defenses by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, which translocates to the nucleus and promotes the transcription of genes encoding endogenous antioxidants like heme oxygenase-1 (HO-1), NAD(P)H:quinone oxidoreductase 1 (NQO1), and glutathione-related enzymes.[142][143]In vitro studies consistently show flavonoids quenching ROS in various cell models, such as endothelial and neuronal cells, thereby reducing markers of oxidative stress like lipid peroxidation and protein carbonylation. For instance, quercetin and kaempferol have been observed to inhibit ROS production induced by hydrogen peroxide in human fibroblasts, preserving cell viability. Animal models further support these findings, with oral administration of flavonoids like apigenin decreasing systemic oxidative stress in rodents exposed to inflammatory stimuli, as measured by lowered malondialdehyde (MDA) levels and elevated total antioxidant capacity.[144][145]Human clinical trials provide evidence of flavonoids' antioxidant effects, with supplementation reducing oxidative stress biomarkers such as F2-isoprostanes and 8-hydroxydeoxyguanosine in plasma. A 2024 retrospective observational study involving flavonoid-rich interventions reported significant decreases in serumoxidative stress levels assessed via the d-ROMs test in the general population. Human trials indicate reductions in oxidative stress markers, though bioavailability influences efficacy, and clinical evidence remains mixed due to factors like absorption and metabolism. The aglycone and conjugated metabolites formed during humanmetabolism contribute to these systemic effects.[146][147]Regarding anti-inflammatory effects, flavonoids suppress inflammation by inhibiting the nuclear factor-kappa B (NF-κB) signaling pathway, preventing its translocation to the nucleus and subsequent activation of pro-inflammatory gene expression. This modulation reduces the production of cytokines such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β). Quercetin, a prototypical flavonol, exemplifies this by dose-dependently inhibiting NF-κBactivation and lowering IL-6 secretion in lipopolysaccharide-stimulated macrophages.[148][149]In vitro and in vivo evidence underscores these mechanisms, with flavonoids like luteolin blocking NF-κB in microglial cells to curb cytokine release, while rodent studies show oral quercetin attenuating paw edema and serum IL-6 elevations in models of acute inflammation. Human intervention trials, including those with citrus flavonoid extracts, demonstrate reductions in circulating C-reactive protein (CRP) and IL-6 following 4-8 weeks of supplementation at 200-500 mg/day. Reviews of randomized trials indicate benefits in reducing inflammatory markers like CRP and IL-6, with stronger effects at higher doses and in populations with elevated baseline inflammation, though evidence is mixed and further RCTs are needed.[150][151]
Cancer Prevention and Therapy
Flavonoids have garnered significant attention for their potential in cancer prevention and therapy due to their multifaceted anticarcinogenic properties observed in preclinical and epidemiological studies. These compounds, abundant in fruits, vegetables, and teas, exhibit inhibitory effects on tumor development through various molecular pathways, with particular emphasis on gastrointestinal (GI) cancers in recent research. For instance, dietary flavonoids such as quercetin and kaempferol have shown promise in reducing the incidence and progression of colorectal cancer by modulating cellular processes that hinder carcinogenesis.[152][153]Key mechanisms underlying the anticancer effects of flavonoids include the induction of apoptosis and inhibition of angiogenesis. Flavonoids like genistein, an isoflavone found in soy, promote programmed cell death in cancer cells by activating caspase pathways and upregulating pro-apoptotic proteins such as Bax, while downregulating anti-apoptotic Bcl-2. In terms of angiogenesis, genistein specifically suppresses vascular endothelial growth factor (VEGF)-induced endothelial cell activation by decreasing protein tyrosine kinase activity and mitogen-activated protein kinase (MAPK) signaling, thereby limiting tumor vascularization and metastasis in models of prostate and breast cancers. These actions are particularly relevant for GI cancers, where flavonoids disrupt epithelial-to-mesenchymal transition and inhibit matrix metalloproteinases to prevent invasion.[154][155][156]Epidemiological evidence supports an inverse association between flavonoid intake and certain cancers, notably colorectal and prostate types. In large cohort studies, higher consumption of flavonols and flavones has been linked to a 20-30% reduced risk of colorectal cancer, with prospective data from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort showing dose-dependent protection among participants with elevated dietary levels. For prostate cancer, meta-analyses of cohort studies indicate that increased intake of isoflavones like genistein correlates with lower incidence, particularly in Asian populations with habitual soy consumption, though results vary by flavonoid subclass. Updates from the Nurses' Health Study have reinforced these findings by demonstrating improved survival post-colorectal cancer diagnosis with higher flavonoid-rich food intake, such as tea and berries.[153][157][158]In therapeutic contexts, flavonoids are increasingly explored in combination with chemotherapy to enhance efficacy and mitigate resistance, with ongoing trials focusing on bioavailability-enhanced formulations. For example, quercetin combined with dasatinib has shown synergistic effects in reducing senescence and improving outcomes in metastatic triple-negative breast cancer when paired with standard chemotherapy regimens, as evaluated in phase II trials initiated in 2024. Recent 2024-2025 studies on nano-encapsulated epigallocatechin gallate (EGCG) from green tea have demonstrated improved oral bioavailability, leading to enhanced apoptosis in GI cancer cell lines and reduced tumor burden in preclinical models of colorectal cancer. A notable example is EGCG's role in breast cancer risk reduction, where epidemiological data from Asian cohorts link regular green tea consumption (providing 200-400 mg EGCG daily) to a 15-25% lower incidence, attributed to its inhibition of estrogen receptor signaling and promotion of DNA demethylation in tumor suppressor genes. These advancements underscore flavonoids' potential as adjuncts in oncology, particularly for GI malignancies, though clinical translation requires further validation through randomized controlled trials.[159][160][161]
Cardiovascular and Metabolic Benefits
Flavonoids exert beneficial effects on cardiovascular health primarily by enhancing endothelial function and promoting vasodilation through increased nitric oxide (NO) production. Endothelial cells, which line blood vessels, respond to flavonoids by upregulating endothelial nitric oxide synthase (eNOS), leading to higher NO bioavailability that relaxes vascular smooth muscle and improves blood flow. This mechanism has been demonstrated in human intervention studies where acute consumption of flavonoid-rich foods, such as black tea or dark chocolate, significantly increased flow-mediated dilation (FMD), a key marker of endothelial health, within hours of intake. Additionally, chronic flavonoid intake from diets high in fruits and vegetables has been linked to sustained improvements in endothelial function, reducing the risk of atherosclerosis progression.[162][163][164]In terms of blood pressure regulation, flavonoids contribute to modest reductions, particularly in hypertensive individuals, via NO-mediated vasodilation and inhibition of angiotensin-converting enzyme (ACE) activity. Meta-analyses of randomized controlled trials (RCTs) indicate that daily intake of flavonoid-rich cocoa flavanols (e.g., 500-1000 mg epicatechin equivalents) lowers systolic blood pressure by 2-4 mmHg on average, with greater effects in those with baseline hypertension. For instance, long-term supplementation with cocoa extract in older adults reduced cardiovascular disease (CVD) mortality by 27%, though overall hypertension incidence was not significantly altered in normotensive subgroups. These effects are attributed to flavanols' ability to enhance NO synthesis in the endothelium, as evidenced by increased plasma NO metabolites post-consumption.[165][166][167]On the metabolic front, flavonoids promote insulin sensitization and lipid lowering, mitigating risks for type 2 diabetes and dyslipidemia. Compounds like naringenin, found in citrus fruits, activate AMP-activated protein kinase (AMPK), a central regulator of energy homeostasis, which enhances glucose uptake in skeletal muscle and adipocytes while suppressing hepatic gluconeogenesis. This leads to improved insulin sensitivity, as shown in high-fat diet models where naringenin supplementation reduced insulin resistance by 20-30% and lowered plasma triglycerides. Soy isoflavones, such as genistein, support glycemic control by modulating insulin signaling pathways; meta-analyses of RCTs report modest improvements in fasting plasma glucose and insulin levels in patients with type 2 diabetes, alongside reductions in LDL cholesterol, though results are mixed and further studies are needed. These metabolic benefits are compounded by flavonoids' role in attenuating postprandial glucose spikes through inhibition of carbohydrate-digesting enzymes.[168][169]Epidemiological evidence from large cohort studies and RCTs underscores that flavonoid-rich diets reduce CVD risk by 10-20%, with highest benefits observed at intakes exceeding 300 mg/day from diverse sources. For example, prospective analyses show an 18% lower risk of fatal CVD events in individuals with the highest total flavonoid consumption compared to the lowest quartile. Recent 2025 research highlights the importance of intakediversity across flavonoid subclasses (e.g., flavanols, flavonols, isoflavones), associating greater variety with 15-25% reduced risks of metabolic syndrome components like hypertension and hyperglycemia, independent of total quantity. These findings are supported by RCTs demonstrating that diverse flavonoid interventions, such as Mediterranean-style diets emphasizing berries, tea, and soy, improve composite CVD risk scores over 6-12 months.[162][123][170]
Emerging Areas: Anti-aging and Nanotechnology
Flavonoids have shown potential in anti-aging research through mechanisms such as sirtuin activation and telomere protection. Quercetin, a prominent flavonol, activates SIRT1, a key sirtuin enzyme involved in cellular longevity pathways, by enhancing its deacetylase activity and promoting mitochondrial function in aging models.[171] Similarly, other flavonoids like kaempferol and resveratrol modulate sirtuin expression to mitigate age-related oxidative stress and inflammation.[171] In telomere protection, genistein and catechins inhibit telomerase activity while preventing telomere shortening, thereby delaying replicative senescence in human cells.[172] Rodent studies further support these effects; for instance, epicatechin supplementation extended median lifespan by 5% in male mice, alongside improvements in healthspan markers like reduced inflammation.[173] Corylin, a prenylated flavonoid, similarly prolonged mouse lifespan by activating anti-senescence pathways.[174]In nanotechnology, flavonoids are being integrated into advanced delivery systems to overcome bioavailability limitations. Nanoencapsulation techniques, such as liposomes, enhance gut delivery of flavonoids like quercetin by protecting them from degradation and improving absorption in the intestinal tract.[175] For brain penetration, quercetin-loaded nanoliposomes have demonstrated superior crossing of the blood-brain barrier, achieving higher bioavailability and neuroprotective effects in Alzheimer's disease models compared to free quercetin.[176] These formulations, including nano-quercetin with lipid carriers, also boost stability and targeted efficacy in preclinical studies.[177]Emerging frontiers include flavonoid modulation of the gut microbiome. Dietary quercetin alters gut microbiota composition, increasing beneficial bacteria like Akkermansia and reducing inflammation-associated taxa, which supports metabolic health.[178]Challenges in clinical translation persist, including variable bioavailability and long-term safety concerns. Recent 2025 reviews highlight the need for optimized formulations to address pharmacokinetic barriers, while toxicity profiles indicate low risk at dietary doses but potential interactions requiring further human trials.[179] Safety assessments emphasize monitoring for off-target effects in chronic use, underscoring gaps in large-scale clinical data.[180]
Analytical and Synthetic Methods
Detection Techniques
Detection of flavonoids often begins with simple colorimetric tests that provide preliminary qualitative identification based on color changes indicative of their chemical structures. The Shinoda test involves treating a sample with magnesium powder and concentrated hydrochloric acid, resulting in a magenta or pink coloration for catechins and related flavonoids due to the reduction of flavones to anthocyanidins.[181] Similarly, the sodium hydroxide test uses dilute NaOH solution, which produces a yellow color shift in samples containing flavonoids with phenolic hydroxyl groups, attributable to the deprotonation and extended conjugation in the chromophore.[181] For proanthocyanidins, a subclass of flavonoids, the p-dimethylaminocinnamaldehyde (DMACA) test employs this reagent in acidic conditions to yield a blue or purple color through reaction with the A-ring, confirming their presence in plant tissues or extracts.[182]Spectroscopic methods offer more specific qualitative detection by exploiting the chromophoric properties of flavonoids. Ultraviolet-visible (UV-Vis) spectroscopy detects the characteristic absorption bands of flavonoids, typically Band II (240-280 nm) from the benzoyl system and Band I (300-380 nm) from the cinnamoyl system, allowing identification of subclasses like flavonols or flavones based on wavelength shifts influenced by substituents.[183]Fluorescence spectroscopy is particularly useful for flavonols, which exhibit native fluorescence under UV excitation (around 360-370 nm) with emission at 450-520 nm due to their rigid planar structure and hydroxyl groups at C3, enabling detection in complex matrices without derivatization.[184]Chromatographic techniques separate flavonoids for qualitative identification based on their polarity and structural differences. Thin-layer chromatography (TLC) uses silica gel plates with solvent systems like ethyl acetate-formic acid-water, where flavonoids appear as fluorescent spots under UV light or colored zones after spraying with reagents like natural products/polyethylene glycol, distinguishing subclasses by Rf values correlated to polarity.[185]High-performance liquid chromatography (HPLC) employs reversed-phase columns (e.g., C18) with gradientelution in methanol-water or acetonitrile-water mobile phases, separating flavonoids by hydrophobicity; detection via UV absorbance or fluorescence confirms identity through retention times matching standards.[185]In recent years, liquid chromatography-mass spectrometry (LC-MS) has become a standard for confirming flavonoid subgroups qualitatively, combining separation with mass spectral fragmentation patterns. High-resolution LC-MS, often using electrospray ionization (ESI) in negative mode, identifies specific flavonoids by accurate mass (e.g., m/z 301 for quercetin) and diagnostic fragments like loss of sugar moieties or retro-Diels-Alder cleavages, as demonstrated in 2020s protocols for plant and food analyses.[186]
Quantification and Structural Analysis
Quantification of flavonoids typically involves chromatographic techniques such as high-performance liquid chromatography (HPLC) coupled with ultraviolet (UV) or diode array detection (DAD), which enable the measurement of total flavonoid content in complex matrices like plant extracts and food samples.[187] These methods separate flavonoids based on their polarity and detect them at wavelengths around 280-370 nm, allowing for accurate determination of individual or total concentrations without prior derivatization.[188] For instance, reversed-phase HPLC-UV/DAD has been widely applied to quantify flavonoids in fruits and vegetables, providing reproducible results for routine analysis.[189]Structural analysis of flavonoids relies on advanced spectroscopic techniques, including nuclear magnetic resonance (NMR) and mass spectrometry (MS), to elucidate molecular structures and confirm identities. High-resolution MS, often in tandem with liquid chromatography (LC-MS), provides molecular weight and fragmentation patterns that distinguish flavonoid subclasses, while NMR spectroscopy, particularly 2D techniques like heteronuclear multiple bond correlation (HMBC), reveals connectivity and substitution patterns such as glycoside positions on the flavonoid backbone.[190] For example, HMBC correlations are essential for assigning the anomeric configuration and linkage sites in flavonoid glycosides isolated from plant sources.[191] These methods complement each other, with MS offering high sensitivity for trace-level detection and NMR providing unambiguous structural proof.[192]Calibration standards for total flavonoid quantification commonly use quercetin equivalents, where sample absorbance is compared against a quercetin calibration curve to express results in milligrams of quercetin per gram of sample.[187] This approach accounts for the structural diversity of flavonoids while standardizing measurements across studies. Limits of detection (LOD) and quantification (LOQ) for HPLC-based methods in food analysis typically range from 0.09-0.49 mg/kg for major flavonols like quercetin and kaempferol, ensuring suitability for low-concentration samples such as processed foods.[193]In practical applications, these quantification and structural analysis techniques validate flavonoid content in dietary supplements, ensuring label accuracy and compliance with regulatory standards through methods like UHPLC-UV.[194] Similarly, in plant breeding programs, HPLC quantification screens genotypes for high flavonoid accumulation, facilitating the selection of cultivars with enhanced nutritional profiles, as demonstrated in legume and blueberry breeding efforts.[195][196]Recent advancements include AI-assisted interpretation of MS data, which automates fragmentation pattern analysis for flavonoid identification, improving efficiency in large-scale metabolomics studies as reported in 2024 machine learning applications for mass spectrometry.[197] This integration enhances structural elucidation by predicting spectral features from databases, reducing manual effort in complex sample profiling.[198]
Synthesis and Biotechnological Production
Flavonoids can be synthesized chemically through total synthesis starting from simple phenolic compounds, enabling the construction of the core flavan skeleton. One prominent method is the Baker-Venkataraman rearrangement, where o-hydroxyacetophenones, derived from phenols, undergo base-catalyzed acylation to form 1,3-diketones, followed by acid-catalyzed cyclization to yield flavones.[199] This approach allows stereoselective control and has been applied to synthesize complex flavones like apigenin. The Allan-Robinson reaction provides an alternative, involving the condensation of o-hydroxyaryl ketones with aromatic anhydrides under basic conditions to directly form flavones, offering efficiency for polyhydroxylated derivatives. Additionally, the Kostanecki acylation utilizes phenols reacted with acid chlorides and anhydrides to produce flavone esters, which are then cyclized, facilitating the introduction of substituents early in the process. These methods, while effective for laboratory-scale production, often require multiple steps and harsh conditions.[199]Semi-synthetic approaches modify naturally occurring flavonoids as precursors to generate analogs with enhanced properties, such as improved bioavailability. For instance, methylation of quercetin using chemical agents like dimethyl sulfate or enzymatic methyltransferases produces tamarixetin (quercetin-3'-O-methyl ether), which exhibits greater metabolic stability.[200] Another example is the semi-synthesis of diosmin from hesperidin, involving selective oxidation at the 5-hydroxy group followed by glycosylation, yielding a rutinoside derivative used in vascular treatments. These modifications leverage the abundance of plant-extracted flavonoids to create targeted variants efficiently.[201]Biotechnological production employs engineered microorganisms to biosynthesize flavonoids, mimicking natural pathways for sustainable output. In Escherichia coli and Saccharomyces cerevisiae, heterologous expression of plant genes such as chalconesynthase (CHS) initiates the pathway from phenylalanine or simple carbon sources, converting them into core flavonoids like naringenin. Recent optimizations, including genome-scale engineering and enzyme screening, have boosted yields; for example, engineered E. coli produced 153 mg/L of pinostrobin, a methylated flavanone, through co-expression of CHS and a 7-O-methyltransferase. Further advancements in 2024-2025 achieved up to 1,500 mg/L for certain glycosylatedflavanones by integrating efflux pumps and pathway balancing. These microbial systems enable post-synthetic alterations, such as glycosylation via glycosyltransferases to attach glucose or rhamnose, enhancing solubility, or halogenation through co-expressed halogenases to create fluorinated or chlorinated analogs for improved bioactivity.[202][203]Compared to traditional plant extraction, biotechnological methods offer scalability for pharmaceutical applications and environmental benefits, reducing reliance on agriculture and minimizing solvent use. Yields from microbial fermentation surpass the low efficiencies of extraction (often <1% from plant material), while avoiding seasonal fluctuations and habitat disruption. This approach supports eco-friendly production of high-purity flavonoids for drug development.[204]