Luteolin

Luteolin at a Glance

Luteolin is a dietary flavone found in celery, thyme and green pepper — quercetin minus one hydroxyl, and the 3’-hydroxy sibling of apigenin.

It is one of the more compelling preclinical molecules in this class, with a signature mast-cell-stabilising property that underlies its anti-allergic and neuroinflammation work.

Its human record sits almost entirely in PEA-luteolin combinations, studied for post-viral smell loss and neuroinflammatory conditions — where palmitoylethanolamide, not luteolin, drives the effect. No rigorous trial of isolated luteolin exists.

What It's Used For

Luteolin is a dietary flavone — structurally quercetin minus one hydroxyl (the 3-OH), and the 3′-hydroxy sibling of apigenin — with an evidence profile that mirrors kaempferol’s: a compelling preclinical molecule with a near-empty human cabinet. There is no rigorous, adequately-powered randomized trial of isolated luteolin for any indication. The only RCT-grade human data come from PEA-luteolin combination products, in which the primary active is palmitoylethanolamide (PEA) and luteolin a minor co-formulant ^{1,2Reference 1Di Stadio A et al. · 2022RCTUltramicronized palmitoylethanolamide and luteolin supplement combined with olfactory training to treat post-COVID-19 olfactory impairment — a multicentre double-blinded randomised placebo-controlled clinical trialView study →Reference 2Di Stadio A et al. · 2023RCTTreatment of COVID-19 olfactory dysfunction with olfactory training, palmitoylethanolamide with luteolin, or combined therapy — a blinded controlled multicentre randomised trialView study →}.

The autism data are one group’s open-label work on a luteolin+quercetin+rutin blend ^{7Reference 7Taliou A et al. · 2013An open-label pilot study of a formulation containing the anti-inflammatory flavonoid luteolin and its effects on behaviour in children with autism spectrum disordersView study →}.

Luteolin’s most-cited property — mast-cell stabilization — is entirely bench-level in humans ^{5Reference 5Tsilioni I · 2024Luteolin is more potent than cromolyn in its ability to inhibit mediator release from cultured human mast cellsView study →}.

All of it is undercut by poor, variable bioavailability: what circulates is sub-micromolar conjugate, not the free aglycone that drives the cell studies ^{14,17,18Reference 14Shimoi K et al. · 1998AnimalIntestinal absorption of luteolin and luteolin 7-O-β-glucoside in rats and humansView study →Reference 17Taheri Y et al. · 2021Paving luteolin therapeutic potentialities and agro-food-pharma applications — emphasis on in-vivo pharmacological effects and bioavailability traitsView study →Reference 18Kaci H et al. · 2023Interaction of luteolin, naringenin and their sulfate and glucuronide conjugates with human serum albumin, CYP (2C9, 2C19, 3A4) enzymes and OATP transportersView study →}.

Evidence by IndicationStrength of support · Beta

Support is an experimental score I’m building — a composite weighted by study type (human > animal > in vitro > review) and study volume, tempered for isolate-vs-formulation match and bioavailability. It’s a beta: a fast way to rank strength of evidence at a glance, not a validated metric. For luteolin every score is capped low — there is no isolate RCT, so even the best “human” evidence is a combination product or an intake association. Each application links to its write-up.

01Post-viral smell loss (PEA-luteolin)Shaky35%Multicenter RCTs — but of a PEA-luteolin combination, PEA-primary ^{1,2Reference 1Di Stadio A et al. · 2022RCTUltramicronized palmitoylethanolamide and luteolin supplement combined with olfactory training to treat post-COVID-19 olfactory impairment — a multicentre double-blinded randomised placebo-controlled clinical trialView study →Reference 2Di Stadio A et al. · 2023RCTTreatment of COVID-19 olfactory dysfunction with olfactory training, palmitoylethanolamide with luteolin, or combined therapy — a blinded controlled multicentre randomised trialView study →}

02Anti-allergic & mast-cellShaky25%Potent in human mast cells in vitro; zero human trials ^{5,6Reference 5Tsilioni I · 2024Luteolin is more potent than cromolyn in its ability to inhibit mediator release from cultured human mast cellsView study →Reference 6Kempuraj D et al. · 2008Luteolin inhibits myelin basic protein-induced human mast cell activation and mast-cell-dependent stimulation of Jurkat T cellsView study →}

03Autism & neuroinflammationShaky20%One group’s open-label combination-formulation pilots ^{7,8Reference 7Taliou A et al. · 2013An open-label pilot study of a formulation containing the anti-inflammatory flavonoid luteolin and its effects on behaviour in children with autism spectrum disordersView study →Reference 8Tsilioni I et al. · 2015Children with autism spectrum disorders who improved with a luteolin-containing dietary formulation show reduced serum levels of TNF and IL-6View study →}

04Dietary epidemiology & anticancerShaky15%Observational intake associations + preclinical mechanism ^{9,12Reference 9Yao X et al. · 2024Dietary intake of luteolin is negatively associated with all-cause and cardiovascular mortality in chronic kidney disease patientsView study →Reference 12Lin Y et al. · 2008ReviewLuteolin, a flavonoid with potential for cancer prevention and therapy — reviewView study →}

Mechanisms

Most of these are shown at 5–50 µM of free aglycone — well above the sub-µM free plasma levels luteolin reaches in people (see Pharmacokinetics), so mechanism-to-clinic translation should be cautious.

Pharmacokinetics

Luteolin is a textbook case of bench promise throttled by poor pharmacokinetics. In plants it is mostly a glycoside (luteolin-7-O-glucoside/cynaroside, luteolin-7-O-rutinoside), and the sugar dictates absorption site — the glucoside is absorbed only after hydrolysis to the aglycone, and luteolin is glucuronidated essentially at the moment it crosses the mucosa ^{14Reference 14Shimoi K et al. · 1998AnimalIntestinal absorption of luteolin and luteolin 7-O-β-glucoside in rats and humansView study →}. So the circulating species are conjugates, not free aglycone: plasma luteolin is recovered overwhelmingly as glucuronides and sulfates, and it is only “seen” analytically after enzymatic deconjugation. Species differ — glucuronides dominate in rats, whereas luteolin-3′-O-sulfate is the main form in humans given the aglycone ^{15Reference 15Hayasaka N et al. · 2018AnimalAbsorption and metabolism of luteolin in rats and humans in relation to in-vitro anti-inflammatory effectsView study →}, a caution against reading human exposure off rodent data — and the disposition is governed by the interplay of UGT and COMT ^{16Reference 16Wang L et al. · 2017AnimalMetabolic disposition of luteolin is mediated by the interplay of UDP-glucuronosyltransferases and catechol-O-methyltransferases in ratsView study →}.

Quantitatively the picture is low and brief: in humans given an artichoke-type extract, total luteolin peaked at only ~0.2–0.55 µM at ~30–40 min with a half-life of ~2–3 h ^{17Reference 17Taheri Y et al. · 2021Paving luteolin therapeutic potentialities and agro-food-pharma applications — emphasis on in-vivo pharmacological effects and bioavailability traitsView study →}. This is the load-bearing in-vitro-vs-in-vivo gap: most of luteolin’s published activity is demonstrated at 5–50 µM of free aglycone, but oral dosing yields only sub-micromolar total luteolin, of which the pharmacologically relevant free aglycone is a small, often undetectable fraction — and the circulating conjugates are much weaker at luteolin’s targets than the parent ^{18Reference 18Kaci H et al. · 2023Interaction of luteolin, naringenin and their sulfate and glucuronide conjugates with human serum albumin, CYP (2C9, 2C19, 3A4) enzymes and OATP transportersView study →}. Concentrations that drive effects in a dish are, for the most part, not reached at the tissue after oral dosing.

Clinical trials

Luteolin has no completed efficacy trial as an isolated molecule — the defining fact of its evidence base. The only randomized human data are of PEA-luteolin combinations (PEA-primary); the autism work is open-label combination pilots; everything else is dietary-intake epidemiology or preclinical.

Efficacy trials (isolate)	Combination-product trials	Dietary epidemiology	Preclinical
None	PEA-luteolin RCTs; NeuroProtek open-label	Several cohorts	Extensive

Last checked: July 2026.

Monoamine oxidase (MAO) inhibition

Luteolin is a MAO-A-preferring flavone inhibitor: in isolated-enzyme work it inhibited MAO-A with an IC50 around 5 µM, versus roughly 60 µM for MAO-B ^{13Reference 13Han XH et al. · 2007Monoamine oxidase inhibitory components from Cayratia japonicaView study →}. As with the other dietary flavonoids the activity is real but modest next to the β-carbolines, and — given luteolin’s low systemic and brain exposure — is best read as an in-vitro property. See the natural MAO inhibitors guide for the comparison.

Isolate vs. Plant Studies

Luteolin’s evidence is rarely about pure luteolin, in three senses. The human trials are of something else: the RCT-grade data are PEA-luteolin combinations (PEA-driven), and the autism data a luteolin+quercetin+rutin blend — the isolate itself is untested ^{1,7Reference 1Di Stadio A et al. · 2022RCTUltramicronized palmitoylethanolamide and luteolin supplement combined with olfactory training to treat post-COVID-19 olfactory impairment — a multicentre double-blinded randomised placebo-controlled clinical trialView study →Reference 7Taliou A et al. · 2013An open-label pilot study of a formulation containing the anti-inflammatory flavonoid luteolin and its effects on behaviour in children with autism spectrum disordersView study →}. In plants it is a glycoside, not the aglycone (cynaroside and others), which absorbs differently and is what a “luteolin-containing” herb delivers ^{14Reference 14Shimoi K et al. · 1998AnimalIntestinal absorption of luteolin and luteolin 7-O-β-glucoside in rats and humansView study →}. And across this database luteolin is named in the flavonoid fraction of many herbs — globe artichoke, chinese-skullcap, yarrow, holy basil, dandelion — usually as a whole-extract contributor. The best-worked example is artichoke’s cholesterol-lowering effect: later work attributed part of the de novo hepatic-cholesterol-synthesis inhibition specifically to luteolin (~30–80% in hepatocytes), alongside the herb’s choleretic action, with the lipid effect confirmed in a whole-herb randomized trial — so luteolin is a plausible active, but the human proof is for the extract, not the molecule ^{19Reference 19Kraft K · 1997Artichoke leaf extract — recent findings reflecting effects on lipid metabolism, liver and gastrointestinal tractsView study →}. Two housekeeping cautions: several repo “luteolin” findings are actually distinct glycosides (cynaroside; orientin = luteolin-8-C-glucoside is a separate molecule), and luteolin is not lutein (the unrelated carotenoid) — do not merge them.

Prevalence in Nature

Luteolin is one of the two most widespread dietary flavones (apigenin being the other), occurring overwhelmingly as O-glycosides — chiefly luteolin-7-O-glucoside (cynaroside) and luteolin-7-O-rutinoside — rather than the free aglycone ^{20Reference 20Muruganathan N et al. · 2022ReviewRecent updates on source, biosynthesis, and therapeutic potential of natural flavonoid luteolin — a reviewView study →}. It concentrates in the Lamiaceae culinary herbs (oregano, thyme, sage, peppermint, rosemary), some Apiaceae (celery and celery seed), and Asteraceae (artichoke, chamomile, chrysanthemum), plus sweet peppers ^{20,23Reference 20Muruganathan N et al. · 2022ReviewRecent updates on source, biosynthesis, and therapeutic potential of natural flavonoid luteolin — a reviewView study →Reference 23U.S et al. · 2014U.S. Department of Agriculture, Agricultural Research Service. USDA Database for the Flavonoid Content of Selected Foods, Release 3.1 (2014) — luteolin, mg/100 g. https://www.ars.usda.gov/arsuserfiles/80400525/data/flav/flav_r03-1.pdfView study →}. The dominant quantitative caveat is basis: dried herbs and seeds carry 100–1000× more luteolin per 100 g than fresh vegetables, because drying removes water and concentrates the flavone — Mexican dried oregano runs ~1,029 mg/100 g and celery seed ~762 mg/100 g, versus ~1 mg/100 g for fresh oregano or a raw celery stalk ^{21,22,23Reference 21Lin LZ et al. · 2007Identification and quantification of flavonoids of Mexican oregano (Lippia graveolens) by LC-DAD-ESI/MS analysisView study →Reference 22Lin LZ et al. · 2007Detection and quantification of glycosylated flavonoid malonates in celery, Chinese celery, and celery seed by LC-DAD-ESI/MSView study →Reference 23U.S et al. · 2014U.S. Department of Agriculture, Agricultural Research Service. USDA Database for the Flavonoid Content of Selected Foods, Release 3.1 (2014) — luteolin, mg/100 g. https://www.ars.usda.gov/arsuserfiles/80400525/data/flav/flav_r03-1.pdfView study →}. The Content-by-Source chart below therefore shows only the comparable fresh herbs and vegetables; the dried outliers would render the fresh bars invisible. (Note parsley and celery stalk are luteolin-poor but apigenin-rich, so parsley is deliberately omitted despite its “flavone herb” reputation.)

Biosynthetically, luteolin is a flavone from the phenylpropanoid → flavonoid pathway: naringenin is desaturated by flavone synthase to apigenin, and flavonoid 3′-hydroxylase adds the B-ring 3′-OH to give luteolin (or acts earlier, via eriodictyol) ^{20Reference 20Muruganathan N et al. · 2022ReviewRecent updates on source, biosynthesis, and therapeutic potential of natural flavonoid luteolin — a reviewView study →}. Structurally this makes luteolin the 3′-hydroxy analogue of apigenin and the flavone (3-deoxy) analogue of the flavonol quercetin — quercetin is simply luteolin plus a 3-OH. There is essentially no non-plant source.

Discovery & Synthesis

The name is literally “little yellow.” Luteolin derives from Latin luteus (“yellow”) via the diminutive luteolus, and reached chemistry through the plant weld (Reseda luteola, also “dyer’s rocket”) — one of the oldest European sources of a clear, lightfast yellow dye for wool and silk, of which luteolin is the principal colorant ^{20Reference 20Muruganathan N et al. · 2022ReviewRecent updates on source, biosynthesis, and therapeutic potential of natural flavonoid luteolin — a reviewView study →}. The compound is commonly credited to the French chemist Michel-Eugène Chevreul, who isolated and named it in 1829 — an attribution well documented in historical sources but not verifiable against a primary indexed record, so treat the exact 1829 date as reported rather than settled.

Structurally luteolin is a flavone (2-phenylchromen-4-one) bearing four hydroxyls — 3′,4′,5,7-tetrahydroxyflavone (C₁₅H₁₀O₆) — with the catechol B-ring that COMT methylates in vivo. Commercially it is produced almost entirely by extraction from plant biomass, not total synthesis: common feedstocks include peanut hulls/skins (a cheap luteolin-rich agro-waste), Reseda luteola, Perilla and chamomile, with the aglycone typically freed by hydrolyzing native glycosides during processing ^{20Reference 20Muruganathan N et al. · 2022ReviewRecent updates on source, biosynthesis, and therapeutic potential of natural flavonoid luteolin — a reviewView study →}.

Patents: not yet researched (future patent-loop pass).

Toxicity & Safety

Luteolin is a widespread dietary flavone (celery, parsley, thyme, chamomile, peppers) with no signal of dietary harm and good tolerability in animals, but isolated-compound human safety data are thin — the main human exposure is a 26-week open tolerability study of a luteolin-containing formulation in children, where transient irritability was the main effect. So it is presumed low-toxicity as a food component, while the high-dose isolate lacks a rigorous safety package. One in-vitro flag for balance: luteolin’s genotoxic potential in human lymphoblastoid cells was enhanced by CYP1A1/1A2 bioactivation — a cell-line observation, not evidence of dietary harm, but an argument against assuming “natural = inert” at concentrated doses ^{26Reference 26Li X et al. · 2021The genotoxicity potential of luteolin is enhanced by CYP1A1 and CYP1A2 in human lymphoblastoid TK6 cellsView study →}.

On interactions: luteolin is an in-vitro CYP inhibitor, most potent at CYP1A (CYP1A1/1A2) with weaker activity at CYP3A4/2C9 ^{24Reference 24Breinholt VM et al. · 2002In vitroIn vitro investigation of cytochrome P450-mediated metabolism of dietary flavonoids (luteolin among the more potent CYP1A inhibitors)View study →} — but the IC50s exceed the sub-µM free-aglycone levels oral dosing achieves, and the circulating conjugates are only weak CYP inhibitors ^{18Reference 18Kaci H et al. · 2023Interaction of luteolin, naringenin and their sulfate and glucuronide conjugates with human serum albumin, CYP (2C9, 2C19, 3A4) enzymes and OATP transportersView study →}, so a clinically meaningful interaction from food is unlikely and only a theoretical caution stands for concentrated supplements (especially with narrow-index CYP1A2/3A4 substrates). Luteolin also behaves as a P-glycoprotein substrate (part of why absorption is poor). Its endocrine activity is genuinely mixed — an estrogen-receptor agonist in some assays and anti-estrogenic in others, i.e. weak and biphasic — relevant to hormone-sensitive contexts ^{25Reference 25Nordeen SK et al. · 2013Endocrine-disrupting activities of the flavonoid nutraceuticals luteolin and quercetinView study →}.

Dosage

There is no evidence-based dose of isolated luteolin, because no trial has tested it. The only human dosing data are for PEA-luteolin combination products (where PEA is the primary active, luteolin a co-formulant, typically tens of milligrams) and the open-label autism formulation (~100 mg luteolin per 10 kg body weight/day, in a blend) ^{1,7Reference 1Di Stadio A et al. · 2022RCTUltramicronized palmitoylethanolamide and luteolin supplement combined with olfactory training to treat post-COVID-19 olfactory impairment — a multicentre double-blinded randomised placebo-controlled clinical trialView study →Reference 7Taliou A et al. · 2013An open-label pilot study of a formulation containing the anti-inflammatory flavonoid luteolin and its effects on behaviour in children with autism spectrum disordersView study →}. Dietary intake from herbs and vegetables is far lower and, given the poor and conjugation-limited absorption, produces only sub-micromolar plasma levels ^{17Reference 17Taheri Y et al. · 2021Paving luteolin therapeutic potentialities and agro-food-pharma applications — emphasis on in-vivo pharmacological effects and bioavailability traitsView study →}.

These are descriptive figures from combination-product research and are not a recommendation — no dose of isolated luteolin has been shown to do anything in a human trial. Anyone considering a concentrated supplement should note the CYP1A/estrogenic signals above and seek professional guidance.

References

1. Di Stadio A, D’Ascanio L, Vaira LA, et al. (2022). Ultramicronized palmitoylethanolamide and luteolin supplement combined with olfactory training to treat post-COVID-19 olfactory impairment — a multicentre double-blinded randomised placebo-controlled clinical trial. Current Neuropharmacology, 20(10), 2001–2012. https://pubmed.ncbi.nlm.nih.gov/35450527/
2. Di Stadio A, Gallina S, Cocuzza S, et al. (2023). Treatment of COVID-19 olfactory dysfunction with olfactory training, palmitoylethanolamide with luteolin, or combined therapy — a blinded controlled multicentre randomised trial. European Archives of Oto-Rhino-Laryngology, 280(11), 4949–4961. https://pubmed.ncbi.nlm.nih.gov/37380908/
3. D’Ascanio L, Vitelli F, Cingolani C, et al. (2021). Randomised clinical trial “olfactory dysfunction after COVID-19 — olfactory rehabilitation therapy vs. intervention treatment with palmitoylethanolamide and luteolin”: preliminary results. European Review for Medical and Pharmacological Sciences, 25(11), 4156–4162. https://pubmed.ncbi.nlm.nih.gov/34156697/
4. Bonzanino M, Riolo M, Battaglini I, et al. (2024). PEALut in the dietary management of patients with acute ischaemic stroke — a prospective randomised controlled clinical trial. Journal of Clinical Medicine, 13(2), 509. https://pubmed.ncbi.nlm.nih.gov/38256644/
5. Tsilioni I, Theoharides TC. (2024). Luteolin is more potent than cromolyn in its ability to inhibit mediator release from cultured human mast cells. International Archives of Allergy and Immunology, 185(6), 587–594. https://pubmed.ncbi.nlm.nih.gov/38588651/
6. Kempuraj D, Tagen M, Iliopoulou BP, et al. (2008). Luteolin inhibits myelin basic protein-induced human mast cell activation and mast-cell-dependent stimulation of Jurkat T cells. British Journal of Pharmacology, 155(7), 1076–1084. https://pubmed.ncbi.nlm.nih.gov/18806808/
7. Taliou A, Zintzaras E, Lykouras L, Francis K. (2013). An open-label pilot study of a formulation containing the anti-inflammatory flavonoid luteolin and its effects on behaviour in children with autism spectrum disorders. Clinical Therapeutics, 35(5), 592–602. https://pubmed.ncbi.nlm.nih.gov/23688534/
8. Tsilioni I, Taliou A, Francis K, Theoharides TC. (2015). Children with autism spectrum disorders who improved with a luteolin-containing dietary formulation show reduced serum levels of TNF and IL-6. Translational Psychiatry, 5(9), e647. https://pubmed.ncbi.nlm.nih.gov/26418275/
9. Yao X, et al. (2024). Dietary intake of luteolin is negatively associated with all-cause and cardiovascular mortality in chronic kidney disease patients. BMC Public Health, 24, 2019. https://pubmed.ncbi.nlm.nih.gov/39080632/
10. Zhang W, et al. (2023). Luteolin intake is negatively associated with all-cause and cardiac mortality among patients with type 2 diabetes mellitus. Diabetology & Metabolic Syndrome, 15, 59. https://pubmed.ncbi.nlm.nih.gov/36966325/
11. Gates MA, Tworoger SS, Hecht JL, et al. (2007). A prospective study of dietary flavonoid intake and incidence of epithelial ovarian cancer. International Journal of Cancer, 121(10), 2225–2232. https://pubmed.ncbi.nlm.nih.gov/17471564/
12. Lin Y, Shi R, Wang X, Shen HM. (2008). Luteolin, a flavonoid with potential for cancer prevention and therapy — review. Current Cancer Drug Targets, 8(7), 634–646. https://pubmed.ncbi.nlm.nih.gov/18991571/
13. Han XH, Hong SS, Hwang JS, Lee MK, Hwang BY, Ro JS. (2007). Monoamine oxidase inhibitory components from Cayratia japonica. Archives of Pharmacal Research, 30(1), 13–17. https://pubmed.ncbi.nlm.nih.gov/17328236/
14. Shimoi K, Okada H, Furugori M, et al. (1998). Intestinal absorption of luteolin and luteolin 7-O-β-glucoside in rats and humans. FEBS Letters, 438(3), 220–224. https://pubmed.ncbi.nlm.nih.gov/9827549/
15. Hayasaka N, Shimizu N, Komoda T, et al. (2018). Absorption and metabolism of luteolin in rats and humans in relation to in-vitro anti-inflammatory effects. Journal of Agricultural and Food Chemistry, 66(43), 11320–11329. https://pubmed.ncbi.nlm.nih.gov/30280574/
16. Wang L, Chen Q, Zhu L, et al. (2017). Metabolic disposition of luteolin is mediated by the interplay of UDP-glucuronosyltransferases and catechol-O-methyltransferases in rats. Drug Metabolism and Disposition, 45(3), 306–315. https://pubmed.ncbi.nlm.nih.gov/28031430/
17. Taheri Y, Sharifi-Rad J, Antika G, et al. (2021). Paving luteolin therapeutic potentialities and agro-food-pharma applications — emphasis on in-vivo pharmacological effects and bioavailability traits. Oxidative Medicine and Cellular Longevity, 2021, 1987588. https://pubmed.ncbi.nlm.nih.gov/34594472/
18. Kaci H, Bodnárová S, Fliszár-Nyúl E, et al. (2023). Interaction of luteolin, naringenin and their sulfate and glucuronide conjugates with human serum albumin, CYP (2C9, 2C19, 3A4) enzymes and OATP transporters. Biomedicine & Pharmacotherapy, 157, 114078. https://pubmed.ncbi.nlm.nih.gov/36481402/
19. Kraft K. (1997). Artichoke leaf extract — recent findings reflecting effects on lipid metabolism, liver and gastrointestinal tracts. Phytomedicine, 4(4), 369–378. https://doi.org/10.1016/S0944-7113(97)80049-9
20. Muruganathan N, Dhanapal AR, Baskar V, et al. (2022). Recent updates on source, biosynthesis, and therapeutic potential of natural flavonoid luteolin — a review. Metabolites, 12(11), 1145. https://pubmed.ncbi.nlm.nih.gov/36422285/
21. Lin LZ, Mukhopadhyay S, Robbins RJ, Harnly JM. (2007). Identification and quantification of flavonoids of Mexican oregano (Lippia graveolens) by LC-DAD-ESI/MS analysis. Journal of Food Composition and Analysis, 20(5), 361–369. https://pubmed.ncbi.nlm.nih.gov/24812440/
22. Lin LZ, Lu S, Harnly JM. (2007). Detection and quantification of glycosylated flavonoid malonates in celery, Chinese celery, and celery seed by LC-DAD-ESI/MS. Journal of Agricultural and Food Chemistry, 55(4), 1321–1326. https://pubmed.ncbi.nlm.nih.gov/17253711/
23. U.S. Department of Agriculture, Agricultural Research Service. USDA Database for the Flavonoid Content of Selected Foods, Release 3.1 (2014) — luteolin, mg/100 g. https://www.ars.usda.gov/arsuserfiles/80400525/data/flav/flav_r03-1.pdf
24. Breinholt VM, Offord EA, Brouwer C, et al. (2002). In vitro investigation of cytochrome P450-mediated metabolism of dietary flavonoids (luteolin among the more potent CYP1A inhibitors). Food and Chemical Toxicology, 40(5), 609–616. https://pubmed.ncbi.nlm.nih.gov/11955666/
25. Nordeen SK, Bona BJ, Jones DN, et al. (2013). Endocrine-disrupting activities of the flavonoid nutraceuticals luteolin and quercetin. Hormones & Cancer, 4(5), 293–300. https://pubmed.ncbi.nlm.nih.gov/23836117/
26. Li X, He X, Chen S, et al. (2021). The genotoxicity potential of luteolin is enhanced by CYP1A1 and CYP1A2 in human lymphoblastoid TK6 cells. Toxicology Letters, 344, 58–68. https://pubmed.ncbi.nlm.nih.gov/33727136/

View all 26 references▾