Naringenin

Naringenin at a Glance

Naringenin is the signature citrus flavanone and the central branch point of the entire flavonoid biosynthetic pathway — nearly every flavonoid in every plant descends from it, which makes it one of the most important molecules in plant chemistry.

It also retires a famous myth. The grapefruit–drug interaction was long attributed to naringenin and its glycoside naringin. It is not: the interaction is caused by furanocoumarins, which irreversibly inhibit intestinal CYP3A4. Naringenin is innocent of the one thing most people know it for.

Most human evidence labelled “naringenin” is really grapefruit juice, citrus extract, or the glycoside naringin, with metabolic and cardiovascular endpoints predominating.

What It's Used For

Naringenin is the signature flavanone of citrus and the central branch point of the entire flavonoid pathway — the node from which flavones, flavonols and the other flavanones diverge. Its evidence, though, is dominated by two substitutions and one myth. Most human “naringenin” data are really grapefruit / citrus / orange-juice interventions or the glycoside naringin, not the pure aglycone ^{3,6Reference 3Demonty I et al. · 2010The citrus flavonoids hesperidin and naringin do not affect serum cholesterol in moderately hypercholesterolaemic men and womenView study →Reference 6Rendeiro C et al. · 2016RCTFlavanone-rich citrus beverages counteract the transient decline in postprandial endothelial function in humans — a randomised, controlled, double-masked, crossover intervention studyView study →}.

Naringin is a poorly-absorbed prodrug that gut bacteria cleave to naringenin in the colon ^{11Reference 11Erlund I et al. · 2001Plasma kinetics and urinary excretion of the flavanones naringenin and hesperetin in humans after ingestion of orange juice and grapefruit juiceView study →}.

— the myth to retire — the grapefruit–drug interaction is caused by furanocoumarins, not naringin or naringenin ^{13Reference 13Paine MF et al. · 2006A furanocoumarin-free grapefruit juice establishes furanocoumarins as the mediators of the grapefruit-juice–felodipine interactionView study →}.

The single thing tested as the pure aglycone for efficacy is one small NAFLD trial ^{1Reference 1Namkhah Z et al. · 2021RCTDoes naringenin supplementation improve lipid profile, severity of hepatic steatosis and probability of liver fibrosis in overweight/obese patients with NAFLD? A randomised, double-blind, placebo-controlled clinical trialView 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-source match and bioavailability. It’s a beta: a fast way to rank strength of evidence at a glance, not a validated metric. Scores are capped for the isolate-vs-source gap — the “Rests on” column names which molecule each really tested. Each application links to its write-up.

01Metabolic — NAFLD, lipids & glucoseShaky40%One small pure-naringenin NAFLD RCT + conflicting naringin trials ^{1,2,3Reference 1Namkhah Z et al. · 2021RCTDoes naringenin supplementation improve lipid profile, severity of hepatic steatosis and probability of liver fibrosis in overweight/obese patients with NAFLD? A randomised, double-blind, placebo-controlled clinical trialView study →Reference 2Barajas-Vega JL et al. · 2022Clinical trialNaringin reduces body weight, plasma lipids and increases adiponectin levels in patients with dyslipidemiaView study →Reference 3Demonty I et al. · 2010The citrus flavonoids hesperidin and naringin do not affect serum cholesterol in moderately hypercholesterolaemic men and womenView study →}

02Cardiovascular & endothelialShaky28%Citrus-flavanone / hesperidin RCTs — naringenin not the proven driver ^{6,7Reference 6Rendeiro C et al. · 2016RCTFlavanone-rich citrus beverages counteract the transient decline in postprandial endothelial function in humans — a randomised, controlled, double-masked, crossover intervention studyView study →Reference 7Rizza S et al. · 2011Clinical trialCitrus polyphenol hesperidin stimulates production of nitric oxide in endothelial cells while improving endothelial function and reducing inflammatory markers in patients with metabolic syndromeView study →}

03Anticancer & antiviralShaky12%Cell + animal mechanism only; no human trials ^{8,9,10Reference 8Faramarzi F et al. · 2022Meta-analysisNaringenin induces intrinsic and extrinsic apoptotic signalling pathways in cancer cells — a systematic review and meta-analysis of in-vitro and in-vivo dataView study →Reference 9Frabasile S et al. · 2017The citrus flavanone naringenin impairs dengue virus replication in human cellsView study →Reference 10Clementi N et al. · 2021In vitroNaringenin is a powerful inhibitor of SARS-CoV-2 infection in vitroView study →}

Mechanisms

Pharmacokinetics

Naringenin’s pharmacokinetics are governed by the sugar it usually arrives with. In food it is almost never the free aglycone — it is stored as naringin (7-O-neohesperidoside) and narirutin (7-O-rutinoside), whose rhamnose-containing disaccharides resist small-intestinal enzymes. Absorption is therefore deferred to the colon, where microbiota strip the sugars to release naringenin — the same colonic-deglycosylation pattern as rutin and hesperidin — giving a long lag and delayed, blunted, highly variable plasma appearance ^{11Reference 11Erlund I et al. · 2001Plasma kinetics and urinary excretion of the flavanones naringenin and hesperetin in humans after ingestion of orange juice and grapefruit juiceView study →}. Human data show it: peak plasma naringenin was ~0.6 µmol/L after orange juice and ~6 µmol/L after grapefruit juice, with large inter-individual variation and a short (~1.3–2.2 h) half-life ^{11Reference 11Erlund I et al. · 2001Plasma kinetics and urinary excretion of the flavanones naringenin and hesperetin in humans after ingestion of orange juice and grapefruit juiceView study →}. Dosing the aglycone directly bypasses the bottleneck and absorbs faster and higher (135 mg gave Cmax ~7.4 µmol/L) ^{12Reference 12Kanaze FI et al. · 2007Clinical trialPharmacokinetics of the citrus flavanone aglycones hesperetin and naringenin after single oral administration in human subjectsView study →}, with dose-proportional exposure across 150–900 mg ^{5Reference 5Rebello CJ et al. · 2020RCTSafety and pharmacokinetics of naringenin — a randomised, controlled, single-ascending-dose clinical trialView study →}.

Whatever is absorbed is rapidly glucuronidated and sulfated, so free aglycone is essentially undetectable in blood — the circulation carries naringenin glucuronides and sulfates, and urinary recovery is only a few percent of dose ^{11,12Reference 11Erlund I et al. · 2001Plasma kinetics and urinary excretion of the flavanones naringenin and hesperetin in humans after ingestion of orange juice and grapefruit juiceView study →Reference 12Kanaze FI et al. · 2007Clinical trialPharmacokinetics of the citrus flavanone aglycones hesperetin and naringenin after single oral administration in human subjectsView study →}. Naringenin also carries one stereocenter (C-2) that racemizes readily in solution, so isolated material is typically near-racemic ^{20Reference 20Caccamese S et al. · 2007Racemisation at C-2 of naringin in sour oranges with increasing maturity determined by chiral HPLCView study →}. The upshot: oral bioavailability is poor and erratic, and — as with the other citrus flavanones — the in-vitro concentrations that drive its mechanisms are not what an oral dose delivers to tissue.

Clinical trials

Naringenin has one small pure-aglycone efficacy RCT (NAFLD) plus a clean safety/PK trial; everything else rests on naringin (conflicting) or citrus/hesperidin mixtures, and its anticancer/antiviral literature is entirely preclinical.

Pure naringenin	Naringin	Citrus / hesperidin	Anticancer / antiviral
1 efficacy (NAFLD) + 1 safety/PK	Conflicting lipid RCTs	Vascular RCTs (mixture)	Preclinical only

Last checked: July 2026.

Isolate vs. Plant Studies

Naringenin is over-credited in three familiar ways. The human evidence is mostly not naringenin: the cardiometabolic and vascular data come from grapefruit/orange juice, citrus extracts, or the glycoside naringin, all of which carry hesperidin, narirutin, vitamin C and fiber alongside — so effects can’t be pinned on the aglycone ^{3,6Reference 3Demonty I et al. · 2010The citrus flavonoids hesperidin and naringin do not affect serum cholesterol in moderately hypercholesterolaemic men and womenView study →Reference 6Rendeiro C et al. · 2016RCTFlavanone-rich citrus beverages counteract the transient decline in postprandial endothelial function in humans — a randomised, controlled, double-masked, crossover intervention studyView study →}. In plants it is a glycoside (or a chalcone): citrus stores it as bitter naringin, oranges as narirutin, and tomato skin as naringenin chalcone (the open-ring precursor) — a “naringenin-containing” food actually delivers one of these forms, absorbed differently ^{11Reference 11Erlund I et al. · 2001Plasma kinetics and urinary excretion of the flavanones naringenin and hesperetin in humans after ingestion of orange juice and grapefruit juiceView study →}. And the most-repeated fact about it is false — naringenin/naringin do not cause the grapefruit–CYP3A4 interaction (furanocoumarins do); their real clinical interaction is the opposite one, OATP inhibition that lowers absorption of drugs like fexofenadine ^{13,17Reference 13Paine MF et al. · 2006A furanocoumarin-free grapefruit juice establishes furanocoumarins as the mediators of the grapefruit-juice–felodipine interactionView study →Reference 17Bailey DG et al. · 2007Naringin is a major and selective clinical inhibitor of organic anion-transporting polypeptide 1A2 (OATP1A2) in grapefruit juiceView study →}. Within this database naringenin appears only at occurrence level (blue-lotus flower, black ant); note the hops “naringenin” is really 8-prenylnaringenin, a distinct prenylflavonoid with its own page, and yerba santa’s are methoxylated relatives — none belong here.

Prevalence in Nature

Naringenin is the signature flavanone of citrus (Rutaceae), but almost never present free in the intact plant — it is stored as glycosides and released only on hydrolysis ^{21Reference 21Gattuso G et al. · 2007Flavonoid composition of citrus juicesView study →}. Grapefruit is the headline, and it is a naringin story: whole white grapefruit carries ~14–17 mg naringin/100 g and grapefruit juice ~10–63 mg/100 mL (white > pink > ruby, plus large brand variation) — the naringin load responsible for grapefruit’s bitterness ^{22,23Reference 22Duda-Madej A et al. · 2022Naringenin and its derivatives — health-promoting phytobiotic against resistant bacteria and fungi in humans (grapefruit naringin content)View study →Reference 23Wanwimolruk S et al. · 2006Variation of flavonoids and furanocoumarins in grapefruit juices — a potential source of variability in grapefruit-juice–drug-interaction studiesView study →}. Other bitter citrus follow (bergamot juice ~17, sour orange ~2 mg naringin/100 mL), while sweet orange contributes mostly narirutin and only trace naringenin, and lemons/limes are minor ^{21,24Reference 21Gattuso G et al. · 2007Flavonoid composition of citrus juicesView study →Reference 24Gardana C et al. · 2008Distribution of flavonoids and furanocoumarins in juices from Citrus bergamia (bergamot) and identification of new compoundsView study →}. The notable non-citrus source is tomato skin, where the form is different again — naringenin chalcone (chalconaringenin), which makes up 35–71% of tomato flavonoids and sits almost entirely in the peel; cooking partially cyclizes it to naringenin, so tomato paste delivers meaningful bioavailable naringenin ^{25,26,27Reference 25Slimestad R et al. · 2008The flavonoids of tomatoesView study →Reference 26Bugianesi R et al. · 2002Naringenin from cooked tomato paste is bioavailable in menView study →Reference 27Kolot C et al. · 2020Bioavailability of naringenin chalcone in humans after ingestion of cherry tomatoesView study →}. There are essentially no non-plant sources.

Biosynthetically naringenin is the central branch point of the flavonoid pathway: chalcone synthase condenses p-coumaroyl-CoA with malonyl-CoA to naringenin chalcone, chalcone isomerase cyclizes it to (2S)-naringenin, and from that single node flavone synthase gives apigenin, F3H+flavonol synthase give kaempferol (and onward to anthocyanins), and B-ring hydroxylation/methylation give the sister flavanones eriodictyol and hesperetin ^{28Reference 28Winkel-Shirley B · 2001Flavonoid biosynthesis — a colourful model for genetics, biochemistry, cell biology and biotechnology (the CHS→CHI→naringenin branch point)View study →}. Tomato peel is unusual in stalling at the chalcone (low chalcone-isomerase activity), which is why the chalcone dominates there.

Discovery & Synthesis

Naringenin is named after naringin, the bitter flavonoid glycoside of grapefruit from which it is released on hydrolysis; “naring-” traces back through scientific and botanical vocabulary to Sanskrit nāraṅga (“orange tree”) — the same root that gave Persian nārang, Spanish naranja and English orange. (The etymology is well documented linguistically; a specific coining author/date, and the frequently-repeated 1928 Asahina–Inubuse structure attribution, could not be confirmed against a primary indexed source — treat them as reported.) Structurally naringenin is 4′,5,7-trihydroxyflavanone, the parent, unsubstituted-B-ring flavanone: add a B-ring 3′-OH and you get eriodictyol; add a 3′-OH plus 4′-O-methyl and you get hesperetin — naringenin is those minus the extra B-ring substituents. It carries one stereocenter at C-2, but the C-2 proton is labile and the molecule racemizes within hours in solution ^{20Reference 20Caccamese S et al. · 2007Racemisation at C-2 of naringin in sour oranges with increasing maturity determined by chiral HPLCView study →}.

Commercial naringenin is overwhelmingly extraction-derived: naringin is recovered from citrus processing waste — chiefly grapefruit peel and albedo — then hydrolyzed to the aglycone, either by acid or, more selectively, by naringinase (an α-L-rhamnosidase + β-glucosidase complex used industrially to “debitter” grapefruit juice). Enzymatic/microbial-fermentation and total-synthesis routes exist but remain minor; citrus extraction plus hydrolysis dominates.

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

Toxicity & Safety

As a dietary flavanone consumed in citrus, naringenin has a low toxicity profile — the single-ascending-dose human trial found no clinically relevant adverse events or blood-marker changes from 150 up to 900 mg, well above dietary intake ^{5Reference 5Rebello CJ et al. · 2020RCTSafety and pharmacokinetics of naringenin — a randomised, controlled, single-ascending-dose clinical trialView study →}.

The grapefruit-interaction clarification is the load-bearing safety point — and it corrects a myth. The dangerous, clinically important grapefruit–drug interaction (sustained inhibition of intestinal CYP3A4 that raises the exposure of felodipine, simvastatin, many calcium-channel blockers and immunosuppressants) is caused by grapefruit FURANOCOUMARINS — bergamottin and 6′,7′-dihydroxybergamottin — not by naringin or naringenin ^{13,14Reference 13Paine MF et al. · 2006A furanocoumarin-free grapefruit juice establishes furanocoumarins as the mediators of the grapefruit-juice–felodipine interactionView study →Reference 14Paine MF et al. · 2005Two major grapefruit-juice components differ in time to onset of intestinal CYP3A4 inhibitionView study →}. Those furanocoumarins are mechanism-based (“suicide”) inhibitors that irreversibly inactivate enterocyte CYP3A4 for 24–72 h; the definitive experiment removed the furanocoumarins while keeping the flavonoids, and the resulting juice did not raise felodipine exposure ^{13Reference 13Paine MF et al. · 2006A furanocoumarin-free grapefruit juice establishes furanocoumarins as the mediators of the grapefruit-juice–felodipine interactionView study →}. Naringin was historically the first suspect (it is grapefruit’s signature bitter compound) ^{15Reference 15Bailey DG et al. · 1993Grapefruit juice–felodipine interaction — mechanism, predictability and effect of naringinView study →}, but naringenin is only a weak, reversible CYP3A4 inhibitor in vitro — far too weak to account for the prolonged clinical effect ^{16Reference 16Lu WJ et al. · 2011Enantiomers of naringenin as pleiotropic, stereoselective inhibitors of cytochrome P450 isoformsView study →}.

Where the flavanone does interact clinically is the opposite direction: inhibition of intestinal OATP uptake transporters (OATP1A2/2B1), which reduces absorption of certain drugs — grapefruit, orange and apple juices cut fexofenadine exposure to ~30–40% of control, and naringin is a major, selective OATP1A2 inhibitor in grapefruit juice ^{17,18Reference 17Bailey DG et al. · 2007Naringin is a major and selective clinical inhibitor of organic anion-transporting polypeptide 1A2 (OATP1A2) in grapefruit juiceView study →Reference 18Dresser GK et al. · 2002Fruit juices inhibit organic anion-transporting polypeptide-mediated drug uptake to decrease the oral availability of fexofenadineView study →}. So the sensible advice is to separate OATP-substrate drugs (fexofenadine, some β-blockers, aliskiren, certain antibiotics) from large citrus-juice loads. Naringenin also has weak, context-dependent estrogen-receptor activity (antiestrogenic in some assays, weakly estrogenic in others), a reason for caution with concentrated supplements in hormone-sensitive conditions ^{19Reference 19Galluzzo P et al. · 2008The nutritional flavanone naringenin triggers antiestrogenic effects by regulating estrogen-receptor-alpha palmitoylationView study →}.

Dosage

There is no established dose of naringenin. The one efficacy trial used 200 mg/day of the pure aglycone for NAFLD ^{1Reference 1Namkhah Z et al. · 2021RCTDoes naringenin supplementation improve lipid profile, severity of hepatic steatosis and probability of liver fibrosis in overweight/obese patients with NAFLD? A randomised, double-blind, placebo-controlled clinical trialView study →}; a safety trial tested single doses up to 900 mg without adverse effect ^{5Reference 5Rebello CJ et al. · 2020RCTSafety and pharmacokinetics of naringenin — a randomised, controlled, single-ascending-dose clinical trialView study →}; and the conflicting lipid trials used naringin at ~450 mg/day ^{2Reference 2Barajas-Vega JL et al. · 2022Clinical trialNaringin reduces body weight, plasma lipids and increases adiponectin levels in patients with dyslipidemiaView study →}. Because naringin is a poorly-absorbed prodrug, the delivered naringenin exposure depends heavily on form and on the individual’s gut microbiome ^{11Reference 11Erlund I et al. · 2001Plasma kinetics and urinary excretion of the flavanones naringenin and hesperetin in humans after ingestion of orange juice and grapefruit juiceView study →}.

These are research figures, not a recommendation — the pure-aglycone evidence is a single small trial, the naringin lipid data conflict, and the vascular evidence belongs to citrus mixtures, not naringenin.

References

1. Namkhah Z, Naeini F, Mahdi Rezayat S, et al. (2021). Does naringenin supplementation improve lipid profile, severity of hepatic steatosis and probability of liver fibrosis in overweight/obese patients with NAFLD? A randomised, double-blind, placebo-controlled clinical trial. International Journal of Clinical Practice, 75(11), e14852. https://pubmed.ncbi.nlm.nih.gov/34516703/
2. Barajas-Vega JL, Raffoul-Orozco AK, Hernández-Molina D, et al. (2022). Naringin reduces body weight, plasma lipids and increases adiponectin levels in patients with dyslipidemia. International Journal for Vitamin and Nutrition Research, 92(4), 292–298. https://pubmed.ncbi.nlm.nih.gov/32513069/
3. Demonty I, Lin Y, Zebregs YE, et al. (2010). The citrus flavonoids hesperidin and naringin do not affect serum cholesterol in moderately hypercholesterolaemic men and women. The Journal of Nutrition, 140(9), 1615–1620. https://pubmed.ncbi.nlm.nih.gov/20660284/
4. Murugesan N, Woodard K, Ramaraju R, et al. (2020). Naringenin increases insulin sensitivity and metabolic rate — a case study. Journal of Medicinal Food, 23(11), 1213–1217. https://pubmed.ncbi.nlm.nih.gov/31670603/
5. Rebello CJ, Beyl RA, Lertora JJL, et al. (2020). Safety and pharmacokinetics of naringenin — a randomised, controlled, single-ascending-dose clinical trial. Diabetes, Obesity & Metabolism, 22(1), 91–98. https://pubmed.ncbi.nlm.nih.gov/31468636/
6. Rendeiro C, Dong H, Saunders C, et al. (2016). Flavanone-rich citrus beverages counteract the transient decline in postprandial endothelial function in humans — a randomised, controlled, double-masked, crossover intervention study. The British Journal of Nutrition, 116(12), 1999–2010. https://pubmed.ncbi.nlm.nih.gov/28065188/
7. Rizza S, Muniyappa R, Iantorno M, et al. (2011). Citrus polyphenol hesperidin stimulates production of nitric oxide in endothelial cells while improving endothelial function and reducing inflammatory markers in patients with metabolic syndrome. The Journal of Clinical Endocrinology & Metabolism, 96(5), E782–E792. https://pubmed.ncbi.nlm.nih.gov/21346065/
8. Faramarzi F, Alimohammadi M, Rahimi A, et al. (2022). Naringenin induces intrinsic and extrinsic apoptotic signalling pathways in cancer cells — a systematic review and meta-analysis of in-vitro and in-vivo data. Nutrition Research, 105, 33–52. https://pubmed.ncbi.nlm.nih.gov/35797732/
9. Frabasile S, Koishi AC, Kuczera D, et al. (2017). The citrus flavanone naringenin impairs dengue virus replication in human cells. Scientific Reports, 7, 41864. https://pubmed.ncbi.nlm.nih.gov/28157234/
10. Clementi N, Scagnolari C, D’Amore A, et al. (2021). Naringenin is a powerful inhibitor of SARS-CoV-2 infection in vitro. Pharmacological Research, 163, 105255. https://pubmed.ncbi.nlm.nih.gov/33096221/
11. Erlund I, Meririnne E, Alfthan G, Aro A. (2001). Plasma kinetics and urinary excretion of the flavanones naringenin and hesperetin in humans after ingestion of orange juice and grapefruit juice. The Journal of Nutrition, 131(2), 235–241. https://pubmed.ncbi.nlm.nih.gov/11160539/
12. Kanaze FI, Bounartzi MI, Georgarakis M, Niopas I. (2007). Pharmacokinetics of the citrus flavanone aglycones hesperetin and naringenin after single oral administration in human subjects. European Journal of Clinical Nutrition, 61(4), 472–477. https://pubmed.ncbi.nlm.nih.gov/17047689/
13. Paine MF, Widmer WW, Hart HL, et al. (2006). A furanocoumarin-free grapefruit juice establishes furanocoumarins as the mediators of the grapefruit-juice–felodipine interaction. The American Journal of Clinical Nutrition, 83(5), 1097–1105. https://pubmed.ncbi.nlm.nih.gov/16685052/
14. Paine MF, Criss AB, Watkins PB. (2005). Two major grapefruit-juice components differ in time to onset of intestinal CYP3A4 inhibition. The Journal of Pharmacology and Experimental Therapeutics, 312(3), 1151–1160. https://pubmed.ncbi.nlm.nih.gov/15485894/
15. Bailey DG, Arnold JM, Munoz C, Spence JD. (1993). Grapefruit juice–felodipine interaction — mechanism, predictability and effect of naringin. Clinical Pharmacology & Therapeutics, 53(6), 637–642. https://pubmed.ncbi.nlm.nih.gov/8275614/
16. Lu WJ, Ferlito V, Xu C, et al. (2011). Enantiomers of naringenin as pleiotropic, stereoselective inhibitors of cytochrome P450 isoforms. Chirality, 23(10), 891–896. https://pubmed.ncbi.nlm.nih.gov/21953762/
17. Bailey DG, Dresser GK, Leake BF, Kim RB. (2007). Naringin is a major and selective clinical inhibitor of organic anion-transporting polypeptide 1A2 (OATP1A2) in grapefruit juice. Clinical Pharmacology & Therapeutics, 81(4), 495–502. https://pubmed.ncbi.nlm.nih.gov/17301733/
18. Dresser GK, Bailey DG, Leake BF, et al. (2002). Fruit juices inhibit organic anion-transporting polypeptide-mediated drug uptake to decrease the oral availability of fexofenadine. Clinical Pharmacology & Therapeutics, 71(1), 11–20. https://pubmed.ncbi.nlm.nih.gov/11823753/
19. Galluzzo P, Ascenzi P, Bulzomi P, Marino M. (2008). The nutritional flavanone naringenin triggers antiestrogenic effects by regulating estrogen-receptor-alpha palmitoylation. Endocrinology, 149(5), 2567–2575. https://pubmed.ncbi.nlm.nih.gov/18239068/
20. Caccamese S, Manna L, Scivoli G. (2007). Racemisation at C-2 of naringin in sour oranges with increasing maturity determined by chiral HPLC. Journal of Agricultural and Food Chemistry, 55(9), 3816–3822. https://pubmed.ncbi.nlm.nih.gov/17417869/
21. Gattuso G, Barreca D, Gargiulli C, et al. (2007). Flavonoid composition of citrus juices. Molecules, 12(8), 1641–1673. https://pubmed.ncbi.nlm.nih.gov/17960080/
22. Duda-Madej A, Stecko J, Sobieraj J, et al. (2022). Naringenin and its derivatives — health-promoting phytobiotic against resistant bacteria and fungi in humans (grapefruit naringin content). Antibiotics, 11(11), 1601. https://pubmed.ncbi.nlm.nih.gov/36421272/
23. Wanwimolruk S, Marquez PV, et al. (2006). Variation of flavonoids and furanocoumarins in grapefruit juices — a potential source of variability in grapefruit-juice–drug-interaction studies. Journal of Agricultural and Food Chemistry / Drug Metabolism and Drug Interactions. https://pubmed.ncbi.nlm.nih.gov/16841515/
24. Gardana C, Nalin F, Simonetti P, et al. (2008). Distribution of flavonoids and furanocoumarins in juices from Citrus bergamia (bergamot) and identification of new compounds. Molecules, 13(9), 2220–2228. https://pubmed.ncbi.nlm.nih.gov/18830151/
25. Slimestad R, Fossen T, Verheul MJ. (2008). The flavonoids of tomatoes. Journal of Agricultural and Food Chemistry, 56(7), 2436–2441. https://pubmed.ncbi.nlm.nih.gov/18318499/
26. Bugianesi R, Catasta G, Spigno P, et al. (2002). Naringenin from cooked tomato paste is bioavailable in men. The Journal of Nutrition, 132(11), 3349–3352. https://pubmed.ncbi.nlm.nih.gov/12421849/
27. Kolot C, Rodriguez-Mateos A, Feliciano R, et al. (2020). Bioavailability of naringenin chalcone in humans after ingestion of cherry tomatoes. International Journal for Vitamin and Nutrition Research, 90(1–2), 25–34. https://pubmed.ncbi.nlm.nih.gov/30961461/
28. Winkel-Shirley B. (2001). Flavonoid biosynthesis — a colourful model for genetics, biochemistry, cell biology and biotechnology (the CHS→CHI→naringenin branch point). Plant Physiology, 126(2), 485–493. https://pubmed.ncbi.nlm.nih.gov/11402179/

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