IngredientsQuinones are a broad class of organic compounds built from a specific ring-like chemical structure. More precisely, quinones are a group of aromatic dioxo compounds derived from benzene or multiple-ring hydrocarbons such as naphthalene, anthracene, etc., and they are classified as benzoquinones, naphthoquinones, anthraquinones, and so forth, on the basis of the ring system. They can be mainly divided into four types, namely benzoquinone, naphthoquinone, phenanthrenequinone, and anthraquinone, according to the number of benzene rings present in their structural skeleton.
Quinones are one of the oldest organic compounds and are of increasing interest due to their abundant presence in a wide range of natural sources and their remarkable biological activity. About 600 naturally occurring quinones have been described. In common usage, the singular term "quinone" most often refers to one of the major biologically active representatives — particularly coenzyme Q10 (ubiquinone), vitamin K (phylloquinone, menaquinones), or, in supplemental and herbal contexts, pyrroloquinoline quinone (PQQ) and the anthraquinones found in medicinal plants. This article covers all major nutritionally and therapeutically relevant quinone classes.
These compounds occur naturally in green leafy vegetables, fruits, herbs, animal and marine sources, and fermented products. Their main plant sources are from the Polygonaceae, Rubiaceae, Leguminosae, Rhamnaceae, Labiatae, and Boraginaceae families.
For CoQ10 specifically: CoQ is used by and found in many organisms, including animals and bacteria; as a result, it can also be obtained from dietary sources such as meat, fish, seed oils, vegetables, and dietary supplements. Coenzyme Q10 is found in highest concentrations in the heart, liver, kidney, and brain.
For vitamin K: The predominant dietary form, phylloquinone or vitamin K1, is found in plants and green vegetables; whereas menaquinone, or vitamin K2, is endogenously synthesized by intestinal bacteria and includes several subtypes that differ in side chain length. Menaquinones generally are of microbial origin.
For PQQ: PQQ is found naturally in a variety of foods, albeit in very small amounts. Some of the richest dietary sources of PQQ include fruits and vegetables: trace amounts of PQQ are found in kiwi, green peppers, parsley, spinach, and papaya.
For anthraquinones: Emodin is a polyphenol found in the roots, leaves, and bark of several plants, including aloe vera (Aloe barbadensis), cascara (Rhamnus pushiana), rhubarb (Rheum officinale), senna (Cassia angustifolia), and Polygonum multiflorum.
Quinones are biosynthesized from acetate/malonate via shikimic acid. Most naturally occurring quinones are synthesized via the shikimate or polyketide pathways that are absent in animals. In mammals, quinones can be formed via the metabolism of endogenous substances, xenobiotics, and drugs.
Supplements offer CoQ10 in either the oxidized form (ubiquinone) or the reduced form (ubiquinol). The redox state of the lipid can be specified: the fully reduced form (the hydroquinone) as "CoQH2" (ubiquinol, UQH2), the singly dehydrogenated radical form (the semiquinone) as "CoQH•" (ubisemiquinone, UQH•), and the oxidized form (the quinone) as "CoQ" (ubiquinone, UQ). CoQ10 in the pure form is a crystalline powder insoluble in water. CoQ10 extracted from living tissues is more expensive than that produced in the laboratory by fermentation, which yields consistent quality and cheaper supplements.
For anthraquinone-containing plants: Standardized commercial dosage forms have been developed and are available as liquids, powders, and nonprescription tablets in over-the-counter laxatives.
Long before anything was known of their chemistry, rhubarb, aloes, senna and cascara were recognized as forming a natural group of laxative drugs. Moreover, certain vegetable and animal dyestuffs such as madder and cochineal were of great economic importance before the introduction of synthetic dyestuffs. Later, the chemical similarity of these laxative drugs and dyestuffs became apparent.
Emodin is a key active component found in several medicinal plants commonly used in traditional Chinese medicine; these plants include Rheum palmatum, Reynoutria japonica, Reynoutria multiflora, and Senna obtusifolia. Traditionally, emodin has primarily been used as a laxative and for managing obesity-related conditions. Rhubarb (Dahuang) is commonly used as a laxative herb in both traditional and modern medicine, and figures prominently in well-known classical Chinese medicinal prescriptions, including the Da Cheng Qi decoction and its derivative decoctions, the Da Huang Mu Dan decoction, and the Da Huang Fu Zi Xi Xin decoction.
Historical indigenous applications of plants for medicinal uses are well known across the globe, with many medicinal applications arising from naphthoquinones (NQ), anthraquinones (AQ), and their quinol or quinone glycosides. Juglone (Juglans spp. — walnut) was long known for its medicinal uses before the development of the scientific method, let alone modern chemistry.
The discovery of vitamin K can be traced back to the research of Carl Peter Henrik Dam at the Biochemical Institute of the University of Copenhagen from 1928 to 1930. In his work on cholesterol metabolism, the Danish biochemist observed a spontaneous tendency to hemorrhage in chicks fed for longer than 2–3 weeks on cholesterol- and fat-free chicken feed. This coagulation disorder was combined with a lowered prothrombin content of the blood. The name derives from the German word koagulation.
A foundational study extracted a "quinone compound Q-275" (absorbing at 275 nm in ethanol) from beef heart mitochondria and demonstrated its role as a coenzyme in the mitochondrial respiratory chain through reversible redox cycling. Coenzyme Q10 is used extensively as a nutritional supplement as well as a pharmacological active agent. It has wide use and acceptance in the treatment of cardiovascular disease in traditional as well as alternative medicine, and is used in treating ischemic heart disease, chronic heart failure, toxin-induced cardiomyopathy, hypertension, and hyperlipidemia.
Long used in traditional medicine, Nigella sativa (NS; Ranunculaceae) has shown significant efficacy as an adjuvant therapy for diabetes mellitus (DM) management by improving glucose tolerance, decreasing hepatic gluconeogenesis, normalizing blood sugar and lipid imbalance, and stimulating insulin secretion from pancreatic cells.
Many natural and artificial coloring substances (dyes and pigments) are quinone derivatives; for instance, lawsone is the active dye compound in henna. Alizarin (1,2-dihydroxy-9,10-anthraquinone), extracted from the madder plant, was the first natural dye to be synthesized from coal tar.
Coenzyme Q10 (CoQ10), also known as ubiquinone, is a fat-soluble, vitamin-like molecule naturally present in every cellular membrane within our bodies. It is an enzyme cofactor found in virtually all cells of the body and participates in many essential energy-producing and antioxidant enzymatic actions.
The primary mechanism of CoQ10 centers on its electron-carrier role: in mitochondria, ubiquinone is reduced to ubiquinol by Complex I or II; Complex III (the Q cycle) re-oxidises ubiquinol to ubiquinone, and extra-mitochondrial oxidoreductase enzymes also participate in the ubiquinone–ubiquinol redox cycle. CoQ10 participates in fatty acid and glucose metabolism by transferring electrons generated from the reduction of fatty acids and glucose to electron acceptors. As a lipid-soluble antioxidant together with vitamin E, it scavenges reactive oxygen species and protects cells against oxidative stress, inhibiting the oxidation of proteins and DNA.
Beyond energy production, CoQ10 can potentially increase the production of vital antioxidants, such as superoxide dismutase, an enzyme that effectively mitigates vascular oxidative stress in individuals with hypertension. In addition, CoQ10 lowers lipid peroxidation levels by diminishing pro-oxidative compounds. Furthermore, CoQ10 can improve blood flow and safeguard blood vessels by preserving nitric oxide.
The term vitamin K is a generic term that refers to a number of related compounds characterized by a methylated naphthoquinone ring as well as an aliphatic side chain. Phylloquinone (vitamin K1), menadione (vitamin K3), and all the menaquinone (vitamin K2) structures are known as vitamers of vitamin K.
Vitamin K compounds undergo oxidation-reduction cycling within the endoplasmic reticulum membrane, donating electrons to activate specific proteins via enzymatic gamma-carboxylation of glutamate groups before being enzymatically reduced. This carboxylation process converts glutamate residues into gamma-carboxyglutamate (Gla) residues. These Gla residues activate clotting proteins like prothrombin, allowing the proteins to bind to calcium ions — a necessary step for the coagulation cascade to proceed and form a blood clot at the site of an injury.
Vitamin K1 (phylloquinone) is more abundant in foods but less bioactive than the vitamin K2 menaquinones (especially MK-7, menaquinone-7). Several studies have suggested that menaquinones, also known as vitamin K2, may be more effective in activating extra-hepatic vitamin K-dependent proteins than phylloquinone.
Senna contains anthraquinones, including dianthrone glycosides (1.5% to 3%), sennosides A and B (rhein dianthrones), and sennosides C and D (rhein aloe-emodin heterodianthrones). Numerous minor sennosides have been identified and appear to contribute to senna's laxative effect. The plant also contains free anthraquinones in small amounts, including rhein, aloe-emodin, chrysophanol, and their glycosides.
As contact cathartics, anthraquinones help relieve constipation by promoting bowel motility and reabsorption of water in the colonic mucosa. At the molecular level, quinones are a stable source of free radicals and are known to complex irreversibly with nucleophilic amino acids in proteins, which leads to inactivation of protein and loss of function — making them potent antimicrobials. Their targets in the microbial cell are surface-exposed adhesins, cell wall polypeptides, and membrane-bound enzymes.
Thymoquinone (TQ) belongs to the family of quinones, naturally derived compounds featuring a conjugated double bond system responsible for their reactivity and an intracellular process known as "redox cycling." Re-oxidation of NADH back to NAD+ via quinone-dependent redox cycling lowers cellular reductive poise and facilitates glucose metabolism. TQ has been shown to have antioxidant, anti-inflammatory, antineoplastic, antimicrobial, analgesic, hypoglycemic, antihypertensive, and hepatoprotective properties.
PQQ has redox properties and exerts antioxidant, neuroprotective, and mitochondrial biogenesis effects. One pivotal study demonstrated that PQQ stimulates mitochondrial biogenesis by activating the cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) and increasing PGC-1α expression in mouse hepatocytes. Although PQQ is not classified as an essential vitamin, studies suggest it may function as a quasi-vitamin due to its health benefits and the role it plays in cellular processes.
Oxidative stress and mitochondrial dysfunction are hallmarks of heart failure (HF). Patients with HF showed CoQ10 deficiency; therefore, a number of clinical trials investigating the effects of CoQ10 supplementation in HF have been conducted.
The landmark Q-SYMBIO trial directly addressed this: previous randomized controlled trials of CoQ10 in HF were underpowered to address major clinical endpoints. Patients with moderate to severe HF were randomly assigned in a 2-year prospective trial to either CoQ10 100 mg 3 times daily or placebo, in addition to standard therapy. The primary short-term endpoints at 16 weeks were changes in New York Heart Association (NYHA) functional classification, 6-minute walk test, and levels of N-terminal pro-B type natriuretic peptide. Long-term CoQ10 treatment of patients with chronic HF was found to be safe, improves symptoms, and reduces major adverse cardiovascular events.
A Cochrane-style systematic review examining mortality data from this trial found that CoQ10 probably reduces all-cause mortality (10% in the intervention group versus 18% in the control group; risk ratio 0.58, 95% CI 0.35 to 0.95; one study, 420 participants; moderate-quality evidence). CoQ10 probably reduces the risk of cardiovascular mortality (9% in CoQ10 group versus 16% in control group; P = 0.039) at 106 weeks.
A 2025 review of this body of evidence concludes: robust evidence, including data from the Q-SYMBIO trial, demonstrates that CoQ10 supplementation can improve functional capacity, ejection fraction, and reduce major cardiovascular events in heart failure with reduced ejection fraction. CoQ10 is generally safe, well-tolerated, and affordable, and emerging research supports its classification as a conditionally essential nutrient in heart failure. Numerous trials during the past 30 years examining CoQ10 in patients with HF have been limited by small numbers and lack of contemporary HF therapies, and these findings warrant future adequately powered randomized controlled trials of CoQ10 supplementation in patients with HF.
Evidence strength (Heart Failure): Moderate-to-strong for functional improvement and reduction of major cardiovascular events, based on at least one well-powered RCT and several smaller trials. The main limitation is the small number of trials powered for hard endpoints.
The small amount of evidence currently available suggests that CoQ10 probably doesn't have a meaningful effect on blood pressure, according to a review by the NIH National Center for Complementary and Integrative Health (NCCIH).
Evidence strength (Blood Pressure): Weak. Insufficient to draw clinically meaningful conclusions based on current evidence.
Statin drugs inhibit the production of an intermediate in the mevalonate pathway — a biochemical route leading to CoQ10 synthesis. Researchers theorize that statin drugs may contribute to CoQ10 depletion. Given that muscle pain and cramping are frequent adverse effects of statins, they attribute these symptoms to the diminished levels of CoQ10.
Although results of individual studies have varied, the overall scientific evidence does not support the idea that CoQ10 can reduce muscle pain caused by the cholesterol-lowering drugs known as statins, according to the NIH NCCIH. In contrast, one observational study enrolled a total of 106 patients with clinically identified statin-associated muscle symptoms (SAMS), with Group A (n=53) receiving CoQ10 (50 mg twice daily). Patients in Group A who received CoQ10 showed a greater reduction in both VAS and pain interference scores compared to Group B; the differences between the two groups were statistically significant (p = 0.001). CoQ10 supplementation (50 mg twice daily) was associated with improved control of statin-associated muscle symptoms in an observational clinical setting. However, this was observational in design, not a blinded RCT, which limits causal inference.
Studies on CoQ10's efficacy for statin myopathy have yielded inconsistent results, with some reporting symptom relief and others showing no significant benefit.
Evidence strength (Statin Myopathy): Mixed and currently insufficient to support a definitive recommendation. RCT data are inconsistent; NCCIH concludes evidence does not support efficacy for this indication.
A major National Institutes of Health-funded study showed that CoQ10, even in higher-than-usual doses, didn't improve symptoms in patients with early Parkinson's disease. A 2017 evaluation of this study and several other, smaller studies concluded that CoQ10 is not helpful for Parkinson's symptoms.
Evidence strength (Parkinson's Disease): Negative. A large, NIH-funded RCT, confirmed by a subsequent systematic review, found no benefit of CoQ10 supplementation for Parkinson's disease symptoms.
CoQ10 has also been studied for a variety of other conditions, including amyotrophic lateral sclerosis (Lou Gehrig's disease), Down syndrome, Huntington's disease, and male infertility, but the research is too limited for any conclusions to be drawn.
There is evidence that CoQ10 may reduce the risk of some complications of heart surgery.
Aside from its established role in blood clotting, several studies now support a critical function of vitamin K in improving bone health. Vitamin K is in fact required for osteocalcin carboxylation, which in turn regulates bone mineral accretion; it seems to promote the transition of osteoblasts to osteocytes and also limits the process of osteoclastogenesis.
Clinical studies have demonstrated the utility of vitamin K2-7 supplementation in ameliorating peripheral neuropathy, reducing bone fracture risk, and improving cardiovascular health. K2-7 acts as a cofactor in converting undercarboxylated osteocalcin (ucOC) and matrix Gla protein (ucMGP) to carboxylated forms, thus facilitating the deposition of calcium in bones and preventing vascular calcification.
However, several observational and interventional studies have examined the relationship between vitamin K and bone metabolism, but findings are conflicting and unclear. Specifically, a systematic review and meta-analysis of randomized controlled trials that tested the effect of phylloquinone (PK) or MK-4 supplementation on age-related bone loss concluded there is little evidence that vitamin K affects bone mineral density (BMD) or vertebral fractures. The authors reported a potentially beneficial effect of PK or MK4 supplementation on clinical fracture risk, but concluded additional studies are needed to confirm this.
Evidence strength (Bone / Vitamin K): Vitamin K's role in coagulation is established and uncontested. Its role in bone health is biologically plausible and supported by some RCT data, but evidence for fracture reduction is mixed, and current dietary reference values for vitamin K are based only on its coagulation function.
In the field of cognitive function, double-blind, placebo-controlled trials have been conducted with PQQ. Various improvements have been reported regarding general memory, verbal memory, working memory, and attention. Furthermore, a stratified analysis of a population with a wide range of ages revealed unique effects in young people (20–40 years old) that were not observed in older adults (41–65 years old). Specifically, cognitive flexibility and executive speed improved more rapidly in young people at 8 weeks.
A randomized controlled trial enrolling thirty-four elderly individuals with mild cognitive impairment (mean age 71.9 ± 3.8 years; 28 females) was assigned in a double-blind parallel-group design to receive either a dihydrogen-PQQ mixture or placebo twice daily for a 6-week intervention period. Dihydrogen-PQQ resulted in a significant elevation in serum BDNF levels at the six-week follow-up (P = 0.01). However, despite the limited number of participants included in the study, the dihydrogen-PQQ mixture blend shows promise as a potential dietary intervention for enhancing mental orientation and brain metabolism in individuals with age-related mild cognitive decline.
Co-administration of PQQ and coenzyme Q10 further enhanced these effects. In an open-label trial, PQQ was shown to improve sleep and mood.
Evidence strength (PQQ / Cognition): Preliminary. Small RCTs show promising signals on memory and brain metabolism; however, sample sizes are small, study durations are short (6–8 weeks), and some positive trials used combined preparations (e.g., PQQ + CoQ10 or PQQ + dihydrogen), making it difficult to isolate PQQ's independent contribution.
Long used in traditional medicine, Nigella sativa has shown significant efficacy as an adjuvant therapy for diabetes mellitus management by improving glucose tolerance, decreasing hepatic gluconeogenesis, normalizing blood sugar and lipid imbalance, and stimulating insulin secretion from pancreatic cells.
A systematic review and meta-analysis of 18 animal studies found that TQ reduced the serum glucose level significantly in the STZ-induced diabetes model (pooled SMD of −9.176 mg/dL; 95% CI: −10.759, −7.593; p = 0.000). However, TQ has been proven to have great therapeutic properties in numerous in vivo and in vitro models; nevertheless, this molecule is not yet in clinical trials, largely because of its poor bioavailability and hydrophobicity. Despite its strong potential to treat DM, Nigella sativa and TQ must be examined in more inclusive clinical studies targeting underrepresented patient populations.
Evidence strength (Thymoquinone / Diabetes): Preclinical only. Evidence is almost exclusively from animal models. Human clinical trial data are insufficient to draw conclusions on efficacy or dosing. Bioavailability limitations are a recognized barrier to clinical development.
The laxative activity of anthraquinone-containing plants (senna, rhubarb, cascara, aloe) is among the best-documented in herbal medicine. Sennosides are the main bioactive components from medicinal plants used for traditional herbal laxatives such as Senna and Rhubarb; among them, sennoside A and B are the main purgative components, first isolated and identified from the leaves of Senna.
Evidence strength (Laxative): Well-established clinical utility. Anthraquinone laxatives from senna and related plants have demonstrated efficacy in multiple clinical settings and are approved over-the-counter preparations in many countries.
In the Q-SYMBIO trial, patients with moderate to severe heart failure were assigned to CoQ10 100 mg three times daily (300 mg/day total) or placebo, in addition to standard therapy, over 2 years.
In a statin myopathy observational study, Group A (n=53) received CoQ10 50 mg twice daily.
In a dose-escalation study in hemodialysis patients, subjects were administered 300 mg CoQ10 for 14 days and then 600, 1200, and 1800 mg CoQ10 daily, each for 14 days. CoQ10 supplementation at doses as high as 1800 mg per day was safe in all subjects and well-tolerated in most.
No adverse effects were observed with daily doses ranging from 600 to 1200 mg in two trials on Huntington's and Parkinson's disease; 2,400 mg/day of CoQ10 was used for 12 months in patients with progressive supranuclear palsy.
Absolute oral bioavailability of CoQ10/ubiquinol is low and highly variable (often reported as less than 10% and sometimes less than 5%). Absorption as a pharmacological substance follows the same process as that of lipids; the uptake mechanism appears to be similar to that of vitamin E, another lipid-soluble nutrient.
Dietary intake of menaquinones accounts for up to 25% of total vitamin K intake and contributes to the biological functions of vitamin K. Existing dietary reference values for vitamin K are based on phylloquinone's coagulation function; specific supplemental doses for MK-7 used in clinical trials vary, and endogenous thrombin potential was not affected by MK-7 intake as high as 360 μg/day for 6 weeks.
The baseline intake level of PQQ is considered to be 20 mg/day. In the 6-week RCT on mild cognitive impairment, participants were assigned to receive a dihydrogen-PQQ mixture or placebo twice daily for a 6-week intervention period.
Coenzyme Q supplements are generally well tolerated and there is no evidence that they cause serum enzyme elevations or clinically apparent liver injury.
Excellent safety and tolerability is a common feature of CoQ10 clinical trial results across multiple disease states, formulations, and dose ranges from 50 to 3600 mg daily. The most common adverse effects are gastrointestinal in nature and can include nausea, epigastric pain, diarrhea, heartburn, and appetite suppression; however, the prevalence of these adverse effects was less than 1% in reported studies. Asymptomatic elevations in serum lactate dehydrogenase and hepatic enzymes were observed and may occur with oral dosages of CoQ10 in excess of 300 mg/day; however, cases of serious hepatotoxicity have not been reported.
Drug interactions: Ubiquinol is generally well tolerated; drug interactions of clinical significance include potential INR reduction with warfarin and absorption interference with bile-acid sequestrants. More specifically, because of its structural similarity to vitamin K, CoQ10 has been suggested that it may have procoagulant activity; this indicates that patients on anticoagulant therapy may need to have their INR monitored and anticoagulant dosage adjusted accordingly. Patients on warfarin should have INR monitored when starting or stopping CoQ10 supplements due to potential interaction.
Although CoQ10 lacks approval from the United States Food and Drug Administration (FDA) for treating any medical condition, it is readily accessible as an over-the-counter dietary supplement.
There are no documented cases of toxicity for phylloquinone or menaquinones. In its safety assessment of menaquinones as a source of vitamin K, the European Food Safety Authority concluded that low doses of menaquinones present no safety concerns. However, the major concerns surrounding vitamin K2 in treatment are focused on the possibility of achieving a hypercoagulable state. Animal data showed this state was not reached at very high experimental doses, and in human subjects not receiving oral anticoagulation treatment, no effects on coagulation were found with highly sensitive assays.
The most clinically significant interaction is with oral anticoagulants: vitamin K is a recognized antagonist of warfarin-type drugs, and changes in dietary or supplemental vitamin K intake can substantially affect anticoagulation control. This is a well-documented pharmacodynamic interaction in clinical practice.
Overdose of anthraquinone laxatives results in intestinal pain and severe diarrhea with consequent electrolyte imbalance and dehydration.
Products containing anthraquinones are mainly used as laxatives and have several biological effects. Long-term use of anthraquinone (AQ) laxatives is associated with an increased risk of serious adverse events, such as colorectal cancer (CRC).
A specific safety finding relates to melanosis coli: melanosis coli tends to occur in individuals who rely on anthraquinone laxatives to relieve constipation and individuals who use laxatives as weight-reducing drugs, beauty products, and health products. Approximately 95% of melanosis coli patients have a medication history of taking anthraquinone laxatives for a prolonged time.
Toxicological studies indicate that two hydroxyanthraquinones — aloe-emodin and emodin, present as minor components in senna — might represent a genotoxic or carcinogenic risk for humans.
Interference with the absorption of other drugs is possible with anthranoid-containing plants, including senna and cascara.
Non-physiologically high and toxic levels of quinones are known to generate excessive levels of reactive oxygen intermediates via quinone-dependent redox cycling, and this causes induction of the NAD(P)H-dependent quinone oxidoreductase 1 (NQO1). Thymoquinone is not yet in clinical trials, largely because of its poor bioavailability and hydrophobicity.
Pyrroloquinoline quinone disodium salt (PQQ) is a red trihydrate crystal that was approved as a new food ingredient by the FDA in 2008. It is now also approved as a food in Japan and the EU. No significant safety concerns have been identified at studied doses in short-term trials. The evidence base for PQQ remains limited to small, relatively short human trials and preclinical models.
Health conditions that Quinone may help support.
Body systems that Quinone may help support.
Go back