Compound Monograph
Sennoside A
Sennoside A is the principal laxative glycoside of senna and a stimulant-laxative component of rhubarb — a rhein dianthrone diglucoside that passes the upper gut intact and is cleaved by colonic bacteria to the active metabolite rhein-anthrone. Together with sennoside B it is the standardised active of senna, one of the most widely used over-the-counter laxatives in the world.
Sources · 4
Where Does It Come From?
Sennoside A is a naturally occurring dianthrone diglucoside (rhein homodianthrone; hydroxyanthracene glycoside), found in Senna — leaf and pod, Rhubarb — rhizome and 2 other sources. It is flagged as moderately toxic.
Concentration
Content by Source
Reported concentrations across the plants that contain sennoside A — the bar marks the typical level, the line shows the reported range.
Literature figures for varying plant parts and preparations. Read them as a comparative guide, not exact assays.
Sennoside A at a Glance
Sennoside A is the principal laxative glycoside of senna and one of the stimulant-laxative components of rhubarb. Chemically it is a rhein dianthrone diglucoside — two rhein-anthrone units joined at their central carbons, each capped with a glucose sugar. That structure is the key to how it works: the sugars make it polar and poorly absorbed, so a swallowed dose survives the stomach and small intestine and travels to the colon essentially unchanged 1,
It is a prodrug. Sennoside A itself does very little; the active molecule is what colonic bacteria make from it. In the large intestine, bacterial enzymes strip the sugars and reduce the freed dianthrone to the reactive anthrone rhein-anthrone, which is the species that actually drives laxation — speeding colonic motility and turning the colon from a net absorber of water into a net secretor of it 1,
With its diastereomer sennoside B, sennoside A is the standardised active of senna — one of the most widely used over-the-counter laxatives in the world, with a genuine human trial record for constipation 3Reference 3RCTSenna Versus Magnesium Oxide for the Treatment of Chronic Constipation: A Randomized, Placebo-Controlled TrialView study →. Almost all of that human evidence, though, is for standardised senna extract (sennosides A + B together), not for the purified isomer. As a member of the hydroxyanthracene family it also carries that class’s stimulant-laxative safety story: electrolyte loss with overuse, melanosis coli with chronic use, and an EU regulatory caution built on the genotoxic potential of the released free anthrones — set against reassuring direct genotoxicity and carcinogenicity testing of senna itself 10,
The Principal Senna Laxative
This is the point of the molecule, so it is worth stating precisely. Sennoside A is the compound that makes senna a laxative, and it does so through a defined prodrug cascade:
- The plant delivers an inert glycoside. Sennoside A is a dianthrone diglucoside — pharmacologically inactive as swallowed, polar, and poorly absorbed. It is stored in senna leaf and pod (and in rhubarb rhizome) as the stable, storable form of the reactive anthrone 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →.
- It reaches the colon intact. Because it is a glycoside, the stomach and small intestine neither absorb nor transform it; it arrives in the large intestine unchanged 1,
2Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →Reference 2Pharmacokinetics of Anthraquinones from Medicinal PlantsView study → . - Colonic bacteria activate it. Bacterial β-glucosidase removes the two glucose units to give the aglycone sennidin A, and bacterial reductase reduces and cleaves the central bond to yield the active metabolite rhein-anthrone 1,
2Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →Reference 2Pharmacokinetics of Anthraquinones from Medicinal PlantsView study → . This step is obligatory — in germ-free rats, sennosides are not converted and the laxative effect does not appear 4Reference 4AnimalThe effect of rhein and rhein anthrone on intestinal fluid transport and on large intestine transit in germ-free ratsView study →. - Rhein-anthrone stimulates the colon. The anthrone acts locally on the colonic wall, producing the two effects that together define stimulant laxation.
The two colonic actions. Rhein-anthrone is prokinetic — it stimulates colonic smooth muscle and the peristaltic reflex, accelerating transit so there is less time for water to be reabsorbed; in guinea-pig ileum it produced a dose-dependent, prostaglandin-mediated rise in muscle tension and peristalsis 8Reference 8Influence of rhein anthrone on peristaltic reflex of guinea-pig isolated ileum: involvement of prostaglandinsView study →. It is simultaneously antiabsorptive/secretory — it reduces net absorption of sodium and chloride and enhances potassium and water secretion, shifting net water movement toward secretion 1,
The clinical laxative evidence. Unlike most of the molecules in this class, senna has a modern randomised trial. In a double-blind, placebo-controlled RCT in chronic idiopathic constipation, standardised senna produced an overall response in ~69% of patients versus ~12% on placebo (statistically indistinguishable from magnesium oxide), with significant gains in spontaneous bowel movements and quality of life 3Reference 3RCTSenna Versus Magnesium Oxide for the Treatment of Chronic Constipation: A Randomized, Placebo-Controlled TrialView study →. That trial — and centuries of pharmacopoeial use — is the real human footprint. The mechanism above is sennoside A’s; the trial is standardised senna’s (sennosides A + B), a distinction the page keeps throughout.
Sennoside A vs. Sennoside B
Senna’s two principal actives are a stereochemical pair, and the distinction explains why they are always quantified together:
- Sennoside A yields, on hydrolysis, the aglycone sennidin A, which is optically active (dextrorotatory) — its two anthrone halves are joined in a chiral, trans configuration at the central C10–C10′ carbons.
- Sennoside B yields sennidin B, the meso form — the same two halves joined so that the molecule is internally compensated and optically inactive.
They are therefore diastereomers, and the C10 centres can epimerise, so the two isomers interconvert and co-occur in the plant. For this reason pharmacopoeial senna is not standardised to sennoside A alone but to total hydroxyanthracene glycosides, conventionally expressed as sennoside B 1,
What It's Used For
The pharmacology is dominated by one well-mapped action — stimulant laxation via the bacterial metabolite — with a scatter of preclinical activities reported for the intact glycoside. The evidence splits sharply by whether the endpoint is the established human laxative use or a cell/rodent finding for isolated sennoside A.
Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. The laxative score reflects genuine human trial evidence (for standardised senna); the other rows are isolated-molecule preclinical signals. Each application links to its write-up.
The marquee use and the only one with human trial evidence. Senna is an established over-the-counter stimulant laxative; in a double-blind, placebo-controlled RCT in chronic idiopathic constipation, standardised senna gave an overall response in ~69% of patients versus ~12% on placebo — comparable to magnesium oxide — with significant improvements in spontaneous bowel movements and quality of life 3Reference 3RCTSenna Versus Magnesium Oxide for the Treatment of Chronic Constipation: A Randomized, Placebo-Controlled TrialView study →.
Mechanistically the effect routes entirely through the bacterial metabolite: sennoside A is cleaved and reduced in the colon to rhein-anthrone, which accelerates colonic transit 8Reference 8Influence of rhein anthrone on peristaltic reflex of guinea-pig isolated ileum: involvement of prostaglandinsView study → and shifts net colonic fluid movement toward secretion via PGE2 and aquaporin-3 downregulation 5,
Onset is ~6–12 h, matching the time to reach and process the drug in the colon 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →.
Gap: the human efficacy is for standardised whole senna (sennosides A + B), not the purified isomer, and the amount of active anthrone actually generated depends on the individual’s colonic microbiota, not on a fixed conversion 1,
A comprehensive review of isolated sennoside A catalogues anti-obesity, hypoglycaemic, hepatoprotective, anti-fibrotic and anti-inflammatory activities in cell and rodent models 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →. These are mechanistically interesting but sit far below the laxative evidence: they are isolated-molecule preclinical findings, several at exposures unrelated to how senna is used, and the same review flags open uncertainty over whether sennoside A or its metabolites are the responsible species 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →.
Gap: no human trial supports any of these uses; they are in-vitro/animal signals for the isolate and do not transfer to senna the laxative herb 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →.
The same review reports antibacterial, antifungal and antiviral activity for isolated sennoside A in vitro 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →. As with the metabolic signals, this is early-stage isolated-molecule work with no clinical correlate, and the relevant exposures bear no relation to oral laxative dosing (where the glycoside is confined to the gut lumen and converted to rhein-anthrone before absorption) 1,
Gap: in-vitro only; no in-vivo antimicrobial efficacy or human data, and the laxative pharmacokinetics make meaningful systemic sennoside A exposure unlikely at normal doses 2Reference 2Pharmacokinetics of Anthraquinones from Medicinal PlantsView study →.
Mechanisms
| Target / pathway | Effect | Relevant to |
|---|---|---|
| Bacterial β-glucosidase + reductase (activation) | removes 2 glucoses → sennidin A → reduces to active rhein-anthrone in the colon | the obligatory activation step |
| Colonic smooth muscle / peristaltic reflex (via rhein-anthrone) | prokinetic — ↑ muscle tension, ↑ peristalsis, faster transit | laxative (motility) |
| Prostaglandin E2 release (luminal, via rhein-anthrone) | drives secretion + motility; indomethacin partially blocks laxation | laxative (secretion) |
| Macrophage activation → ↓ aquaporin-3 (via rhein-anthrone) | less water reabsorption from lumen → looser stool | laxative (secretion) |
| Na⁺/K⁺-ATPase-linked ion transport (via rhein-anthrone) | ↓ Na⁺/Cl⁻ absorption, ↑ K⁺/water secretion → net secretion | laxative (antiabsorptive) |
| Air / in-vivo oxidation of anthrone → rhein | active anthrone → largely inactive anthraquinone; rhein is what circulates | pharmacokinetics; why rhein is the measured species |
| Colonic epithelial apoptosis (chronic, class effect) | lipofuscin-laden macrophages → melanosis coli pigment | toxicity (chronic use) |
The load-bearing point: sennoside A is a delivery vehicle. Every therapeutic action in the table is really rhein-anthrone’s — the glycoside’s job is to survive the upper gut and release the reactive anthrone exactly where laxation is wanted.
Pharmacokinetics
Sennoside A’s pharmacokinetics are the pharmacokinetics of a colon-targeted prodrug. Because it is a polar diglucoside, oral absorption of the intact molecule is minimal — it is not meaningfully taken up in the small intestine, which is precisely what lets it reach the colon 1,
Clinical Trials
Human evidence is for standardised senna, not the isolated isomer. Senna is an established OTC laxative with a modern double-blind, placebo-controlled RCT in chronic idiopathic constipation 3Reference 3RCTSenna Versus Magnesium Oxide for the Treatment of Chronic Constipation: A Randomized, Placebo-Controlled TrialView study → on top of pharmacopoeial recognition and long use; the preclinical (metabolic, antimicrobial, antitumour) activities of isolated sennoside A remain cell/animal-stage 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →.
| Completed | Planned | Terminated | Preclinical |
|---|---|---|---|
| Laxative: established (RCT + OTC use, standardised senna) | — | — | Metabolic / hepatoprotective / antimicrobial / antitumour (isolated sennoside A) |
Last checked: July 2026.
Isolate vs. Plant Studies
Sennoside A shows the usual two-layer split, but with a strong human core. The efficacy evidence is at the whole-herb / standardised-extract level: senna is dosed and trialled by its combined sennoside content, and the randomised laxative data are for standardised senna (sennosides A + B), not the purified isomer 3Reference 3RCTSenna Versus Magnesium Oxide for the Treatment of Chronic Constipation: A Randomized, Placebo-Controlled TrialView study →. The mechanism is genuinely sennoside A’s — the prodrug-to-rhein-anthrone cascade is well mapped — but it is shared with sennoside B, which converges on the same metabolite 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →. Where the isolated molecule has been studied directly (the metabolic, hepatoprotective and antimicrobial reports), the work is preclinical, and even the authoritative review is candid that it is unclear whether sennoside A or a metabolite is responsible 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →. So the honest framing: take the laxative efficacy from the standardised plant, take the mechanism from the molecule, and treat the isolated-molecule pharmacology as a preclinical frontier.
Prevalence in Nature
Sennoside A is a stored dianthrone glycoside of a small set of anthraquinone-bearing medicinal plants — unlike its metabolite rhein-anthrone, which is not stored pre-formed. Its principal sources are:
- Senna (Senna alexandrina, syn. Cassia angustifolia / Cassia senna) — leaf and pod, its defining source. Senna leaf and pod store sennosides A and B as their principal actives alongside minor sennosides C and D (rhein–aloe-emodin heterodianthrones); pharmacopoeial material is standardised to total hydroxyanthracene glycosides expressed as sennoside B, typically ~2–3% in leaf and ~3–4% in pod 1,
14Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →Reference 14Safety of hydroxyanthracene derivatives for use in foodView study → . - Rhubarb (Rheum spp., e.g. R. palmatum) — rhizome, where sennoside A occurs alongside the free anthraquinones rhein, emodin, aloe-emodin, chrysophanol and physcion; it is a minor share (~3.9%) of a representative rhubarb free-anthraquinone extract 16Reference 16AnimalPharmacokinetics and pharmacodynamics of rhubarb anthraquinones extract in normal and disease ratsView study →.
Content in both plants swings with species, plant part and processing — leaf is more potent (and more griping) than pod, and raw rhubarb is more purgative than steamed or charred forms 1,
Major Natural Sources
| Source (Botanical) | Part | Sennoside content | Note |
|---|---|---|---|
| Senna (Senna alexandrina) | Pod | ~3–4% total sennosides (as sennoside B) | The standardised laxative drug; milder/less griping than leaf 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study → |
| Senna (Senna alexandrina) | Leaf | ~2–3% total sennosides (as sennoside B) | More potent but more cramping than pod 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study → |
| Rhubarb (Rheum palmatum) | Rhizome | ~3.9% of the anthraquinone extract | One anthraquinone among many; raw > processed 16Reference 16AnimalPharmacokinetics and pharmacodynamics of rhubarb anthraquinones extract in normal and disease ratsView study → |
Discovery & Synthesis
Sennoside A entered the literature as one of the two crystalline active glycosides that finally explained senna’s laxative action. Stoll, Becker and Kussmaul, working at Sandoz in Basel, isolated and named sennosides A and B from senna in 1949, showing that each hydrolyses to two molecules of glucose and a sennidin aglycone — sennidin A dextrorotatory, sennidin B its meso form. That work converted senna from a crude drug of variable strength into a standardisable one, since the sennoside content could now be measured. The molecule is a rhein homodianthrone diglucoside: two rhein-anthrone units linked at C10–C10′ and glucosylated. There is no meaningful “total synthesis” story of practical importance — sennoside A is obtained by extraction and purification from senna, and the article of commerce is standardised senna extract itself rather than the pure isomer, because the two isomers interconvert and converge on the same colonic metabolite. Where pure sennoside A is wanted as a reference standard, it is isolated chromatographically from senna material 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →.
Patents: not yet researched.
Toxicity & Safety
Sennoside A carries a moderate flag — heavier than an inert dietary glycoside would warrant — because it is an active stimulant laxative and a member of the hydroxyanthracene-derivative class that sits under regulatory scrutiny. The caveats are the stimulant-laxative / anthranoid cautions, applied to senna’s principal active.
- An established laxative with human evidence. Senna standardised to its sennosides is an OTC stimulant laxative with a placebo-controlled RCT behind its use for constipation 3Reference 3RCTSenna Versus Magnesium Oxide for the Treatment of Chronic Constipation: A Randomized, Placebo-Controlled TrialView study →.
- Direct testing of senna is reassuring. Standard genotoxicity batteries on senna, the sennosides and rhein were negative, and a 2-year oral carcinogenicity study of senna in rats found no carcinogenic effect 10,
11, .12Reference 10The genotoxicity status of sennaView study →Reference 11Assessment of the genotoxic risk from laxative senna productsView study →Reference 12AnimalAn oral carcinogenicity and toxicity study of senna (Tinnevelly senna fruits) in the ratView study → - Stimulant-laxative class risks. Electrolyte loss (especially potassium) with overuse — which can compound digoxin, diuretic and antiarrhythmic effects — plus cramping/griping, and dependence with reduced bowel tone on chronic daily use.
- Melanosis coli with chronic use. Long-term use pigments the colonic mucosa (lipofuscin in macrophages) from laxative-induced epithelial apoptosis — benign and reversible, not linked to increased colon-cancer risk, but a marker of sustained use 13Reference 13ReviewReview on melanosis coli and anthraquinone-containing traditional Chinese herbs that cause melanosis coliView study →.
- Regulatory context — short-term use. Hydroxyanthracene derivatives sit under EU/EFSA scrutiny because the released free anthrones are the structural basis for the class genotoxicity concern; senna laxatives are intended for occasional, short-term use 1,
14Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →Reference 14Safety of hydroxyanthracene derivatives for use in foodView study → .
Full Safety & Interactions Detail
Genotoxicity — the class concern vs the direct data. The EU restriction on hydroxyanthracene derivatives rests on the reactive free anthrones (the aglycone end-products), which are the structural basis for a class genotoxicity flag 14Reference 14Safety of hydroxyanthracene derivatives for use in foodView study →. Against that structural concern, the direct testing of senna itself has been largely reassuring: senna, the sennosides and rhein did not increase mutation frequencies across bacterial and mammalian assays (aloe-emodin was the class member showing in-vitro mutagenicity, without an in-vivo effect) 10Reference 10The genotoxicity status of sennaView study →, and a formal assessment concluded the genotoxic risk to patients using senna laxatives is not established 11Reference 11Assessment of the genotoxic risk from laxative senna productsView study →.
Carcinogenicity — negative in the pivotal study. A 2-year oral carcinogenicity and toxicity study of Tinnevelly senna fruits in rats found no treatment-related carcinogenic effect at daily doses up to the high range, with only minor non-neoplastic intestinal and renal changes 12Reference 12AnimalAn oral carcinogenicity and toxicity study of senna (Tinnevelly senna fruits) in the ratView study →. Chronic use produces melanosis coli — dark colonic pigmentation from laxative-induced epithelial apoptosis and lipofuscin-laden macrophages — which is benign, reversible on stopping, and not associated with increased colorectal-cancer risk 13Reference 13ReviewReview on melanosis coli and anthraquinone-containing traditional Chinese herbs that cause melanosis coliView study →. A comprehensive review of isolated sennoside A does, however, note that long-term high-dose exposure has been linked in some contexts to aberrant crypt foci and colonic changes, keeping the “short-term use” framing appropriate 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →.
Class laxative cautions. As an active stimulant laxative, sennoside A underlies the familiar anthranoid concerns: potassium and fluid loss with excessive use, abdominal cramping/griping (worse with leaf than pod), and — with habitual daily use — laxative dependence and diminished spontaneous bowel function. These are dose- and duration-driven, tied to the very motility/secretion mechanism that makes it work.
Pregnancy and lactation (prose only). Senna is one of the better-characterised laxatives in pregnancy and is generally regarded as acceptable for short-term use where a stimulant laxative is needed. A large population-based case-control study (Hungarian Case-Control Surveillance System) found no association between maternal senna treatment and congenital abnormalities in offspring (adjusted OR ~1.0), and concluded senna is not contraindicated when constipation requires drug treatment in pregnancy 15Reference 15ObservationalSenna treatment in pregnant women and congenital abnormalities in their offspring—a population-based case-control studyView study →. In lactation, systemic exposure is largely to the oxidation product rhein (sennoside A and the anthrone act locally and are poorly absorbed) 1,
Dosage
There is no dose for isolated sennoside A as a stand-alone drug — it is not administered as the pure isomer. Human dosing is entirely of senna preparations standardised to their sennoside / hydroxyanthracene-glycoside content 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study →:
| Application | Form | Dose |
|---|---|---|
| Constipation (adult, OTC) | Standardised senna | ~15–30 mg sennosides/day, short-term |
| Chronic constipation (RCT) | Standardised senna, 28 days | 1.0 g senna/day (double-blind, placebo-controlled) 3Reference 3RCTSenna Versus Magnesium Oxide for the Treatment of Chronic Constipation: A Randomized, Placebo-Controlled TrialView study → |
| Herbal / traditional | Senna leaf or pod tea | Dosed to sennoside content; pod milder, leaf more griping 1Reference 1Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural CompoundView study → |
The amount of active rhein-anthrone actually generated depends on the individual’s colonic microbiota, not on a fixed conversion, so response varies between people 1,
References
- Le J, et al. (2021). Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural Compound. Frontiers in Pharmacology. https://pubmed.ncbi.nlm.nih.gov/34764866/
- Wang D, et al. (2021). Pharmacokinetics of Anthraquinones from Medicinal Plants. Frontiers in Pharmacology. https://pubmed.ncbi.nlm.nih.gov/33935728/
- Morishita D, et al. (2021). Senna Versus Magnesium Oxide for the Treatment of Chronic Constipation: A Randomized, Placebo-Controlled Trial. The American Journal of Gastroenterology. https://pubmed.ncbi.nlm.nih.gov/32969946/
- Van Hoestenberghe A, et al. (1992). The effect of rhein and rhein anthrone on intestinal fluid transport and on large intestine transit in germ-free rats. European Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/1555634/
- Kon R, et al. (2014). Rheinanthrone, a metabolite of sennoside A, triggers macrophage activation to decrease aquaporin-3 expression in the colon, causing the laxative effect of rhubarb extract. Journal of Ethnopharmacology. https://pubmed.ncbi.nlm.nih.gov/24412547/
- Yagi T, et al. (1990). Prostaglandin E2-mediated stimulation of mucus synthesis and secretion by rhein anthrone, the active metabolite of sennosides A and B, in the mouse colon. Journal of Pharmacy and Pharmacology. https://pubmed.ncbi.nlm.nih.gov/1981580/
- Yagi T, et al. (1991). Suppression of the purgative action of rhein anthrone, the active metabolite of sennosides A and B, by indomethacin in rats. Journal of Pharmacy and Pharmacology. https://pubmed.ncbi.nlm.nih.gov/1680171/
- Nijs G, et al. (1993). Influence of rhein anthrone on peristaltic reflex of guinea-pig isolated ileum: involvement of prostaglandins. British Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/8094026/
- Nakajima K, Yamauchi K, Kuwano S (1985). Isolation of a new aloe-emodin dianthrone diglucoside from senna and its potentiating effect on the purgative activity of sennoside A in mice. Journal of Pharmacy and Pharmacology. https://pubmed.ncbi.nlm.nih.gov/2867138/
- Heidemann A, Miltenburger HG, Mengs U (1993). The genotoxicity status of senna. Pharmacology. https://pubmed.ncbi.nlm.nih.gov/8234427/
- Brusick D, Mengs U (1997). Assessment of the genotoxic risk from laxative senna products. Environmental and Molecular Mutagenesis. https://pubmed.ncbi.nlm.nih.gov/9020301/
- Mitchell JM, et al. (2006). An oral carcinogenicity and toxicity study of senna (Tinnevelly senna fruits) in the rat. Archives of Toxicology. https://pubmed.ncbi.nlm.nih.gov/16205914/
- Zhang R, et al. (2023). Review on melanosis coli and anthraquinone-containing traditional Chinese herbs that cause melanosis coli. Frontiers in Pharmacology. https://pubmed.ncbi.nlm.nih.gov/37214441/
- EFSA ANS Panel (2018). Safety of hydroxyanthracene derivatives for use in food. EFSA Journal. https://pubmed.ncbi.nlm.nih.gov/32625659/
- Acs N, et al. (2009). Senna treatment in pregnant women and congenital abnormalities in their offspring—a population-based case-control study. Reproductive Toxicology. https://pubmed.ncbi.nlm.nih.gov/19491001/
- Li P, et al. (2017). Pharmacokinetics and pharmacodynamics of rhubarb anthraquinones extract in normal and disease rats. Biomedicine & Pharmacotherapy. https://pubmed.ncbi.nlm.nih.gov/28475921/
