Solanum nigrum · PhytoNexus

01 Identity and provenance

Accepted binomial: Solanum nigrum
Common names: Makoi
Family (APG IV): Solanaceae
Part used: Whole plant
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): PMC9424827 (traditional uses, phytochemistry, pharmacology review) | J Agric Sci Bangladesh review of S. nigrum toxicity | VERIFIED 2026 (batch 4) - synthetic analogue, application, interactions, side effects and references populated from retrieved primary/regulatory sources. Interactions labelled CLINICAL vs THEORETICAL. Marketed-formulation column intentionally blank. | COMPOSITION

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Steroidal alkaloids	Solasodine, Solanine Whole plant	No analogue. Solasodine has been used as a starting material for steroid semi-synthesis.

The analogue column is what makes the interaction reasoning tractable: where a constituent has a marketed structural counterpart, the counterpart's interaction profile is the starting hypothesis for the plant.

Looking up structures and physicochemical properties from PubChem…

03 Stated application

Reported activity: Ayurvedic (Makoi) use for liver disorders, ulcer, diarrhoea and skin disease; TCM for inflammation and oedema. Ripe berries and cooked leaves are eaten as food in India and parts of Africa.
Reported adverse effects: TOXICITY IS RIPENESS- AND PART-DEPENDENT - THIS IS THE WHOLE POINT. Glycoalkaloids (solanine, solasonine, solamargine) are concentrated in GREEN UNRIPE BERRIES and leaves; content falls sharply as fruit ripens, and fully ripe black berries are eaten as food. Leaves must be cooked to detoxify. Solanine poisoning: nausea, vomiting, abdominal pain, diarrhoea, headache, vertigo, chills, sweating, speech impairment, confusion, hallucination, arrhythmia, seizure, coma, death in severe cases. FOOD-CHAIN ROUTE: contamination of commercially frozen green beans with unripe S. nigrum caused a cluster of solanine poisonings in the UK, with symptoms 7-10 h after exposure. Alkaloid content varies markedly between strains.

04 Interaction matrix

Source column, verbatim: THEORETICAL: additive with hepatotoxic drugs. Cholinesterase-inhibiting activity of glycoalkaloids is described but clinical relevance is unclear.
Normalised onto 1 canonical drug class below.

Curated from the reviewed source

Drug class	Severity	Mechanism type	Provenance	Expected effect
Hepatotoxic drugs Organ toxicity	3Major	Organ-toxicity additive	curated A	Transaminase elevation, cholestasis, sinusoidal obstruction syndrome, acu…	why ▾
Class mechanism. Pyrrolizidine alkaloids, high-dose anthraquinones, kava constituents and germander-type diterpenes cause hepatocellular or sinusoidal injury that adds to the risk from paracetamol, isoniazid, methotrexate, azoles and statins. Expected Transaminase elevation, cholestasis, sinusoidal obstruction syndrome, acute liver failure. Management Baseline and 4-weekly ALT and bilirubin. Stop the botanical at any transaminase rise above three times the upper reference limit. Onset unspecified Evidence A - human data with a cited source Matched on “hepatotoxic drugs” Find evidence for this pair Map this mechanism

Predicted from constituent chemistry

These edges are not clinical findings. Each one is a rule inference: a constituent class in this plant is known to act on a target that the drug class also acts on. They are shown because a blank cell reads as “safe”, and for a Tier 1 entry a blank cell only means “not yet looked at”. Treat them as a literature-search agenda, not as a warning.

Drug class	Severity	Mechanism type	Provenance	Expected effect
Narrow-therapeutic-index CYP3A4 substrates Pharmacokinetic	4Contraindicated	PK-CYP3A4	predicted D	Toxic accumulation or subtherapeutic failure of the co-prescribed drug, s…	why ▾
Chemistry of this pair. Alkaloidal bases have pH-dependent absorption and commonly interact with hepatic CYP isoenzymes and efflux transporters. Class mechanism. Furanocoumarins, bergamottin, piperine, glabridin and berberine inhibit CYP3A4; hyperforin, andrographolide and several diterpenes induce it through PXR. Because CYP3A4 handles roughly half of marketed drugs, the affected list is broad and the direction is product-specific. Expected Toxic accumulation or subtherapeutic failure of the co-prescribed drug, sometimes fatal for antiarrhythmics, immunosuppressants and oncology agents. Management Screen the full regimen for 3A4 substrates. Where the substrate has a narrow index, avoid rather than monitor. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Antacids, PPIs and H2 blockers Gastrointestinal	2Moderate	PK-absorption	predicted D	Reduced or erratic absorption of alkaloids; heartburn and reflux from pre…	why ▾
Chemistry of this pair. Alkaloidal bases have pH-dependent absorption and commonly interact with hepatic CYP isoenzymes and efflux transporters. Class mechanism. Gastric pH elevation alters the dissolution and ionisation of alkaloidal and enteric-coated botanical products; menthol- and peppermint-oil products lose their enteric protection at high pH and can be released prematurely. Expected Reduced or erratic absorption of alkaloids; heartburn and reflux from premature release of volatile-oil preparations. Management Separate administration by 2 hours. Avoid non-enteric peppermint oil in reflux disease. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism

05 Hazard register

ripeness and plant part - green berries and raw leaves toxic, ri

06 Confusable material

These entries could be mistaken for this one in trade, in the herbarium, or in a prescription. Powdered material is often indistinguishable, so the check is macroscopic, microscopic and chromatographic rather than nominal.

Solanum virginianum

Kantakari

Solanaceae

Same genus (Solanum)

07 Mechanism map

Chemistry sorts to the left, pharmacology to the right. Dashed edges are predicted. Drag nodes, scroll to zoom, export at 3× for a figure.

species

chemical class

marker compound

drug class

expected effect

hazard

08 Open literature

Abstract-scoped query built from this binomial, its common names and its marker compounds, run live against Europe PMC, PubMed and OpenAlex, then ranked locally against an evidence hierarchy.

Checking openFDA spontaneous reports…

09 Isomechanistic neighbours

Species whose interaction profile overlaps this one, ranked by shared severity weight rather than by count — a shared contraindication counts for more than a shared minor signal. Practical use: these are the plants you should not stack with this one, because the mechanisms summate.

Species	Family	Shared classes	Jaccard
Piper methysticum Kava	Piperaceae	3	0.30
Chelidonium majus Greater Celandine	Papaveraceae	3	0.60
Tussilago farfara Coltsfoot	Asteraceae	3	0.38
Melaleuca alternifolia Tea Tree	Myrtaceae	2	0.40
Amomum subulatum Black Cardamom	Zingiberaceae	2	0.40
Salvia rosmarinus Rosemary	Lamiaceae	2	0.40

10 References and notes

Source column: Encyclopedia of Toxicology, 4th ed., Solanum nigrum (frozen bean contamination cluster)

Encyclopedia of Toxicology, 4th ed., Solanum nigrum (frozen bean contamination cluster)

manual

BibTeX for all 1 records

@article{anon,
  title = {Encyclopedia of Toxicology, 4th ed., Solanum nigrum (frozen bean contamination cluster)},
}

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