Fact-checked by Grok 2 weeks ago

Ginkgotoxin

Ginkgotoxin, chemically known as 4'-O-methylpyridoxine (MPN), is a potent neurotoxin primarily found in the seeds of the Ginkgo biloba tree, where it occurs at concentrations of 170–404 μg/g, along with its less toxic glucoside derivative, MPN-5'-O-glucoside.^[1] This compound, structurally analogous to vitamin B6 (pyridoxine) but featuring a methyl group at the 4' position, functions as an antivitamin by competitively inhibiting pyridoxal kinase, thereby reducing the levels of the active vitamin B6 form, pyridoxal-5'-phosphate (PLP), and disrupting γ-aminobutyric acid (GABA) synthesis in the brain.^[2] Ingestion of ginkgo seeds containing ginkgotoxin can lead to acute poisoning, particularly in children and with consumption exceeding 10–20 seeds, manifesting as tonic-clonic seizures, vomiting, loss of consciousness, and in severe cases, coma or death.^[3] Ginkgotoxin was first identified as the primary toxic agent in G. biloba seeds in 1985, though reports of ginkgo seed poisoning date back to 1881 in Japan, with over 170 cases documented there historically, including a 13% mortality rate before widespread recognition of vitamin B6 treatment.^[1] While G. biloba leaves contain trace amounts (<9 μg/g), the seeds remain the main source of exposure, especially in traditional Asian cuisines where they are consumed as "ginnan" after cooking—a process that reduces ginkgotoxin levels to about 1% of raw values due to its water solubility, though risks persist with overconsumption.^[3] The toxin's mechanism mimics vitamin B6 deficiency, elevating glutamate excitability and suppressing inhibitory neurotransmission, with serum MPN levels in poisoned individuals ranging from 37–1280 ng/mL.^[2] Treatment for ginkgotoxin poisoning involves prompt intravenous administration of pyridoxine (vitamin B6), which effectively reverses symptoms in most cases without long-term sequelae, as evidenced by recoveries in pediatric and adult incidents reported in Japan, Korea, and Switzerland.^[1] Safety guidelines for G. biloba products, including standardized leaf extracts used in supplements, limit ginkgotoxin-related contaminants like ginkgolic acids to below 5 ppm to minimize neurotoxic risks, though seed-derived foods require strict portion control.^[3] Despite its dangers, G. biloba remains valued in traditional medicine, but awareness of ginkgotoxin's presence underscores the need for processed, low-toxin preparations.^[2]

Chemical Properties

Structure and Nomenclature

Ginkgotoxin, also known as 4'-O-methylpyridoxine, is a pyridine derivative with the molecular formula C₉H₁₃NO₃ and a molar mass of 183.207 g/mol.^[4] Its preferred IUPAC name is 5-(hydroxymethyl)-4-(methoxymethyl)-2-methylpyridin-3-ol, reflecting the substituted pyridine core central to its chemical identity.^[4] The molecular structure features a pyridine ring, a six-membered heterocyclic ring containing nitrogen at position 1. Substituents are positioned as follows: a methyl group (-CH₃) at carbon 2, a hydroxy group (-OH) at carbon 3, a methoxymethyl group (-CH₂OCH₃) at carbon 4, and a hydroxymethyl group (-CH₂OH) at carbon 5. This arrangement positions the methoxymethyl at the 4-position, distinguishing it from related compounds.^[4] Ginkgotoxin bears a close structural resemblance to vitamin B6 (pyridoxine), differing primarily by the 4'-O-methylation on the hydroxymethyl group at the 4-position of the pyridine ring.^[5] In pyridoxine, this group is a free hydroxymethyl (-CH₂OH), whereas in ginkgotoxin, it is modified to -CH₂OCH₃, altering the substituent without changing the overall ring framework.^[5]

Physical and Chemical Characteristics

Ginkgotoxin is typically isolated and observed as a white to off-white crystalline powder.^[6] Its molecular formula is C₉H₁₃NO₃, corresponding to a molecular weight of 183.20 g/mol.^[7] The compound has a reported melting point of 181 °C.^[8] Ginkgotoxin demonstrates moderate solubility in water, achieving up to 10 mg/mL in phosphate-buffered saline at pH 7.2, and is highly soluble in polar organic solvents such as dimethyl sulfoxide (up to 100 mg/mL), ethanol (1 mg/mL), chloroform, dichloromethane, ethyl acetate, and acetone.^[9]^[10]^[11] The calculated logP value of -0.299 reflects its slightly hydrophilic character, facilitating solubility in aqueous environments while retaining affinity for polar solvents.^[12] Ginkgotoxin maintains stability for at least four years when stored as a solid under recommended conditions, such as protection from moisture and extreme temperatures.^[13] As a structural analog of pyridoxine (vitamin B6), it shares comparable chemical reactivity, including potential sensitivity to light, heat, and alkaline conditions that may lead to degradation.^[14] Spectroscopic characterization of ginkgotoxin commonly employs UV detection in analytical methods, leveraging absorption bands associated with its pyridine ring system, often monitored around 280–300 nm.^[15]

Natural Sources

Occurrence in Ginkgo biloba

Ginkgotoxin, also known as 4'-O-methylpyridoxine, is predominantly concentrated in the seeds (ginkgo nuts) of Ginkgo biloba, where it serves as the primary reservoir within the plant. Studies have reported concentrations ranging from 0.173 to 0.4 mg/g fresh weight in raw seeds collected from various locations, highlighting variability due to geographic and environmental factors.^[16] These levels underscore the seeds as the main site of accumulation, far exceeding those in other plant parts. In contrast, leaves contain significantly lower amounts, with maximum reported concentrations of up to 5 μg/g dry weight, often approaching detection limits in commercial extracts.^[17] The distribution of ginkgotoxin in seeds shows notable seasonal variation, with concentrations increasing during the growing period and reaching a peak in August before declining toward seed maturation.^[18] This temporal pattern aligns with the plant's reproductive cycle in temperate regions. Additionally, seed maturity influences toxin levels, as immature seeds exhibit higher ginkgotoxin content compared to fully mature ones, contributing to their greater overall toxicity.^[19] A key derivative, ginkgotoxin-5'-glucoside, occurs at lower baseline levels in raw seeds but becomes more prevalent during heating or processing, where it can accumulate to levels substantially exceeding the free ginkgotoxin form in processed samples.^[20] This glycosylated compound arises from enzymatic or thermal transformations, altering the toxin's solubility and bioavailability. Ginkgotoxin and its derivatives may function as natural defenses against herbivores and microbial threats in G. biloba.^[17]

Presence in Other Plants

Ginkgotoxin and structurally related antivitamin B<sub>6</sub> compounds occur in various species of the genus Albizia within the Fabaceae family. Notably, Albizia julibrissin (the silk tree) contains derivatives such as the glycosides julibrine I and II, which have been isolated from its seeds and leaves.^[21] Similarly, Albizia tanganyicensis produces ginkgotoxin itself along with 5'-O-acetylginkgotoxin in its pods. Levels of these compounds in Albizia species are substantially lower than those typically observed in Ginkgo biloba. For example, extraction from 26 kg of A. tanganyicensis pods yielded 980 mg of ginkgotoxin, equating to approximately 0.038 mg/g (or 38 mg/kg), which is substantially lower than levels in G. biloba seeds. Trace quantities of ginkgotoxin or analogous pyridoxine derivatives are documented in additional Fabaceae plants, supporting the view that such compounds function as widespread secondary metabolites across this family. In an ecological context, these toxins in Albizia species contribute to defense mechanisms against herbivores, as evidenced by neurotoxic syndromes in livestock grazing on pod-bearing plants; affected animals exhibit hypersensitivity, tetanic spasms, and convulsions, which respond to vitamin B<sub>6</sub> supplementation.^[22]^[23]

Biosynthesis

Pathway Overview

The de novo biosynthesis of ginkgotoxin in Ginkgo biloba commences with the pentose phosphate pathway intermediates ribulose 5-phosphate and dihydroxyacetone phosphate as starting substrates.^[24] These precursors are condensed and cyclized through a series of reactions to form a pyridoxal phosphate intermediate, which undergoes specific modifications, including 4'-O-methylation, to yield ginkgotoxin.^[24] This pathway represents a specialized branch of primary metabolism adapted for the production of this antivitamin compound. The biosynthetic process is localized primarily in the seeds and leaves of G. biloba, where it is catalyzed by plastidial enzymes within the chloroplasts.^[24] This compartmentalization aligns with the organelle's role in integrating carbohydrate metabolism and secondary metabolite synthesis, ensuring efficient precursor availability. Evolutionarily, the ginkgotoxin pathway exhibits conservation with the vitamin B6 de novo biosynthesis route observed in bacteria and higher plants, sharing core glutamine amidotransferase domains and subunit interactions that facilitate pyridoxal phosphate formation. This similarity underscores a common ancestral mechanism, with plant-specific adaptations enabling the divergence toward ginkgotoxin production in G. biloba.^[24] The pathway connects to general vitamin B6 synthesis by utilizing analogous DXP-independent mechanisms prevalent in photosynthetic organisms.

Key Enzymes and Steps

The biosynthesis of ginkgotoxin in Ginkgo biloba involves key enzymes from the vitamin B6 pathway, adapted to produce this methylated derivative. The primary enzymes are the pyridoxal 5'-phosphate (PLP) synthase complex, composed of Pdx1 and Pdx2 subunits, which catalyze the glutamine-dependent formation of pyridoxal 5'-phosphate (PLP) from pentose phosphate pathway precursors. Pdx1 forms a dodecameric structure that interacts with Pdx2, the glutaminase subunit, to facilitate the condensation of ribulose 5-phosphate and dihydroxyacetone phosphate into PLP, the initial ring-closed product in the pathway.^[25]^[26] In G. biloba, orthologs such as GbPDX1 and GbPDX2 have been cloned and characterized, confirming their role in this deoxyxylulose-independent pathway.^[26]^[27] Subsequent steps convert PLP to pyridoxine through dephosphorylation and reduction, followed by methylation to yield ginkgotoxin. A dehydrogenase enzyme reduces PLP to pyridoxine or its 5'-phosphate, setting the stage for the final modification. The critical methylation step is performed by an O-methyltransferase that adds a methyl group at the 4'-O position of pyridoxine, utilizing S-adenosylmethionine as the methyl donor; this enzyme acts on either free pyridoxine or its phosphorylated form.^[25]^[28] The overall sequence thus proceeds as: (1) precursor condensation and ring closure to form PLP via the Pdx1/Pdx2 complex; (2) reduction to pyridoxine; and (3) 4'-O-methylation to produce ginkgotoxin. This process links directly to broader vitamin B6 pathway intermediates, diverging only at the methylation step unique to G. biloba.^[25] Gene regulation of these biosynthetic enzymes is tightly linked to seed development in G. biloba. Expression of GbPDX1 is highest in developing seeds, peaking in August when ginkgotoxin accumulation reaches approximately 85 µg per seed, indicating upregulation coordinated with toxin production. Similarly, multiple GbPDX2 orthologs show elevated transcription in reproductive tissues, underscoring their role in modulating vitamin B6 derivative levels during embryogenesis.^[25]^[29]

Mechanism of Action

Antivitamin B6 Properties

Ginkgotoxin, chemically known as 4'-O-methylpyridoxine, functions as an antivitamin B6 by acting as a structural analog of pyridoxine, the alcohol form of vitamin B6. This similarity enables ginkgotoxin to interfere with the metabolic activation of vitamin B6, preventing the formation of its biologically active cofactor, pyridoxal 5'-phosphate (PLP), which is essential for numerous enzymatic reactions including amino acid metabolism and neurotransmitter synthesis. The key structural feature responsible for this antivitamin activity is the 4'-O-methyl group attached to the pyridine ring, which differentiates ginkgotoxin from pyridoxine. While ginkgotoxin can be phosphorylated by pyridoxal kinase to form 4'-O-methylpyridoxine 5'-phosphate, this modified product cannot be further converted to an active form analogous to PLP, as the phosphorylated product is not a substrate for pyridoxamine 5'-phosphate oxidase. As a result, ginkgotoxin traps the kinase in a non-productive cycle, depleting cellular PLP levels and disrupting vitamin B6-dependent processes. The 4'-O-methyl group also enhances binding affinity through hydrophobic interactions with kinase residues such as Thr47 and Val231, further promoting its inhibitory role. Ginkgotoxin exerts its effects through competitive inhibition of pyridoxal kinase, the enzyme responsible for phosphorylating vitamin B6 vitamers to their 5'-phosphate derivatives. It binds to the kinase's active site with high affinity but lacks catalytic productivity in downstream steps, thereby reducing the enzyme's availability for genuine substrates. Kinetic studies have determined an inhibition constant (Ki) of approximately 3 μM for human pyridoxal kinase, underscoring its potency as an antimetabolite. This classification of ginkgotoxin as an antivitamin B6 emerged from investigations into ginkgo seed poisoning in the mid-20th century, with definitive structural and functional identification confirmed in 1985 through isolation from Ginkgo biloba seeds and analysis of its interference with vitamin B6 metabolism.

Biochemical Interactions

Ginkgotoxin primarily targets human pyridoxal kinase (PLK), the enzyme responsible for phosphorylating vitamin B6 forms such as pyridoxal (PL) to produce pyridoxal 5'-phosphate (PLP), the active cofactor. By acting as an alternate substrate with a higher affinity (Km = 4.95 × 10⁻⁶ M) compared to PL (Km = 5.87 × 10⁻⁵ M), ginkgotoxin competes for the enzyme's active site, leading to its own phosphorylation and a subsequent reduction in PLP availability.^[12] This inhibition is competitive, with a Ki value of approximately 3 µM, effectively delaying or suppressing PLP formation at physiological concentrations.^[30] The shortage of PLP as a cofactor directly impairs the activity of PLP-dependent enzymes, notably glutamate decarboxylase (GAD), which catalyzes the decarboxylation of glutamate to γ-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the central nervous system. Reduced PLP levels decrease GAD function, thereby limiting GABA synthesis without direct inhibition of GAD isoforms at relevant concentrations (IC50 > 2 mM for ginkgotoxin phosphate).^[12]^[30] This disruption results in a neurotransmitter imbalance, characterized by lowered GABA levels alongside relatively elevated excitatory glutamate signaling, which promotes neuronal hyperexcitability. The competitive nature of the inhibition can be modeled by the Michaelis-Menten equation adjusted for a competitive inhibitor:

v = \frac{V_{\max} [S]}{K_m (1 + \frac{[I]}{K_i}) + [S]}

where v is the reaction velocity, V_{\max} is the maximum velocity, [S] is the substrate concentration, K_m is the Michaelis constant, [I] is the inhibitor (ginkgotoxin) concentration, and K_i is the inhibition constant.^[30] This mechanism underscores ginkgotoxin's role as an antivitamin in B6 metabolism, exacerbating the cofactor deficiency.^[12]

Toxicity

Symptoms and Clinical Effects

Ingestion of ginkgotoxin, primarily from overconsumption of Ginkgo biloba seeds, leads to acute gastrointestinal symptoms including nausea, vomiting, diarrhea, and abdominal pain, typically onsetting within 1 to 12 hours post-ingestion.^[31] These initial manifestations are often followed by neurological effects such as confusion and loss of consciousness.^[1] Neurological symptoms are particularly prominent and include tonic-clonic convulsions and epileptic seizures, which can be severe and life-threatening.^[32] These effects are linked to disruption of GABA-mediated neurotransmission due to ginkgotoxin's antivitamin B6 activity.^[33] In children, toxicity is especially pronounced, with as few as 10 cooked seeds potentially inducing convulsions and other severe symptoms.^[31] Lethality is rare but documented in cases of significant overconsumption (e.g., 50–100 or more seeds), though exact toxic thresholds are derived from animal data and case reports, with fatalities noted in historical incidents. Infants and individuals with pre-existing vitamin B6 deficiency represent vulnerable populations, exhibiting heightened susceptibility to these clinical effects.^[33]

Treatment and Management

The primary treatment for ginkgotoxin toxicity involves intravenous administration of vitamin B6 (pyridoxine) to counteract the toxin's antivitamin B6 effects and restore normal biochemical function. Typical doses range from 50 to 100 mg, often given promptly upon suspicion of poisoning to reverse the induced vitamin B6 deficiency. Vitamin B6 supplementation directly overcomes ginkgotoxin's competitive inhibition of pyridoxal kinase, thereby alleviating neurotoxic symptoms. Supportive care is essential and includes the use of anticonvulsants such as diazepam to control seizures, particularly in cases presenting with tonic-clonic convulsions. For recent ingestions, gastric lavage may be performed to remove unabsorbed ginkgotoxin from the stomach, reducing further absorption. Prevention focuses on limiting consumption of ginkgo seeds, with recommendations to restrict intake to fewer than 5–10 cooked seeds per day for adults and to avoid them entirely in children due to heightened sensitivity. As of 2023, health authorities recommend limiting intake to a few seeds per day for adults and avoiding them in children.^[31] Proper cooking methods, such as boiling or roasting, can significantly reduce levels of both ginkgotoxin-5'-glucoside (through hydrolysis and leaching) and free ginkgotoxin (through thermal degradation and solubility), though they do not eliminate the toxins completely.^[34] With prompt administration of vitamin B6, full recovery is typical, and no long-term effects are generally observed if treatment occurs early in the course of toxicity.

Historical Context

Discovery and Research

Ginkgotoxin was first isolated in 1985 from the seeds of Ginkgo biloba by Japanese researchers investigating incidents of nut poisoning, which had been reported in traditional literature and modern cases involving convulsions and neurological symptoms. This discovery identified the compound as the primary neurotoxin responsible for "gin-nan sitotoxism," linking overconsumption of raw or underprocessed seeds to vitamin B6 antagonism. Early studies confirmed its structural similarity to pyridoxine, establishing it as an antivitamin that disrupts B6-dependent enzymatic processes.^[1] Subsequent research expanded on ginkgotoxin's biochemical interactions. A seminal 2007 study published in the FEBS Journal demonstrated that ginkgotoxin serves as an alternate substrate for human pyridoxal kinase, the enzyme responsible for phosphorylating vitamin B6 forms to their active cofactor, pyridoxal 5'-phosphate; this occurs with a Ki value of approximately 0.4 μM, explaining its neurotoxic effects through reduced GABA synthesis.^[12] These findings underscored the dual nature of ginkgo as both therapeutic and hazardous. Recent advances have focused on detection, mitigation, and genetic underpinnings. Recent 2023 analyses have examined ginkgotoxin persistence in processed foods, such as boiled or fermented seeds, despite heat treatment, highlighting the need for advanced detoxification techniques. Concurrently, genetic studies have explored biosynthetic pathways associated with secondary metabolite production in G. biloba during seed development.^[35]^[36] Ongoing research gaps include the long-term impacts of chronic low-dose exposure, which may contribute to subtle neurological deficits without acute poisoning, and the development of high-sensitivity analytical methods to ensure product safety. These areas remain critical for regulatory standardization and clinical translation.^[35]

Traditional Uses

In traditional Chinese medicine, ginkgo seeds have been employed for centuries to address respiratory and urinary conditions, including cough, asthma, and enuresis. These applications are detailed in classical texts such as the Bencao Gangmu (Compendium of Materia Medica), compiled by Li Shizhen and published in 1596, which lists 17 therapeutic uses for the seeds, primarily targeting lung ailments like chronic cough and bronchial issues.^[37] Preparations often involved boiling or processing the seeds to mitigate potential risks, reflecting an early recognition of their dual nature as both medicinal and hazardous.^[38] In Japan, roasted ginkgo seeds, known as ginnan, have long been valued as a seasonal delicacy and occasional folk remedy, sometimes used to alleviate symptoms associated with alcohol intoxication. Folklore traditions emphasize moderation, with stories warning of adverse effects from excessive intake, underscoring the seeds' role in cultural cuisine alongside precautionary tales.^[39] Historical awareness of the seeds' toxicity dates to the 19th century, with reports of ginkgo seed poisoning in Japan dating back to 1881, highlighting risks even in small quantities for vulnerable individuals.^[39] Ginkgotoxin, the primary toxin present in these traditionally used seeds, contributes to such incidents when ingestion exceeds safe limits.^[1] In contemporary settings, ginkgo's applications have shifted toward regulated supplements derived from leaf extracts, which are naturally free of ginkgotoxin and processed to ensure safety. These extracts are utilized in treatments for dementia, showing modest improvements in cognitive function for patients with Alzheimer's disease when administered at doses of 120-240 mg daily for 3-6 months.^[40]

References

[1]
Review of Ginkgo biloba-induced toxicity, from experimental studies ...
Ginkgo seed poisoning is primarily due to the neurotoxic compound 4'-O-methylpyridoxine (MPN, also known as ginkgotoxin) and MPN glucoside in ginkgo seeds. MPN ...
[2]
Ginkgo biloba: A Treasure of Functional Phytochemicals with ...
The neurotoxic chemical MPN, also known as ginkgotoxin, and its derivative MPN glucoside are the primary sources of toxicity. MPN is structurally similar to ...
[3]
The Potential of Ginkgo biloba as a Source of Biologically Active ...
While eating cooked ginkgo seeds is safer than eating them raw, they can be toxic if consumed in large amounts or over a long period of time, especially in ...
[4]
Ginkgotoxin | C9H13NO3 - ChemSpider
Molecular formula: C9H13NO3. Average mass: 183.207. Monoisotopic mass ... [IUPAC name – generated by ACD/Name]. 5-(Hydroxymethyl)-4-(methoxymethyl)-2 ...
[5]
The human pyridoxal kinase, a plausible target for ginkgotoxin from ...
Ginkgotoxin (4'-O-methylpyridoxine) occurring in the seeds and leaves of Ginkgo biloba, is an antivitamin structurally related to vitamin B(6).
[6]
https://cymitquimica.com/cas/1464-33-1/
[7]
4'-O-Methylpyridoxine
**Summary of 4'-O-Methylpyridoxine (CID 76581) Properties:**
[8]
Showing metabocard for Ginkgotoxin (HMDB0029455)
Sep 11, 2012 · Ginkgotoxin belongs to the class of organic compounds known as pyridoxines. ... LogP, Not Available, Not Available. Experimental Chromatographic ...
[9]
Ginkgotoxin | CAS NO.:1464-33-1 - GlpBio
Ginkgotoxin is a pyridoxine antimetabolite that has been found in G. biloba. 1,2 It inhibits pyridoxal kinase (Ki = 3 µM), the enzyme that converts ...<|separator|>
[10]
https://www.medchemexpress.com/4-o-methylpyridoxine.html
[11]
4'-O-Methylpyridoxine | CAS:1464-33-1 | Piperidines - BioCrick
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. Chemical Name, 5-(hydroxymethyl)-4-(methoxymethyl)-2-methylpyridin-3-ol. SMILES, CC1=NC=C( ...
[12]
The human pyridoxal kinase, a plausible target for ginkgotoxin from ...
Jan 19, 2007 · For ginkgotoxin a logP value of −0.299 was found. This is significantly higher than the logP value determined for PL (−1.182) ...
[13]
https://www.caymanchem.com/product/33460/ginkgotoxin
[14]
Biological properties of vitamins of the B-complex, part 2
May 30, 2025 · Vitamin B6 in foods is stable under acidic conditions but unstable in neutral and alkaline environments, particularly when exposed to heat or ...
[15]
Improved extraction of ginkgotoxin (4'-O-methylpyridoxine ... - PubMed
Determination was by liquid chromatography with UV or fluorescence detection. Recoveries of ginkgotoxin from a spiked and unspiked natural health product ( ...<|separator|>
[16]
A critical review of current technologies used to reduce ginkgotoxin ...
Jul 15, 2022 · Ginkgotoxin (MPN) concentrations in fresh GBS range from 170 − 404 μg/g ... leaves. The side-chains carbon atom number at the sixth ...
[17]
Ginkgo biloba and Ginkgotoxin | Journal of Natural Products
Dec 30, 2009 · The present paper summarizes recent experiences with G. biloba and its derived products and explains why their restricted use is recommended.Missing: Leistner Drewke 2010
[18]
The Potential of Ginkgo biloba as a Source of Biologically Active ...
However, it has been shown that the concentration of ginkgotoxin in the protein of ginkgo seeds increases during the growing season and reaches its maximum in ...
[19]
The Ginkgo – A Living Fossil with Poisonous Seeds
It is worth noting that immature and uncooked ginkgo seeds are more toxic. Examples of food poisoning cases caused by plant and mushroom toxins in Hong Kong ...
[20]
Toxicity of 4′-O-methylpyridoxine-5′-glucoside in Ginkgo biloba ...
Jun 1, 2011 · A vitamin B6 derivative, 4′-O-methylpyridoxine (MPN) is responsible for food poisoning by Ginkgo biloba seeds. MPN-5′-glucoside is also ...Missing: melting point
[21]
Vitamin B6: A Long Known Compound of Surprising Complexity
The best known of these derivatives is probably 4'-O-methylpyridoxine or ginkgotoxin from the tree Ginkgo biloba [12,97]. The compound has been found in ...
[22]
Albizia Versicolor Poisoning of Sheep and Goats in Malawi - PubMed
Approximately 800 animals are estimated to have died over a 9-year period on a government farm near Lake Malawi.
[23]
Experimental Albizia versicolor poisoning in sheep and its ... - PubMed
Five sheep developed severe nervous signs after being drenched with Albizia versicolor pod-material. Four of these sheep were treated with pyridoxine ...Missing: livestock | Show results with:livestock
[24]
https://doi.org/10.1021/np9005019
[25]
(PDF) Ginkgo biloba and Ginkgotoxin - ResearchGate
The 4′- O-methylating enzyme system accepts pyridoxine (11) as well as its 5′-phosphate (10) in the presence of S-adenosylmethionine (AdoMet).
[26]
The Pdx1 family is structurally and functionally conserved between ...
Here we describe the cloning of a vitamin B6 biosynthetic gene GbPDX1 from Ginkgo biloba. The gene is expressed in seeds, leaf and trunk tissue. Using yeast 2- ...
[27]
Functional and Bioinformatic Analysis of PDX2 from Ginkgo biloba
May 21, 2025 · The PDX2 gene serves as a critical catalytic component in vitamin B6 (VB6) biosynthesis pathways and plays pivotal regulatory roles in plant growth.
[28]
Biosynthesis of 4'-O-Methylpyridoxine (Ginkgotoxin) from Primary ...
Dec 31, 1999 · This indicates that ginkgotoxin is likely to be derived by 4'-O-methylation of pyridoxine (1). The G. biloba cell suspension culture may be a ...
[29]
Systematic Identification and Functional Study of Vitamin B6-Related ...
This study provides the first comprehensive functional analysis of the PDX2 gene family in Ginkgo and confirms their critical role in VB6 biosynthesis. These ...Missing: ginkgotoxin | Show results with:ginkgotoxin
[30]
Insights into Pyridoxal Kinase Inhibition | PLOS One
Jul 18, 2012 · We have performed structural and kinetic studies on hPL kinase with several potential inhibitors, including ginkgotoxin and theophylline.<|separator|>
[31]
Ginkgo Seed Poisoning - Centre for Food Safety
Jul 19, 2023 · Eating excessive amounts of ginkgo seeds in one go can cause food poisoning due to the natural toxins present in the seeds.
[32]
Epileptic Seizure from Ginkgo Nut Intoxication in an Adult - PMC
Jan 28, 2020 · We report a 48-year-old male patient experiencing acute convulsions presumably due to overconsumption of gingko nuts.
[33]
Ginkgotoxin Induced Seizure Caused by Vitamin B6 Deficiency
We experienced a case of a 51-year-old female patient with generalized tonic clonic seizure and postictal confusion after eating large amounts of ginkgo nuts.Missing: toxicity | Show results with:toxicity
[34]
Permitted daily exposure from preclinical studies of Ginkgo biloba L ...
Leistner and Drewke (2010) reported that the highest concentration of ginkgotoxin in Ginkgo biloba L. leaves was 5 µg, corresponding to 7 µg/g in leaves ...
[35]
Efficacy and safety of ginkgo preparation in patients with vascular ...
Sep 11, 2020 · This systematic review will explore whether ginkgo preparation is an effective and safe intervention for vascular dementia.
[36]
glucoside in Ginkgo biloba L. seeds - ScienceDirect
Overconsumption of Ginkgo biloba seeds leads to poisoning. Ginkgotoxin and ginkgotoxin-5′-glucoside is responsible for Ginkgo biloba seeds poisoning.
[37]
Novel mechanisms for the synthesis of important secondary ...
Jun 6, 2023 · The results showed that most of the metabolites in ginkgo seeds were more active in June and August, and 208 of them (Group 1) significantly ...
[38]
Ginkgo - Institute for Traditional Medicine
In 1930, a Japanese researcher reported on the effect of ginkgotoxin on isolated frog heart; in the same year he also reported on skin irritation caused by ...
[39]
Ginkgo: Cultural Background and Medicinal Usage in China
Sep 7, 2022 · Today, the gingko seed continues to be prescribed regularly by traditional Chinese medicine practitioners around the world, either as a lung ...
[40]
Ginkgo Seed Poisoning | Pediatrics - AAP Publications
Feb 1, 2002 · A 2-year-old girl presented with vomiting and diarrhea 7 hours after eating a large quantity of ginkgo seeds. She exhibited an afebrile convulsion 9 hours ...Missing: ginkgotoxin vulnerable
[41]
The Efficacy of Ginkgo biloba on Cognitive Function in Alzheimer ...
There is a small but significant effect of 3- to 6-month treatment with 120 to 240 mg of G biloba extract on objective measures of cognitive function in AD.Missing: ginkgotoxin removal