Grayanotoxins in Mad Honey: Therapeutic Potential, Regional Comparison, and the 2025 Research Frontier

This 2025 review from Tribhuvan University in Kathmandu, Nepal, is the most recent peer-reviewed synthesis of grayanotoxin research in the CMHI library. It is also the first paper in the library authored by someone from Nepal. That provenance matters. The review is not a narrow technical paper; it draws together the chemical composition of mad honey, the toxicological profile from animal studies, a regional comparison of concentration data between Nepal and Turkey, documented human case records from both countries, the molecular mechanism of grayanotoxin action, evidence for therapeutic applications, and a policy framework for what the field needs next.

What distinguishes this paper from the earlier three CMHI entries is scope and orientation. Jansen (2012) established the mechanism and clinical case record. Ahn (2022) documented batch-level concentration variability. Ullah (2018) built the diagnosis and treatment protocol. This paper situates all of that within the current state of the research in 2025, and makes an honest accounting of what still needs to happen before therapeutic potential can move from animal evidence to clinical application.

Contents

1. What the Paper Covers
2. Nepal and Turkey: What the Regional Concentration Data Shows
3. The Sodium Channel Mechanism: What the 2025 Review Adds
4. Animal Study Evidence for Therapeutic Applications
5. Genotoxicity: Evidence the CMHI Library Has Not Addressed Until Now
6. Blood Concentration Thresholds: A New Clinical Reference Point
7. Human Case Records: Nepal and Turkey in the Same Frame
8. Policy and Future Research: What the 2025 Review Calls For
9. What We Don’t Know Yet
10. Index Verdict
11. Sources

What the Paper Covers

The paper is organised around six areas. It begins with the sources and chemical composition of mad honey, documenting how different plant species, altitudes, climates, and harvest seasons drive variation in grayanotoxin content. It then reviews the toxicological effects of GRAYs across animal studies, a body of literature that now includes hepatotoxicity, genotoxicity, ovarian toxicity, and cardiovascular effects in addition to the better-known bradycardia and hypotension. The third section presents human intoxication cases from Nepal and Turkey side by side. 

 

The fourth section covers the molecular mechanism of GRAY-induced voltage-gated sodium channel dysfunction, building on and extending the mechanistic record established in earlier literature. The fifth section addresses what has become an open clinical question in the field: whether grayanotoxins have genuine therapeutic applications, and what the current evidence base actually supports. The sixth section lays out the policy and research agenda, which standardisation, regulatory oversight, and study design the field requires before therapeutic applications can be responsibly pursued.

Nepal and Turkey: What the Regional Concentration Data Shows

One of the most practically useful parts of this paper is Table 1, which brings GRAY concentration data from Nepal (Himalayan region) and Turkey (Black Sea region) together in one review. The 2023 EFSA assessment had already tabulated most of the same studies side by side in its occurrence data (Schrenk et al. 2023). This paper assembles the data in one place.

The table below brings together concentration data from studies the 2025 review cites; the values are taken from the primary papers and the 2023 EFSA assessment (Schrenk et al. 2023). All values are in µg/g (micrograms per gram of honey) unless noted.

 

What the comparison does and does not show

Several things emerge from reading this data together. First, both regions produce honey with substantial concentration variability, not just between regions but within them. The Nepal data from Ahn et al. (2022) alone spans a factor of 86 for GRAY-I and 255 for GRAY-III across the 33 of 60 samples in which toxin was quantified. Turkish data shows comparable internal variation. No single figure characterises either region’s honey.

Second, the regions do not have clearly ranked profiles. Turkish honey, in some studies, shows higher GRAY-III dominance. Aygun et al. (2018) found mean GRAY-III at 27.60 µg/g versus GRAY-I at 8.73 µg/g, while Nepal honey from Ahn et al. (2022) shows both isoforms reaching similar high-end values. Only one Turkish sample in the table, the honey analysed by These et al. (2015), has a reported GRAY-II value, a semi-quantitative 2.0 µg/g; the Aygun studies measured GRAY-I and GRAY-III only, and GRAY-II was also found, at up to 1.1 µg/g, in honey imported from Nepal (Lee et al. 2008).

Third, and most importantly, the comparison is not methodologically controlled. The studies in Table 1 used different analytical methods, different sample sources, and were conducted at different times. Aggregating them gives a useful empirical picture but not a head-to-head comparison. The paper is explicit about this. Environmental factors, altitude, climate, soil composition, harvest season, and specific plant species, are as likely to drive concentration differences as geography alone.

The Sodium Channel Mechanism: What the 2025 Review Adds

The foundational mechanistic account of how grayanotoxins work on voltage-gated sodium channels is covered in depth in the Jansen (2012) CMHI entry. The 2025 paper builds on that record with a more detailed structural description of the channels themselves and some additional mechanistic pathways that were not part of the 2012 treatment.

Voltage-gated sodium channel structure

GRAYs disrupt voltage-gated sodium channels (VGSCs), complex heteromultimeric structures consisting of a pore-forming α subunit and auxiliary β subunits. The α subunit is organised into four homologous transmembrane domains (DI–DIV), each containing six helical segments (S1–S6). The S1–S4 segments form the voltage-sensing domain, characterised by positively charged lysine and arginine residues along the S4 helix that enable voltage detection and channel activation. The S5 and S6 segments form the pore through which sodium ions pass (Schrenk et al. 2023).

Site-directed mutagenesis of the rat skeletal muscle sodium channel (Nav1.4) has placed the grayanotoxin receptor on the S6 segments of all four domains, which line the pore (Ishii et al. 1999; Kimura et al. 2000; Maejima et al. 2003). Within domain IV segment 6, Maejima et al. (2003) proposed that Phe-1579 controls the toxin’s access to its receptor and that Tyr-1586, the more critical of the two, controls its binding. Grayanotoxin removes fast inactivation and shifts activation to more negative voltages, so affected channels stay open (Maejima et al. 2003).

Downstream effects beyond vagal stimulation

The consequence of persistent channel activation is sustained sodium influx into excitable cells. Neurons experience increased energy demands as a result of continuous depolarisation, and if the resting potential is not restored, cellular damage can follow. The accumulation of intracellular sodium also triggers secondary calcium influx through voltage-dependent calcium channels, a pathway that impacts neurotransmitter release and muscle activity, and that underlies some of the cardiac and neurological symptoms seen in poisoning cases.

The paper also covers the neurological effects of poisoning. EFSA lists convulsions, mental confusion, agitation and loss of consciousness among the effects of higher doses (Schrenk et al. 2023). In rats, however, grayanotoxin injected into the brain suppressed epileptiform activity, and those authors concluded that it is not directly responsible for the seizures seen in mad honey poisoning (Gündüz et al. 2012). In the heart, sustained VGSC activation disrupts conduction, creating the conditions for arrhythmias, including atrial fibrillation and ventricular tachycardia. GRAYs also induce vasodilation through mechanisms not fully characterised, which contributes to the hypotension documented in clinical cases.

Animal Study Evidence for Therapeutic Applications

The therapeutic potential of mad honey and grayanotoxins is one of the most discussed and least clearly evidenced topics in the field. This paper addresses it directly, synthesizing the available animal study data across several application areas. The discipline required in this section is the same as in the clinical signs sections: document what the evidence shows, attribute it to the right study, and state clearly what level of evidence that represents.

The table below organises the documented therapeutic findings from the 2025 review and the studies it cites.

 

The fracture healing finding in context

The fracture healing result in this paper comes from Sahin et al. (2018), who gave female Sprague-Dawley rats with a femur fracture 80 mg/kg of mad honey a day. At 15 days mad honey made no significant difference, while propolis did. At 30 days both the mad honey and propolis groups healed significantly better than controls, with no significant difference between the two, and at neither time point did mad honey differ significantly from normal honey. The grayanotoxin content of the honey was not measured. Propolis is widely regarded in ethnopharmacology for its wound healing properties, which makes this a meaningful comparison rather than a trivial one.

What it is not is clinical evidence. The study used a rat fracture model, an oral dose of 80 mg/kg, and a 30-day observation window. Translating that to human therapeutic use would require dose-escalation trials, pharmacokinetic data in humans, and a safety assessment that accounts for the genotoxicity findings documented elsewhere in the same literature. None of those studies exists yet.

Blood glucose and blood pressure: the folk medicine connection

The blood glucose reduction documented by Oztasan et al. (2005) and the blood pressure reduction documented by Turkmen et al. (2013) are the two findings that most directly connect to the historical folk use record. Mad honey has been used for centuries in Turkey and Nepal for hypertension and diabetes management. These animal studies are consistent with those uses, but they do not establish a mechanism: Oztasan et al. (2005) suggested that grayanotoxin may raise insulin secretion by stimulating the parasympathetic nervous system or M2 muscarinic receptors, and Turkmen et al. (2013) reproduced in rats the fall in blood pressure and heart rate seen in poisoning. They do not, by themselves, establish therapeutic efficacy in humans. The paper is explicit that clinical trials are the next required step.

Genotoxicity: Evidence the CMHI Library Has Not Addressed Until Now

None of the previous three CMHI articles, Ahn (2022), Jansen (2012), or Ullah (2018), documents genotoxic effects of grayanotoxins or mad honey. The 2025 review is the first paper in the CMHI library to synthesize this body of evidence, and it warrants its own section rather than a footnote to the animal toxicity data.

Genotoxicity refers to the capacity of a substance to damage genetic material, DNA, chromosomes, or the replication machinery that copies them. The concern is not theoretical. Two animal studies, in rats and mice, have reported genotoxic signals from mad honey or GRAY-III; EFSA judged the mouse study clearly positive and the rat study unclear (Schrenk et al. 2023).

What the animal studies document

• Eraslan et al. (2018) administered mad honey to Wistar male rats at three dose regimens: acute (12.5 g/kg single dose), subacute (7.5 g/kg daily for 21 days), and chronic (5 g/kg daily for 60 days); the honey contained about 34 µg/g GRAY-I and 6.5 µg/g GRAY-III (Schrenk et al. 2023). Oxidative stress markers rose in every exposure period, and the Comet assay, which measures DNA strand breaks in individual cells, showed changes in tail intensity in some tissues in each period, but micronucleus counts did not change. EFSA judged the evidence for genotoxicity from this study unclear because of poor reporting (Schrenk et al. 2023).
• Rasgele et al. (2021) found increased chromosomal aberrations at every tested dose, and increased micronucleated erythrocytes at the highest dose, in mice given Rhododendron honey containing GRAYs, which the authors read as genotoxic and cytotoxic effects on bone marrow cells. The micronucleus test is a standard genotoxicity biomarker; elevated micronucleated erythrocytes reflect chromosomal damage during cell division.
• Cakmak-Arslan et al. (2020) found changes consistent with lipid peroxidation, increased membrane fluidity and protein denaturation in the livers of mice given GRAY-III or the highest dose of mad honey. Oxidative stress is one route by which indirect DNA damage could occur, but EFSA found no evidence to say whether grayananes damage DNA directly or indirectly (Schrenk et al. 2023).
• In the Rasgele et al. (2021) study, GRAY-III given alone by injection, at one dose level of 0.01 mg/kg, did not increase chromosomal aberrations, but did increase micronucleated polychromatic erythrocytes (MNPCE) and reduce the PCE/NCE ratio in bone marrow, which EFSA read as a genotoxic effect in the presence of bone marrow toxicity (Schrenk et al. 2023).

The ovarian toxicity finding

A specific genotoxicity-adjacent concern documented in this paper involves female reproductive tissue. Yeşil Sarsmaz et al. (2024) administered mad honey to female Sprague-Dawley rats at 80 mg/kg oral gavage over 30 days. The treated animals showed moderate to strong caspase-3 immunostaining, a marker of apoptosis, TUNEL-positive staining in most Graafian follicles, and high expression of inducible nitric oxide synthase (iNOS). These findings indicate that mad honey may promote ovarian follicular atresia: accelerated cell death in developing ovarian follicles.

Follicular atresia is a normal physiological process, but its acceleration can affect fertility. The clinical relevance of this finding in humans at typical mad honey intake amounts is not established. No human study has examined ovarian function in relation to mad honey consumption. The paper documents the finding; it does not extrapolate it to human clinical risk.

The scope of what is and is not known

Blood Concentration Thresholds: A New Clinical Reference Point

One of the most practically significant pieces of data in the 2025 paper is the blood concentration threshold information compiled from Choi et al. (2017). Earlier CMHI articles, particularly Ullah (2018), document intake-weight thresholds for poisoning: approximately 15–30 grams of mad honey are associated with intoxication onset in documented cases. What Choi et al. (2017) add is a pharmacokinetic reference: what GRAY blood concentrations actually correspond to clinical outcomes.

Choi et al. (2017) analysed GRAY-I and GRAY-III blood concentrations in six patients who consumed Rhododendron liqueur. The liqueur itself contained 1.436 ng/mL of GRAY-I and 16.907 ng/mL of GRAY-III. Initial blood levels ranged from 2.9 to 58.0 ng/mL for GRAY-III and from below the quantification limit to 8.33 ng/mL for GRAY-I. The authors estimated that the minimum blood levels that caused hypotension were between 17.83 and 27.3 ng/mL for GRAY-III and between 2.52 and 4.55 ng/mL for GRAY-I.

Why this matters beyond the case report record

The intake-weight data from case reports, 15–30 grams, reflect what patients reported consuming before symptoms appeared. That figure is useful but limited, because the same gram weight of honey can contain radically different GRAY concentrations depending on the batch. A jar with 0.75 µg/g of GRAY-I and a jar with 64.86 µg/g, both documented in the Ahn (2022) Nepal sample set, represent an 86-fold difference in actual GRAY content for the same physical amount of honey.

The blood concentration data bridges that gap. It gives an estimate, from six patients who drank the same liqueur, of the blood level, rather than the intake weight, that corresponds to the clinical effect. It comes from a small dataset, and a larger series has not confirmed a link between blood levels and symptoms: Aygun et al. (2018), in 25 patients, found no association between blood grayanotoxin levels and clinical data.

The EFSA assessment (Schrenk et al. 2023) found that selected concentrations of 1 and 10 mg/kg of GRAY-I and GRAY-III combined in honey raised health concerns for acute toxicity, and calculated 0.05 mg/kg as the highest concentration it was at least 75% certain would protect all age groups, toddlers included, from acute intoxication. This is a relevant caution for public health guidance: the primary poisoning literature is dominated by cases in middle-aged men, which may not represent the full risk profile.

Human Case Records: Nepal and Turkey in the Same Frame

The paper’s Table 3 compiles mad honey case reports from Nepal and Turkey side by side. It covers cases spanning decades, documenting intake amounts (where available), presenting vital signs, cardiac rhythm abnormalities, treatment protocols, and recovery times.

What the Nepal cases document

Several Nepal cases in the table are noteworthy for the specificity of their clinical details. Aryal et al. (2017), a paper also authored from Nepal, reported a 73-year-old man who presented with cardiovascular collapse, with severe bradycardia, AV block and hypotension, after eating wild honey. Thapa et al. (2024) reported five cases from 2022–23, with intake of one to two teaspoons (about 10–20 mL), treated with intravenous fluids and, depending on the case, atropine, noradrenaline or adrenaline. Two patients were discharged after 24 hours and three, who needed intensive care, after 48 hours.

Across the Nepal cases in the review, intake amounts are frequently recorded in teaspoons or milliliters rather than grams, reflecting the way mad honey is typically consumed in Nepal: as a folk medicine taken in small, deliberate doses rather than as a food. This is a meaningful distinction. The case in which a patient consumed about 200 mL (Adhikari and Bhandari 2021) represents a different exposure scenario than someone taking two teaspoons.

Turkey and Nepal: the same clinical picture

Despite the different regional context and, in many cases, different Rhododendron species involved, the clinical presentation across Turkish and Nepalese cases follows the same pattern: bradycardia, hypotension, dizziness, nausea, and in severe cases cardiac rhythm abnormalities including AV block and atrial fibrillation. Treatment response is also consistent: with intravenous fluids and atropine, patients were generally discharged within 24 hours after recovery in the 1,199 cases reviewed by Silici and Atayoglu (2015), and EFSA describes recovery as generally within 1 to 2 days (Schrenk et al. 2023). Temporary pacemaker use is documented in Turkish cases involving complete AV block (Ullah et al. 2018).

This consistency reinforces what the mechanism literature establishes: the toxin is the same, the channel target is the same, and the clinical presentation follows predictably from the pharmacology, regardless of where the honey was produced.

Policy and Future Research: What the 2025 Review Calls For

The final section of the paper does something none of the three prior CMHI entries do: it addresses what still needs to happen. This matters for a research index because it marks the current boundary of the literature, what is established, and what remains to be done.

The research agenda

The paper explicitly calls for three research priorities. First: pharmacokinetic studies to clarify how GRAYs are metabolised and excreted in humans. The rapid symptom resolution, typically within 24 hours, suggests efficient clearance, but the metabolic pathway is not characterised. Understanding it is the precondition for developing standardised dosing guidance. Second: diagnostic biomarkers for rapid clinical identification. No blood or urine test for GRAYs is commercially available (Ullah et al. 2018). Diagnosis rests on the history of honey intake and the clinical findings. A validated biomarker would significantly improve both the speed and accuracy of diagnosis, particularly in non-endemic regions where clinicians have limited experience with the presentation. Third: clinical trials to evaluate therapeutic efficacy. The animal evidence for fracture healing, blood glucose reduction, and blood pressure lowering is sufficiently documented to justify well-designed human studies. None has been conducted.

The regulatory position

The paper cites the 2023 EFSA risk assessment (Schrenk et al. 2023), a scientific opinion prepared for the European Commission rather than a regulation. It assesses the risk of acute poisoning, including from honey taken as folk medicine, but not any therapeutic benefit. The paper calls for enhanced regulatory oversight and public health awareness, particularly given that mad honey is increasingly available internationally through online retail, often without adequate labelling of grayanotoxin content or concentration.

The paper’s concluding recommendation is that scientists, policymakers, and local communities, specifically naming Nepal and Turkey, need to work together to reconcile traditional knowledge with evidence-based medicine. That is not a hedge. It is a statement that neither the folk medicine tradition nor the toxicological risk profile alone gives an adequate picture of what mad honey is and how it should be managed.

What We Don’t Know Yet

The 2025 paper is explicit about its limitations in a way that strengthens rather than weakens its credibility. A research review that accurately maps the boundaries of what is known is more useful than one that overstates its conclusions. The limitations below are drawn directly from the paper’s own statements and from the structural gaps in the studies it cites.

• No clinical trial for any therapeutic application: every therapeutic finding documented in this paper is animal study evidence or case report level. The paper explicitly calls for clinical trials as a research priority, not as a hedge, but as an acknowledged gap in the current literature.
• Pharmacokinetics are incompletely characterised: rapid absorption is documented and clearance within 24 hours is inferred from symptom resolution, but the full metabolic pathway for GRAYs in humans is not established. Without this, standardised dosing is not possible.
• No diagnostic biomarker exists: diagnosis still rests on the history and clinical picture, as described by Ullah et al. (2018) and Thapa et al. (2024). The paper identifies biomarker development as a research priority.
• Genotoxicity data are animal-only: documented in rats and mice at doses that may not correspond to typical human consumption in GRAY exposure terms. No equivalent human data exists. Cucer and Eroz (2010) found no genotoxic effects on cultured human lymphocytes, but that is an in vitro model under different exposure conditions.
• Ovarian toxicity is not characterised in humans: the Yeşil Sarsmaz et al. (2024) finding in female rats at 80 mg/kg over 30 days has no human equivalent study. Clinical relevance is unknown.
• The Nepal vs Turkey comparison is not methodologically controlled: Table 1 aggregates studies using different analytical methods, different sample origins, and different time periods. It gives a useful empirical picture but not a direct comparison. Environmental factors drive at least as much of the variation as geography.
• No standardised dosing framework exists: variable toxin concentrations between batches, different susceptibility profiles across populations, and the absence of pharmacokinetic data make a universal safe threshold impossible to establish with the current evidence base. This is the most consequential gap for anyone seeking to use mad honey for therapeutic purposes.

Index Verdict

This 2025 review from Tribhuvan University, Kathmandu, Nepal, is the most recent synthesis of grayanotoxin research in the CMHI library and the anchor article for its therapeutic framing.

What it confirms is nuanced. The pharmacological basis for several traditional therapeutic uses, blood pressure reduction, blood glucose lowering, and fracture healing, is documented in animal models at specific doses. The fracture healing finding (Sahin et al. 2018) comes from a single rat study, in which mad honey and propolis both improved healing over controls at 30 days and mad honey did not outperform propolis or normal honey. None of these findings has been tested in controlled clinical trials in humans. The paper is direct about this: clinical trials are not a future refinement of the evidence base; they are the missing layer without which therapeutic recommendations cannot responsibly be made.

What the paper also documents is a genotoxicity and ovarian toxicity concern in animal studies that has not been previously addressed in the CMHI library. These findings are not grounds for categorical rejection of therapeutic interest; they are animal evidence at doses that may not correspond to typical human consumption. But they are also not grounds for dismissal. They belong in the record, accurately scoped.

The regional comparison confirms what the Ahn (2022) entry established at the batch level: neither Nepal nor Turkey produces honey with a uniform concentration profile. Both regions show wide variability. Batch-level testing remains the only reliable basis for knowing what is in any specific jar.

The paper’s conclusion positions mad honey at the intersection of ethnopharmacology and contemporary toxicology, two frameworks that have historically been treated as opposites. The 2025 review argues they need to be reconciled. CMHI will update this entry when any of the research priorities the paper calls for, pharmacokinetic studies, diagnostic biomarkers, or clinical trials, produce peer-reviewed results.

Anyone experiencing symptoms consistent with grayanotoxin poisoning, bradycardia, hypotension, or significant dizziness after honey consumption should seek emergency medical attention immediately.

 

Sources

• Adhikari S, Bhandari A (2021), Wild Honey Poisoning: A Case Report from Remote Mountains. Global Journal of Medical Research 21(5):33-35.
• Ahn SY, Kim S, Cho H (2022), Determination of Grayanotoxin I and Grayanotoxin III in mad honey from Nepal using liquid chromatography-tandem mass spectrometry. Analytical Science and Technology 35(2):82-91.
• Aryal BD, et al. (2017), Cardiovascular collapse due to wild honey Intoxication: A case report. Health Renaissance 13(2):170-172.
• Aygun A, et al. (2015), Examination using LC-MS/MS determination of grayanotoxin levels in blood, urine, and honey consumed by patients presenting to the emergency department with mad honey intoxication and relations with clinical data: a preliminary study. Annals of Saudi Medicine 35(2):161-164.
• Aygun A, et al. (2018), Grayanotoxin levels in blood, urine and honey and their association with clinical status in patients with mad honey intoxication. Turkish Journal of Emergency Medicine 18(1):29-33.
• Cakmak-Arslan G, et al. (2020), Determination of the dose-dependent toxic effects of mad honey on mouse liver using ATR-FTIR spectroscopy. Spectrochimica Acta Part A: Molecular and Biomolecular Spectroscopy 228:117719.
• Choi HL, et al. (2017), Relationship between blood toxin level and clinical features in patients with grayanotoxin poisoning: six clinical cases. Clinical Toxicology 55(9):991-995.
• Cucer N, Eroz R (2010), Investigation of mutagenic effects of grayanotoxins II and III on cultured human lymphocytes. Al Ameen Journal of Medical Sciences 4:293-299.
• EFSA CONTAM Panel (2023), Risks for human health related to the presence of grayanotoxins in certain honey. EFSA Journal 21(3):7866.
• Eraslan G, et al. (2018), Effect on oxidative stress, hepatic chemical metabolizing parameters, and genotoxic damage of mad honey intake in rats. Human & Experimental Toxicology 37(9):991-1004.
• Gül A, Pehlivan T (2018), Antioxidant activities of some monofloral honey types produced across Turkey. Saudi Journal of Biological Sciences 25(6):1056-1065.
• Gündüz A, et al. (2012), Is grayanotoxin directly responsible for mad honey poisoning-associated seizures?. Turkish Journal of Medical Sciences 42:1086-1092.
• Ishii H, et al. (1999), Point-Mutations Related to the Loss of Batrachotoxin Binding Abolish the Grayanotoxin Effect in Na+ Channel Isoforms. The Japanese Journal of Physiology 49(5):457-461.
• Jansen SA, et al. (2012), Grayanotoxin Poisoning: ‘Mad Honey Disease’ and Beyond. Cardiovascular Toxicology 12(3):208-215.
• Kimura T, et al. (2000), On site of action of grayanotoxin in domain 4 segment 6 of rat skeletal muscle sodium channel. FEBS Letters 465(1):18-22.
• Lee SY, et al. (2008), Determination and monitoring of grayanotoxins in honey using LC-MS/MS. Korean Journal of Food Science and Technology 40:8-14.
• Maejima H, et al. (2003), Distinct Sites Regulating Grayanotoxin Binding and Unbinding to D4S6 of Nav1.4 Sodium Channel as Revealed by Improved Estimation of Toxin Sensitivity. Journal of Biological Chemistry 278(11):9464-9471.
• Nassibou S, et al. (2020), Mad honey of Nepalese origin-related grayanatoxin intoxication. Toxicon 184:202-203.
• Öztaşan N, et al. (2005), Effects of mad honey on blood glucose and lipid levels in rats with streptozocin-induced diabetes. Turkish Journal of Veterinary and Animal Sciences 29(5):1093-1096.
• Rasgele PG, et al. (2021), Investigation of genotoxic effects of rhododendron honey using three mammalian bioassays in vivo. Drug and Chemical Toxicology 45(5):2301-2310.
• Sahin A, et al. (2018), A Comparison of the Effects of Grayanotoxin-Containing Honey (Mad Honey), Normal Honey, and Propolis on Fracture Healing. Medical Principles and Practice 27(2):99-106.
• Silici S, Sagdic O, Ekici L (2010), Total phenolic content, antiradical, antioxidant and antimicrobial activities of Rhododendron honeys. Food Chemistry 121(1):238-243.
• Silici S, Atayoglu AT (2015), Mad honey intoxication: A systematic review on the 1199 cases. Food and Chemical Toxicology 86:282-290.
• Thapa AJ, et al. (2024), Mad honey (wild honey) poisoning: clinical case series from Nepal. Annals of Medicine & Surgery 86(9):4975-4978.
• These A, et al. (2015), A case of human poisoning by grayanotoxins following honey ingestion: elucidation of the toxin profile by mass spectrometry. Food Additives & Contaminants: Part A 32(10):1674-1684.
• Türkmen S, et al. (2013), The dose-dependent effect of grayanotoxin on the cardiovascular system. Turkish Journal of Medical Sciences 43(5):700-705.
• Ullah S, et al. (2018), Mad honey: uses, intoxicating/poisoning effects, diagnosis, and treatment. RSC Advances 8(33):18635-18646.
• Yeşil Sarsmaz H, et al. (2024), The relationship between oxidative stress and apoptosis of histopathological changes in the ovary made by mad honey containing grayanotoxin. Food and Chemical Toxicology 187:114634.