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The aim of this paper is to highlight the symptomatology in three Conium maculatum intoxication incidents, one of which was fatal. A number of studies were reviewed in order to update and summarize the relevant literature on the incidence, sociodemographic variables, method of poisoning, pathophysiology, diagnosis, variables associated with survival and fatality, management, and treatment of C. maculatum intoxication as well as the biosynthesis and biological effects of poison hemlock alkaloids. Results show that hemlock poisoning is relatively rare, although incidence varies in different regions, despite its worldwide distribution. Hemlock poisoning is more common in European and especially Mediterranean countries. The majority of the patients are adult males over 38 years of age. The clinical course of hemlock poisoning includes neurotoxicosis, tremor, vomiting, muscle paralysis, respiratory paralysis/failure, rhabdomyolysis, and acute renal failure. The therapeutic management focuses on absorption reduction, close observation for complications, and supportive therapy (especially for respiration). Acute occurrence is severe and life-threatening, but the survival rate is high if treatment is provided promptly. Recovery is rapid, generally taking only a few days.

Conium maculatum extract is used as a traditional medicine for cervix carcinoma including homeopathy. However, no systematic work has so far been carried out to test its anti-cancer potential against cervix cancer cells in vitro. Thus, in this study, we investigated whether ethanolic extract of conium is capable of inducing cytotoxicity in different normal and cancer cell lines including an elaborate study in HeLa cells. Conium's effects on cell cycle, reactive oxygen species (ROS) accumulation, mitochondrial membrane potential (MMP) and apoptosis, if any, were analyzed through flow cytometry. Whether Conium could damage DNA and induce morphological changes were also determined microscopically. Expression of different proteins related to cell death and survival was critically studied by western blotting and ELISA methods. If Conium could interact directly with DNA was also determined by circular dichroism (CD) spectroscopy. Conium treatment reduced cell viability and colony formation at 48 h and inhibited cell proliferation, arresting cell cycle at sub-G stage. Conium treatment lead to increased generation of reactive oxygen species (ROS) at 24 h, increase in MMP depolarization, morphological changes and DNA damage in HeLa cells along with externalization of phosphatidyl serine at 48 hours. While cytochrome c release and caspase-3 activation led HeLa cells toward apoptosis, down-regulation of Akt and NFkB inhibited cellular proliferation, indicating the signaling pathway to be mediated via the mitochondria-mediated caspase-3-dependent pathway. CD-spectroscopy revealed that Conium interacted with DNA molecule. Overall results validate anti-cancer potential of Conium and provide support for its use in traditional systems of medicine.

Coniine, a polyketide-derived alkaloid, is poisonous to humans and animals. It is a nicotinic acetylcholine receptor antagonist, which leads to inhibition of the nervous system, eventually causing death by suffocation in mammals. Coniine’s most famous victim is Socrates who was sentenced to death by poison chalice containing poison hemlock in 399 BC. In chemistry, coniine holds two historical records: It is the first alkaloid the chemical structure of which was established (in 1881), and that was chemically synthesized (in 1886). In plants, coniine and twelve closely related alkaloids are known from poison hemlock (Conium maculatum L.), and several Sarracenia and Aloe species. Recent work confirmed its biosynthetic polyketide origin. Biosynthesis commences by carbon backbone formation from butyryl-CoA and two malonyl-CoA building blocks catalyzed by polyketide synthase. A transamination reaction incorporates nitrogen from l-alanine and non-enzymatic cyclization leads to γ-coniceine, the first hemlock alkaloid in the pathway. Ultimately, reduction of γ-coniceine to coniine is facilitated by NADPH-dependent γ-coniceine reductase. Although coniine is notorious for its toxicity, there is no consensus on its ecological roles, especially in the carnivorous pitcher plants where it occurs. Lately there has been renewed interest in coniine’s medical uses particularly for pain relief without an addictive side effect.

Poison hemlock (Conium maculatum L.) is a weed that grows rampant in many areas of North America. Forensic toxicology laboratories rarely receive requests to analyze biological specimens for the presence of poison hemlock. This report discusses two postmortem cases that were encountered over a decade apart and describes different analytical approaches that may be used to quantify coniine, a primary poison hemlock alkaloid, in biological specimens. The first case is from 2004 and involves a 27-year-old female that was found deceased in a relatively isolated area of California. Based on the presence of plant material at the scene and signs of its ingestion at autopsy, the possibility of hemlock poisoning was considered. Toxicological testing of the blood and gastric content by quantitative selected-ion monitoring Gas Chromatography/Mass Spectrometry (SIM-GC/MS) revealed the presence of coniine at concentrations of 410 ng/mL and 9300 ng/mL, respectively. The second case is from Pennsylvania and was sent for analysis in the spring of 2019. In this case, a male in his forties was found deceased in the kitchen area of a camper. Green substances, in liquid and residue forms, were observed in the sink. Mixtures of leaf-like material were also found in several bowls and pans. Subclavian blood screened positive for coniine by full-scan Gas Chromatography/Mass Spectrometry (GC/MS). Semi-quantitative confirmation testing was performed by Liquid Chromatography Tandem Mass Spectrometry (LC-MS/MS) and showed the presence of coniine at a concentration of 35 ng/mL. These analytical approaches can be used to substantiate or exclude poison hemlock exposure as a cause of death. •Poison hemlock toxicity is due to several piperidine alkaloids, including coniine.•Two case studies are presented where coniine was attributed to the cause of death.•GC/MS and LC-MS/MS methods were developed to quantitate coniine in blood.

Increased muscular activity and damage results in a metabolic acidosis. 6, 8 Acute renal failure secondary to rhabdomyolysis has been reported. 8, 9 Treatment is symptomatic. [...]of this the hospital has now invested in specific resources that relate to plant poisoning, and people in the community who have expertise in plant identification have been identified, and have agreed to be contacted in the event of suspected poisoning.

Furanocoumarins, such as psoralen, xanthotoxin and bergapten, serve as protectants against phytopathogens and are used in pharmaceutical applications e.g. as DNA-crosslinking agents against non-melanoma skin cancers. Poison hemlock plants (Conium maculatum L.) are a known source of furanocoumarins and toxic alkaloids, but systematic research on callus and suspension cultures with the aim of eliciting secondary metabolites is lacking. Therefore callus cultures of poison hemlock were induced with 0.186 mg L−1 6-benzylaminopurine and 2 or 4 mg L−1 naphthalene acetic acid on McCown’s Woody plant medium. A broad variety of elicitors (alginic acid, cellulase, chitosan, ethylene, methyl jasmonate, salicylic acid, copper(II) sulphate and silver nitrate) were tested with an established cell suspension culture for their capacity to trigger differential metabolite accumulation. Samples were extracted and analysed by gas chromatography-mass spectrometry. Elicitation with alginic acid, cellulase, chitosan, silver nitrate and copper(II) sulphate induced furanocoumarins. Plant hormones (ethylene, methyl jasmonate and salicylic acid) were not able to induce furanocoumarins. Extracts contained bergapten, columbianetin, isopimpinellin, marmesin, oroselone, psoralen and xanthotoxin but not piperidine alkaloids. The relative amount of furanocoumarins was generally higher in the medium than in the cells. The report describes the angular furanocoumarins oroselone and columbianetin together with the linear furanocoumarin marmesin, elicited for the first time in poison hemlock.

Background Poison hemlock ( Conium maculatum ) is a common plant with a significant toxicity. Data on this toxicity is sparse as there have been few case reports and never a documented poisoning after intravenous injection. Objectives We present a case of intravenous poison hemlock injection encountered in the emergency department. Case Report We describe a 30-year-old male who presented to the emergency department after a brief cardiac arrest after injecting poison hemlock. The patient had return of spontaneous circulation in the emergency department but had prolonged muscular weakness and encephalopathy later requiring tracheostomy. Conclusion Intravenous injection of poison hemlock alkaloids can result in significant toxicity, including cardiopulmonary arrest, prolonged weakness, and encephalopathy.

In this paper histochemical investigations of the secretory structures ofConium maculatumL., are described that discriminated between ducts and vittae. The localization of alkaloids in seedlings, vegetative organs, flowers, and in the mericarp (during its development from ovary to full maturity), was achieved using specific histochemical tests.