Toxicity Of Metaldehyde Research Articles

Research on the Mechanism of Metaldehyde on Pomacea canaliculata.

Golden apple snail (Pomacea canaliculata), a major alien invasive organism in China, affects food production and poses a threat to human health. Metaldehyde is a highly effective, commonly used snail killer with low toxicity. Virulence determination, tissue section, iTRAQ and RNA interference were used to systematically study the toxicity of metaldehyde on P. canaliculata. The molluscicidal activity tests showed that metaldehyde exhibits strong toxicity against P. canaliculata. Physiological and biochemical data indicate that metaldehyde can cause damage to the gills, liver, pancreas, and kidneys of snails, also reduce the oxygen consumption rate and ammonia excretion rate of golden apple snails, and cause neurological diseases. The proteome of the gill region of the golden apple snail after exposure to metaldehyde was analyzed by using iTRAQ technology. A total of 360 differential proteins were identified, and four target proteins were screened, namely, alpha-protein kinase 1 (ALPK1), cubilin (CUBN), sodium- and chloride-dependent GABA transporter 2 (GAT2), and acetylcholinesterase (AChE). RNAi was used to target the four proteins. After the ALPK1 and CUBN protein genes were interfered with by metaldehyde treatment, it was found that the mortality rate of the golden apple snail significantly increased. However, interference of GAT2 and AChE protein genes by metaldehyde led to no significant change in the mortality rates of the snails. The histopathological observation of the gill showed that the rate of cilia shedding in the gill decreased after the interference of ALPK1 and CUBN protein genes.

Assessing the combined toxic effects of metaldehyde mollucide

The excessive use of metaldehyde in agriculture to combat mollusks endangers both the environment and non-target organisms. The aim of this study is to investigate the toxicity caused by metaldehyde in Alliumcepa with the help of physiological, cytogenetic, biochemical and anatomical parameters. Also, DNA fragmentation caused by metaldehyde in root tip cells was measured by the "Comet Assay" method. The control group was germinated with tap water and the application groups were germinated with 20 mg/L metaldehyde, 40 mg/L metaldehyde, 100 mg/L metaldehyde and 200 mg/L metaldehyde for 72 h. The results of the physiological parameters showed that metaldehyde had a growth-limiting effect in A.cepa, depending on the application dose. According to root elongation levels, the EC50 (effective concentration) value for metaldehyde was 60.6 mg/L in A.cepa. As the treatment dose increased, the incidence of micronucleus and chromosomal aberrations gradually increased while mitotic index decreased. Metaldehyde exposure induced damages such as sticky chromosome, fragment, unequal distribution of chromatin, reverse polarization, bridge, and multipolar anaphase. In addition, metaldehyde caused cell damage in epidermis and cortex, thickening of the cortex cell wall and flattened cell nucleus in root meristem. Increasing doses of metaldehyde application also increased malondialdehyde levels, superoxide dismutase and catalase activities. As a result, it has been determined that the toxicity of metaldehyde in plants is versatile and the A.cepa test material is a suitable biological indicator to determine this toxicity.

Acute metaldehyde poisoning from ingestion: clinical features and implications for early treatment.

AimsTo describe and compare the clinical features of patients with acute metaldehyde toxicity from suicidal and accidental ingestion of metaldehyde, and to elucidate factors influencing early treatment and disposition.MethodsWe undertook a systematic review and retrospective analysis of the clinical characteristics and outcomes of patients with acute toxicity from ingesting metaldehyde.ResultsTwenty‐one cases identified between 1965 and 2021 were analyzed. The median age was 32 years (range, 3–68 years), and two‐thirds of patients experienced symptoms (14/21, 67%). In symptomatic patients, gastrointestinal symptoms were present in two‐thirds (9/14, 64%), and half experienced neurologic complications (8/14, 57%); of those with neurologic complications, half experienced seizures (8/14, 57%). There were near‐equal cases of accidental and suicidal poisoning. Those who attempted suicide were likelier to develop symptoms (90% versus 45%, P = 0.031), experience seizures (60% versus 18%, P = 0.049), require intensive care (50% versus 9%, P = 0.038), and suffer longer hospitalizations (13.3 days versus 2.9 days, P = 0.005), despite no statistically significant differences in the doses of metaldehyde consumed when compared against patients with accidental ingestion (9.04 g versus 2.03 g, P = 0.09).ConclusionThe circumstances in which metaldehyde is consumed heavily influence clinical symptoms and outcomes. Early and close observation for seizures and adopting a lowered threshold for escalation to the intensive care unit are recommended in patients attempting suicide even when the dose ingested cannot be determined at that time, which is common during the early phases of treatment.

Acute Toxicity of Metaldehyde in the Invasive Rice Snail Pomacea canaliculata and Sublethal Effects on Tadpoles of a Non-target Species (Rhinella arenarum)

We investigated the effects of exposure to molluscicidal metaldehyde (MET) on golden apple snail (GAS) Pomacea canaliculata and Rhinella arenarum tadpoles by assessing mortality and/or other effects via: acute toxicity assays; B-esterase activities (acetilcholinesterase (AChE) and carboxilesterase (CbE)) and oxidative responses (glutathione-S-transferase (GST) and catalase (CAT)). The effect of sublethal concentrations of MET was also analysed by assessing biochemical changes and swimming parameters in tadpoles. The LC50 value in P. canaliculata was as 0.50 mg L−1 and in R. arenarun tadpoles, 229.7 mg L−1 at 48 h. The intestine of MET-exposed P. canaliculata exhibited a significant reduction in CbE and CAT activities, but not in AChE activity; hepatopancreas of GAS showed a decreased GST activity decreased with respect to control individuals. In addition, a significant reduction of CbE activities was detected in R. arenarum tadpoles exposed to MET, and AChE presented lower values than the control but without statistical differences. Antioxidant enzymes (GST and CAT) were significantly reduced in tadpoles exposed to MET compared with the control group. In addition, MET had a significant effect on the swimming behaviour of R. arenarum. Finally, since amphibian tadpoles and P. canaliculata often co-occur, other native amphibian species should be studied to elucidate the ecological risk of MET to amphibian populations.

Developmental toxicity of metaldehyde in the embryos of Lymnaea stagnalis (Gastropoda: Pulmonata) co-exposed to the synergist piperonyl butoxide

Metaldehyde is a widely used molluscicide in countries where damage to crops from slugs and snails is a major problem associated with warm and wet winters. In the UK it is estimated that over 8% of the area covered by arable crops is treated with formulated granular bait pellets containing metaldehyde as the main active ingredient. Metaldehyde is hydrophilic (log Kow=0.12), water soluble (200mg·L−1 at 17°C) and has been detected in UK surface waters in the concentration range of typically 0.2–0.6μg·L−1 (maximum 2.7μg·L−1) during 2008–2011. In the absence of chronic data on potential hazards to non-target freshwater molluscs, a laboratory study was conducted to investigate the impact of metaldehyde on embryo development in the gastropod Lymnaea stagnalis (RENILYS strain) and using zinc as a positive control. L. stagnalis embryos were exposed to metaldehyde under semi-static conditions at 20±1°C and hatching success and growth (measured as shell height and intraocular distance) examined after 21d. Exposure concentrations were verified using HPLC and gave 21d hatchingNOEC and hatchingLOEC mean measured values of 36 and 116mgMET·L−1, respectively (equal to the 21d shell heightNOEC and shell heightLOEC values). For basic research purposes, a second group of L. stagnalis embryos was co-exposed to metaldehyde and the pesticide synergist piperonyl butoxide (PBO). Co-exposure to the PBO (measured concentrations between 0.47–0.56mg·L−1) reduced hatching success from 100% to 47% and resulted in a 30% reduction in embryo growth (shell height) in snail embryos co-exposed to metaldehyde at 34–36mg·L−1 over 21d. In conclusion, these data suggest mollusc embryos may have some metabolic detoxication capacity for metaldehyde and further work is warranted to explore this aspect in order to support the recent initiative to include molluscs in the OECD test guideline programme.

Metaldehyde intoxication in a red fox (Vulpes vulpes)

Metaldehyde toxicity has been commonly reported in different species, including dogs, cats, horses, livestock and wildlife, but the authors are not aware of previously described cases in red foxes. A...

Effect of prolonged status epilepticus as a result of intoxication on epileptogenesis in a UK canine population

The aim of the present study was to investigate if prolonged status epilepticus (SE), secondary to a chemoconvulsant, can induce spontaneous recurrent seizures in dogs. Clinical records at two UK...

The relative toxicity of metaldehyde and iron phosphate-based molluscicides to earthworms

Slugs are suppressed by cereal flour-based baits or pellets containing metaldehyde, or containing iron phosphate plus chelating agents, which are also consumed by earthworms and other invertebrates. These studies compared the effects of metaldehyde and iron phosphate alone, with those of iron phosphate plus chelating agents EDDS and EDTA, and of the chelating agents alone on earthworms. OECD artificial soil test Earthworms ( Eisenia fetida) were exposed directly to the molluscicides in artificial soil. The test chemicals were: metaldehyde; iron phosphate; ethyldiaminetetraceticacid (EDTA), ethylenediaminesuccinicacid (EDDS) and mixtures of iron phosphate and these latter two chemicals. LD 50 values were more than 10,000 mg kg −1 for metaldehyde and iron phosphate, 156.5 mg kg −1 for EDTA, 145.6 mg kg −1 for EDDS, 72.2 mg kg −1 for iron phosphate/EDTA, and 83.0 mg kg −1 for iron phosphate/EDDS. Microcosm test Four mature Lumbricus terrestris were exposed in each microcosm (15 cm diam. × 30 cm deep) to pellets containing: no active ingredient; metaldehyde (4%); iron phosphate/EDTA (1%) (Sluggo ®); iron phosphate (3%); EDTA (3%); EDDS (3%). Metaldehyde and iron phosphate did not affect earthworm feeding, growth or mortality. Sluggo ® decreased earthworm feeding and caused loss of weight and mortality. Earthworms consumed fewer pellets containing EDDS or EDTA and lost weight.

Self-poisoning with metaldehyde

Metaldehyde poisoning is rare. This case report details the largest toxic dose of self-poisoning with metaldehyde ever recorded in the literature to the authors’ knowledge, the aim being to emphasise...

Clinical, neurological and clinicopathological signs, treatment and outcome of metaldehyde intoxication in 18 dogs

To describe the clinical signs, clinicopathological abnormalities and outcome of metaldehyde intoxication in dogs. Medical records of dogs presenting between 1989 and 2005 with a diagnosis of metaldehyde toxicity were reviewed retrospectively. Data obtained from the medical record included signalment, history, clinical signs, laboratory tests results, hospitalisation period length, treatments and outcome. Eighteen dogs fulfilled the inclusion criteria. The most prevalent clinical signs were seizures, hyperthermia, tachycardia and muscle tremors. Serum biochemistry abnormalities included increased serum muscle enzymes activities, acidaemia (six dogs) and decreased blood bicarbonate (eight dogs). Treatment was symptomatic and supportive. Hyperbilirubinaemia was observed in two dogs. Diazepam was the most commonly used anticonvulsant followed by phenobarbitone and pentobarbital. General inhalant anaesthesia was required in nine of 18 dogs with seizures unresponsive to anticonvulsants. The survival was 83 per cent (15 of 18 dogs). This clinical study recorded, for the first time in the veterinary literature, several clinicopathological abnormalities from severely intoxicated dogs. Metabolic acidosis was common, while acute or delayed hepatotoxicity was an uncommon complication.

Toxic and excitatory effects of the molluscicide metaldehyde on the biofouling bivalveDreissena polymorpha Pallas

The zebra mussel, Dreissena polymorpha Pallas, is a biofouling freshwater pest for which alternative control methods to the use of chlorine are sought. Metaldehyde, a molluscicide used primarily for control of terrestrial slugs, has also been shown to have efficacy and specificity in the control of aquatic snails. To test its potential for zebra mussel control, we investigated its effects on zebra mussel viability and on contractility of siphon/mantle muscle preparations in vitro. Metaldehyde caused zebra mussel mortality within 48 h at concentrations of approximately 0.1 and 0.2 g litre−1. The same concentrations of metaldehyde activated a complex, excitatory response in previously quiescent siphon/mantle preparations but did not modify the contractile responses of the preparations to acetylcholine. The relatively low level of toxicity of metaldehyde to zebra mussels, compared to its toxicity to snails and slugs, and the difficulty of applying this relatively insoluble molluscicide in the aqueous environment suggest that metaldehyde would not be an effective zebra mussel control agent. © 2000 Society of Chemical Industry

Metaldehyde Molluscicide Action in Mice: Distribution, Metabolism, and Possible Relation to GABAergic System

Two proposed modes of toxic action of the molluscicide metaldehyde are considered here by studies in orally treated mice of symptomatology, acetaldehyde and metaldehyde concentrations in tissues, and characteristics of the γ-aminobutyric acid (GABA) receptor complex. An earlier proposal that metaldehyde-induced poisoning is due to acetaldehyde liberation is not supported by either their different symptomatology or tissue analyses. Unmetabolized metaldehyde is excreted to the extent of 8% and the urinary metabolites from [13C]metaldehyde and [13C]acetate are consistent with primary degradation of metaldehyde via acetaldehyde and acetate. Poisoning signs are initiated at ∼12 ppm metaldehyde in brain, progressing to tonic convulsions and death at ∼40 ppm and lessened by diazepam and phenobarbital without greatly altering the tissue levels of metaldehyde. Possible involvement of the GABAergic system in metaldehyde toxicity is suggested by the lowered levels of GABA in the brain of poisoned mice determined by (1) earlier chemical analysis of the whole brain (Homeida and Cooke,J. Vet. Pharmacol. Ther.5,77 (1982)) and (2) the presently observed reduced effect of endogenous inhibitors (primarily GABA) in preventing binding of [3H]ethynylbicycloorthobenzoate ([3H]EBOB) to brain membranes. Metaldehyde (1 mM) does not: (1) inhibit [3H]EBOB bindingin vitroat the noncompetitive blocker site, (2) alter the coupled effects on [3H]EBOB binding of GABA as an inhibitor (acting at the GABA recognition site) and the amidine steroid RU 5135 in reversing this inhibition (acting primarily as a competitive antagonist), or (3) inhibit glutamic acid decarboxylase activity. Thus, the toxicity of metaldehyde is not due to degradation to acetaldehyde but instead may result from disrupting the GABAergic system by a mechanism which remains to be determined.

An investigation of metaldehyde and acetaldehyde toxicities in dogs

Acetaldehyde has been reported, but has not been proven, to be the toxic entity resulting from metaldehyde ingestion. To investigate this, male dogs were given a single dose of 600 mg metaldehyde or acetaldehyde/kg of body wt via stomach tube. Clinical signs were monitored, and plasma and urine were assayed for metaldehyde and acetaldehyde. Vomiting occurred less often and in a significantly lower number of metaldehyde-dosed dogs than in acetaldehyde-dosed dogs. Ataxia and tremors occurred significantly more often in metaldehyde-dosed dogs than in acetaldehyde-dosed dogs. Acetaldehyde was not detected in the plasma or urine of metaldehyde-dosed dogs, however, it was found in a sample of vomitus from one of the metaldehyde-dosed dogs. Metaldehyde was found in plasma and urine of metaldehyde-dosed dogs. Urinary excretion of metaldehyde from the metaldehyde-dosed dogs was less than 1%. Urinary excretion of acetaldehyde from acetaldehyde-dosed dogs was essentially nonexistent. Metaldehyde has a larger role in the mechanism of metaldehyde toxicity than previously thought. While acetaldehyde appeared to be of significantly lesser importance, we could not eliminate it as a factor in metaldehyde toxicity in dogs.

Letter: Toxicity of metaldehyde to dogs.

Letter: Toxicity of metaldehyde to dogs.