[Determination of methomyl by using chemical ionization mass fragmentography. Experimental studies and a case report of methomyl poisoning].
Explore the source record for details and available documents.
Adult↗
SEARCH · PubMed Health
Results for “Methomyl”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Lithium-methomyl induced seizures in rats: a new model of status epilepticus?
Behavioral, electroencephalographic (EEG) and neuropathological effects of methomyl, a carbamate insecticide reversibly inhibiting acetylcholinesterase activity, were studied in naive or lithium chloride (24 h, 3 mEq/kg, s.c.) pretreated male Wistar rats. In naive animals, methomyl with equal potency produced motor limbic seizures and fatal status epilepticus. Thus, the CD50 values (50% convulsant dose) for these seizure endpoints were almost equal to the LD50 (50% lethal dose) of methomyl (13 mg/kg). Lithium pretreated rats were much more susceptible to convulsant, but not lethal effect of methomyl. CD50 values of methomyl for motor limbic seizures and status epilepticus were reduced by lithium pretreatment to 3.7 mg/kg (a 3.5-fold decrease) and 5.2 mg/kg (a 2.5-fold decrease), respectively. In contrast, lithium pretreatment resulted in only 1.3-fold decrease of LD50 value of methomyl (9.9 mg/kg). Moreover, lithium-methomyl treated animals developed a long-lasting status epilepticus, which was not associated with imminent lethality observed in methomyl-only treated rats. Scopolamine (10 mg/kg) or diazepam (10 mg/kg) protected all lithium-methomyl treated rats from convulsions and lethality. Cortical and hippocampal EEG recordings revealed typical epileptic discharges that were consistent with behavioral seizures observed in lithium-methomyl treated rats. In addition, convulsions induced by lithium-methomyl treatment were associated with widespread neurodegeneration of limbic structures. Our observations indicate that lithium pretreatment results in separation between convulsant and lethal effects of methomyl in rats. As such, seizures induced by lithium-methomyl administration may be an alternative to lithium-pilocarpine model of status epilepticus, which is associated with high lethality.
Animals↗
Role of selenium on antioxidant capacity in methomyl-treated mice.
Methomyl carbamate is a pesticide widely used in the control of insects. The present work aims at studying the effect of selenium on the antioxidant system of methomyl-treated mice. Swiss albino mice were intraperitoneally administered a single dose of methomyl (7 mg/Kg body weight). Mice of another group were injected with sodium selenite (5 pmole/Kg b.wt.) 7 days before methomyl intoxication. After 24 hours, methomyl exposure resulted in significant increase in lactic dehydrogenase activity (LDH). The antioxidant capacity of hepatic cells in terms of the activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione-S-transferase (GST) and glutathione (GSH) content was diminished. It appears that methomyl exerts its toxic effect via peroxidative damage to hepatic, renal and splenic cell membranes. Also, methomyl induced DNA damage in these organs as detected by alkaline filter elution technique. The distribution of methomyl in different organs of mice was detected by HPLC. Selenium administration prior to methomyl injection produced pronounced protective action against methomyl effects. It is observed that selenium enhances the endogenous antioxidant capacity of the cells by increasing the activities of SOD, CAT, GR and GST as well as increasing GSH content. The activity of LDH was decreased in blood and the damage of DNA was suppressed comparable to controls. In conclusion, the adverse effects of methomyl in mice could be ameliorated by selenium.
Animals↗
Penetration and fate of methomyl and its oxime metabolite in insects and twospotted spider mites.
The penetration and fate of methomyl and its oxime metabolite, methomyl oxime or S-methyl N-hydroxythioacetimidate, were examined in house flies (Musca domestica Linnaeus), face flies (Musca autumnalis De Geer), black cutworm larvae (Agrotis ipsilon (Hufnagel), and twospotted spider mites (Tetranychus urticae Koch). Generally, penetration and metabolism of methomyl-1-14C were rapid in insects and spider mites although differences in rates among the different test organisms were observed. Metabolites from methomyl included CO2, methomyl oxime, and several unknowns. Penetration and metabolism of methomyl oxime-1-14C also were rapid in insects. Metabolites from methomyl oxime included a small amount of CO2 and several unidentified compounds. Organosoluble metabolites from methomyl oxime generally displayed similar chromatographic behavior as those from methomyl. Methomyl was hydrolyzed to its oxime metabolite, which, apparently, was further metabolized to 14CO2 presumably via a Beckmann rearrangement reaction.
Animals↗
Transfer of methomyl and HmT-toxin sensitivity from T-cytoplasm maize to tobacco.
The mitochondrial gene, T-urf13, which is unique to the T-cytoplasm of maize, has been expressed in tobacco plants using the Cauliflower Mosaic Virus 35S promoter. Tobacco plants expressing T-urf13 exhibit a variety of responses to methomyl. Leaf discs and petiole sections bleach when exposed to methomyl or HmT-toxin; this effect increases with the age of the tissue. The bleaching effect is not however observed when light is excluded. Plants homozygous for T-urf13 exhibit extreme sensitivity when sprayed with methomyl. The growth of seedling which are either homozygous or heterozygous for T-urf13 is inhibited by methomyl and by kanamycin, whereas seedlings from untransformed tobacco or tobacco which has lost the T-urf13 gene through segregation are sensitive to kanamycin but develop normally when exposed to methomyl. The results demonstrate that T-URF13 need not be specifically targeted to the mitochondrion for it to induce methomyl or HmT-toxin sensitivity in tobacco.
Base Sequence↗
Analysis and toxicity of methomyl and ametryn after biodegradation.
The controlled biodegradation of ametryn and methomyl has been performed, in accordance with the OECD Zahn-Wellens/EMPA procedure, by use of an enriched mixture of activated sludge collected from three domestic waste-water-treatment plants (WWTP). During the process concentrations of ametryn and methomyl in the water samples were isolated by solid-phase extraction (SPE); recovery rates were 98.9 and 93.2 for methomyl and ametryn, respectively. Liquid chromatography-mass spectrometry (LC-MS) was used to determine final pesticide concentrations and for metabolite identification. The efficiency of aerobic biodegradation of ametryn and methomyl was evaluated by measuring both the decrease in the concentration of the pesticides and global properties such as the chemical oxygen demand (COD). The acute toxicity of ametryn and methomyl was evaluated by use of the ToxAlert100 biological test, which is based on inhibition of the bioluminescence of Vibrio fischeri. There was significant correlation between results from primary and ultimate biodegradation and those from determination of toxicity. Pesticide concentrations were always reduced to below the limit of detection in less than 17 days. High COD removal (90-96%) was achieved in 28 and 18 days for methomyl and ametryn, respectively.
Biodegradation, Environmental↗
Fatal and non-fatal methomyl intoxication in an attempted double suicide.
A 79-year-old man and his 73-year-old wife attempted double suicide by ingesting methomyl powder. The woman died 19 h after ingestion in spite of intensive care. At autopsy a large number of miliary hemorrhages were found in both thalami of the brain. Her husband, however, recovered after 10 days of treatment. Methomyl (CAS No. 16752-77-5, Lannate) in the biological materials was analyzed by gas chromatography-mass spectrometry. The methomyl concentration was 44 micrograms/g in the wife's serum sample collected 1 h after ingestion, and 0.2 microgram/g in the blood sample collected at autopsy. The methomyl concentration in the husband's blood sample collected 28 h after ingestion was from 0.01 to 0.1 microgram/g. It is suggested that prompt and adequate intensive care including a direct hemoperfusion is necessary to effect the recovery of patients with lethal blood levels of methomyl. The miliary hemorrhages found in the thalami of the brain are suspected to have been caused by asphyxia induced by methomyl intoxication.
Aged↗
A case of poisoning in a man who drank a nutrition supplement containing methomyl, a carbamate pesticide.
A 50-year-old man was admitted to the emergency room complaining oppression on his chest, sweating and vomiting. He had drunk a 30 ml volume nutrition supplement 60 minutes before. As myosis and decrease of serum choline esterase activity were observed on admission examination, poisoning was suspected and toxicological analyses were carried out on the heeltap of the drink. Drug screening by gas chromatography-mass spectrometry (GC/MS) revealed the presence of methomyl and the concentration of methomyl in the heeltap determined by liquid chromatography was 2.1 mg/ml. Methomyl concentrations in the serum and urine were determined after converting methomyl to its oxime form followed by derivatization and GC/MS. Methomyl concentration in the serum collected 6 hours after ingestion was 0.63 microg/ml, and that in the urine collected 7-20 hours after ingestion was 0.10 microg/ml. Based on these values and reported data, the amount of methomyl contaminated to the drink was considered to be a toxic dose.
Cholinesterase Inhibitors↗
MRG1-1, a dominant allele that confers methomyl resistance in yeast expressing the cytoplasmic male sterility T-urf13 gene from maize.
We have previously described a eukaryotic heterologous expression system, with the urf13TW gene in yeast, which mimics the disease susceptibility associated with the Texas cytoplasmic male sterility in maize. This yeast model was used to isolate yeast nuclear mutants conferring methomyl resistance. The genetic strategy we have developed focused on screening for nuclear dominant yeast mutations which restore methomyl resistance. MRG1-1, a yeast nuclear dominant allele, was identified as a methomyl-resistance restorer. We have shown that methomyl resistance co-segregated with a pleiotropic phenotype in the heterozygous MRG1-1/MRG1 diploids, detectable even in the absence of the maize-derived mitochondrial protein and/or methomyl. We observed an increase in oxygen uptake, a significant decrease of the levels of cytochrome aa3, and a decrease in the growth yield. This phenotype is influenced by the carbon source and the results suggest a defect in the adaptation to the respiratory pathway in MRG1-1 yeast cells.
Alleles↗
Effects of weathering and flue-curing on methomyl residues on tobacco.
A replicated field experiment was conducted at two locations to determine the disappearance of methomyl from flue-cured tobacco. Immediately after application, methomyl residues were 88 and 113 ppm at Clayton and 44 and 105 ppm at Reidsville, respectively, for 0.56 and 1.12 kg/ha application rates. After 5 days these levels dropped to 0.7 and 2.8 ppm at Clayton and 1.4 and 4.1 ppm at Reidsville. At 9 days after application, 99% of the methomyl had disappeared at both locations. Losses of methomyl during flue-curing averaged 96% over locations, rates of application, and times of harvest, compared to an average loss of 98% due to weathering in the field for 5 days. The disappearance of methomyl during the curing process was approximately the same for both locations.
Chromatography, Gas↗
A fatal poisoning caused by methomyl and nicotine.
A 35-year-old male was found lying in a prone position in his room. He was in cardiopulmonary arrest on arrival to hospital and was pronounced dead. There was no attempt at resuscitation. No miosis was observed on admission. At post-mortem his stomach contained 170 g greenish liquid with a small amount of shredded tobacco leaves. The serum cholinesterase activities were 47-90 IU (normal range for male: 200-440 IU). GC and GC-MS analyses showed nicotine (21.8 mg), methomyl (304 mg), and triazolam (1.69 mg) in his stomach. He had consumed tobacco leaves, Lannate containing water soluble methomyl (45%), and Halcion tablets containing 0.25 mg triazolam. Methomyl concentrations in blood were 3-8 ng/ml. Substantial amounts of methomyl (2260-2680 ng/ml) were detected in cerebrospinal fluid and vitreous humor. Nicotine concentrations in blood ranged from 222 to 733 ng/ml. A small amount of triazolam was detected only in bile (176 ng/ml) and liver (23 ng/g). The cause of death was respiratory paralysis produced by the additive effects of methomyl and nicotine shortly after consumption.
Adult↗
Targeting the maize T-urf13 product into tobacco mitochondria confers methomyl sensitivity to mitochondrial respiration.
The URF13 protein, which is encoded by the maize mitochondrial T-urf13 gene, is thought to be responsible for pathotoxin and methomyl sensitivity and male sterility. We have investigated whether T-urf13 confers toxin sensitivity and male sterility when expressed in another plant species. The coding sequence of T-urf13 was fused to a mitochondrial targeting presequence, placed under the control of the cauliflower mosaic virus 35S promoter, and introduced into tobacco by Agrobacterium tumefaciens-mediated transformation. Plants expressing high levels of URF13 were methomyl sensitive. Subcellular analysis indicated that URF13 is mainly associated with the mitochondria. Adding methomyl to isolated mitochondria stimulated NADH-linked respiration and uncoupled oxidative phosphorylation, indicating that URF13 was imported into the mitochondria, and conferred toxin sensitivity. Most control plants, which expressed the T-urf13c construct lacking the mitochondrial presequence, were methomyl sensitive and contained URF13 in a membrane fraction. Subcellular fractionation by sucrose gradient centrifugation showed that URF13 sedimented at several positions, suggesting the protein is associated with various organelles, including mitochondria. No methomyl effect was observed in isolated mitochondria, however, indicating that URF13 was not imported and did not confer toxin sensitivity to the mitochondria. Thus, URF13 confers toxin sensitivity to transgenic tobacco with or without import into the mitochondria. There was no correlation between the expression of URF13 and male sterility, suggesting either that URF13 does not cause male sterility in transgenic tobacco or that URF13 is not expressed in sufficient amounts in the appropriate anther cells.
Amino Acid Sequence↗
Acute pancreatitis subsequent to voluntary methomyl and dichlorvos intoxication.
INTRODUCTION: Acute pancreatitis subsequent to methomyl (Lannate) had not been reported until 2005, when Markides published the first case. In our study, we report for the first time 2 cases of acute pancreatitis complicating voluntary methomyl intoxication and compare them with 5 cases of pancreatitis subsequent to dichlorvos poisoning admitted to our toxicological unit during the same period, between July 2001 and June 2003. CASE REPORTS: Patients included in this study were seriously poisoned because all developed muscarinic and nicotinic syndromes. Deep coma and respiratory failure requiring mechanical ventilation were noted in all methomyl-poisoned patients and in only 3 dichlorvos-poisoned patients. Acute pancreatitis occurred 24 to 72 hours after dosing and was characterized by painless abdominal paralytic ileus and vomiting. Clinical features and laboratory examinations were normalized by the fifth day under medical treatment. Complications such as intrapancreatic fluid collection occurred later between days 10 and 20 in 1 methomyl-poisoned patient who required secondary surgical drainage and in 1 dichlorvos-poisoned patient who was treated conservatively. Outcome was favorable in all cases. CONCLUSION: The developing of acute pancreatitis is a serious adverse effect following insecticide intoxication and is better known with dichlorvos than methomyl.
Acute Disease↗
Response of insecticide-resistant and susceptible houseflies (Musca domestica) to a commercial granular bait formulation containing methomyl.
Female houseflies (Musca domestica L.) from a susceptible and a multi-insecticide-resistant strain were used to evaluate the relative toxicity of an insecticide bait formulation of the carbamate insecticide methomyl. Individual flies were allowed to feed on bait granules for an unrestricted period or for 5 s. Resistant flies took longer than susceptible flies to initiate a feeding response. When allowed to feed continuously, those from the resistant strain spent longer feeding than susceptible ones. The time taken to knock-down (KD), including feeding times, was significantly greater for resistant than susceptible flies (P less than 0.001), but once the proboscis was withdrawn from the granule there was no difference in KD times between the strains. All flies from both strains were knocked down, and only a very small number of resistant and susceptible flies recovered. The toxic effects of methomyl on flies which were restricted to a 5 s feed ranged from no observed effect to KD in less than 1 min. After feeding for 5 s, 81% of resistant and 98% of susceptible flies developed signs of methomyl poisoning. More resistant than susceptible flies recovered from KD, giving final mortalities of 46% and 88% respectively. With both feeding regimes, some flies of both strains which had apparently recovered from KD had lost their ability to fly. Observations have also shown that 8% of resistant flies may have been repelled by methomyl granules. The implication of these results on the survival of M. domestica in intensive animal units following exposure to methomyl bait is also discussed.
Animals↗
An insensitive acetylcholinesterase confers resistance to methomyl in the beet armyworm Spodoptera exigua (Lepidoptera: Noctuidae).
Two forms of acetylcholinesterase were identified in field populations of the beet armyworm, Spodoptera exigua (Hübner), collected from cotton in San Joaquin Valley, CA. Strains (BESS and BKRR) homogeneous for each variant were isolated and their relative susceptibilities to methomyl, chlorpyrifos, and chlorpyrifos-oxon assessed by topical application bioassay. In comparisons with a laboratory susceptible strain (DOW), BKRR and BESS expressed 68-fold and sevenfold resistance, respectively, to the carbamate methomyl. Neither strain was cross-resistant to chlorpyrifos or its oxygen analog (chlorpyrifos-oxon). In biochemical studies, the BKRR AChE enzyme was approximately 30-fold and sixfold more insensitive to methomyl and chlorpyrifos-oxon, respectively, compared with the DOW enzyme. The correlation between the toxicological and biochemical studies provides strong evidence that target-site insensitivity is an important mechanism of resistance to methomyl. The lack of significant cross-resistance to chlorpyrifos suggests that the insensitive AChE in these field populations was selected by methomyl alone and not by the organophosphate.
Acetylcholinesterase↗
Increase in lactate dehydrogenase isoenzyme-4 and splenocyte toxicity in methomyl-treated rats.
The toxic effect of methomyl was studied in rats after a single or repeated oral administration. Rats treated with a single dose of methomyl (3, 5, or 7 mg/kg) showed significant increase (P < 0.05) in total lactate dehydrogenase (LDH) activity on day 1. The highest level of LDH activity was observed on day 3 in rats receiving 7 mg/kg of methomyl. The total LDH activity returned to normal on day 7 after dosing. Specific increases in LDH-3 and LDH-4 isoenzyme activities were observed. In rats treated with a single dose of 6 and 8 mg/kg of methomyl, spleen weight and splenocyte viability significantly dropped (P < 0.05) on days 1 and 3, respectively. Splenotoxicity was prevented by pretreatment with 60 mg/kg of N-acetylcysteine. The results suggest that the splenotoxic effect of methomyl is more likely directly related to oxidative cell injury than to cholinesterase inhibition. The significance of cytotoxic effects and the nature of cytotoxicity in relation to reactive oxidative damage deserve further investigation.
Animals↗
Pesticide deposition in hair: preliminary results of a model study of methomyl incorporation into rabbit hair.
This work studied the incorporation of methomyl, a carbamate insecticide, into the hair of New Zealand white rabbits. A total of 600 mg methomyl was administered by drinking water over 4 mo, and acetylcholinesterase activity in serum was monitored. At the end of the dosing period, hair from the back of the rabbits was cut off, and the methomyl concentration was measured using ELISA and HPLC. A decrease of serum acetylcholinesterase occurred. The top cm of hair contained no methomyl, the second cm contained 0.9 ng/mg and the 3rd cm of hair contained 3 ng methomyl/mg. Methomyl was incorporated into the rabbit hair in a process independent of gender but dependent on the hair growth rate.
Acetylcholinesterase↗
Genotoxic effects of the carbamate insecticide methomyl. I. In vitro studies with pure compound and the technical formulation "Lannate 25".
The carbamate insecticide methomyl and the methomyl-containing technical formulation "Lannate 25" were tested on whole blood human lymphocyte cultures. Both products induced dose-dependent increases in chromosome aberrations and micronuclei. Lannate 25 induced DNA damage as measured by the alkaline elution assay and hydroxylation of guanine at the C8 position. Sister chromatid exchanges were not increased significantly with either product. Overall, the technical formulation was more active than the pure compound, when compared at similar concentrations of active principle. Moreover, a different ratio of CREST-positive/CREST-negative micronuclei was observed with the two products, pure methomyl being relatively more active than Lannate 25 in the induction of CREST-positive micronuclei. On the basis of these results, previous evaluations of methomyl as a nongenotoxic compound should be reconsidered.
8-Hydroxy-2'-Deoxyguanosine↗