Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Methyl Parathion”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1991

The effect of glutathione monoethyl ester on the potentiation of the acute toxicity of methyl parathion, methyl paraoxon or fenitrothion by diethyl maleate in the mouse.

Depletion of hepatic glutathione in the mouse by pretreatment with diethyl maleate (DEM) is known to potentiate the acute toxicities of many dimethyl-substituted organothiophosphate insecticides. However, certain studies have raised doubts regarding the participation of glutathione in the detoxification of methyl parathion in the mouse, and hence the putative mechanism of action of DEM-induced potentiation of this insecticide. The present study evaluates the hypothesis that DEM potentiates the acute toxicities of methyl parathion, methyl paraoxon, and fenitrothion by a mechanism other than glutathione depletion. One hour following pretreatment of mice with DEM (0.75 ml/kg i.p.), glutathione was markedly depleted and the acute toxicities of methyl parathion, methyl paraoxon and fenitrothion were potentiated. Administration of glutathione monoethyl ester (20 mmol/kg p.o.) to DEM-pretreated mice attenuated DEM-depletion of hepatic glutathione, or maintained glutathione at or above control levels. However, glutathione monoethyl ester did not alter the DEM-induced potentiation of the lethality of these insecticides. Furthermore, administration of glutathione monoethyl ester to naive mice increased hepatic glutathione levels, but did not affect the percentage of animals succumbing to a challenge dose of methyl parathion, methyl paraoxon, or fenitrothion. These data indicate that DEM potentiates the toxicity of methyl parathion, methyl paraoxon or fenitrothion by a mechanism unrelated to hepatic glutathione content.

Animals↗
PubMed2002

In vitro effects of chlorpyrifos, parathion, methyl parathion and their oxons on cardiac muscarinic receptor binding in neonatal and adult rats.

Organophosphorus insecticides elicit toxicity by inhibiting acetylcholinesterase. Young animals are generally more sensitive than adults to these toxicants. A number of studies reported that some organophosphorus agents also bind directly to muscarinic receptors, in particular the m(2) subtype, in tissues from adult rats. As both the density and agonist affinity states of cardiac muscarinic receptors (primarily m(2)) have been reported to change in an age-related manner, we evaluated the relative in vitro sensitivity of cardiac muscarinic receptors in tissues from neonatal (7-11 days of age) and adult (90 days of age) rats to selected organophosphorus compounds (chlorpyrifos, parathion, methyl parathion and their oxygen analogs or oxons). The effects of the cholinergic agonist carbachol (100 pM-5 microM) or an organophosphorus toxicant (50 pM-10 microM) on muscarinic receptor binding were determined using the nonselective muscarinic ligand [3H]quinuclidinyl benzilate or the m(2)-preferential ligand [3H]oxotremorine-M acetate. Carbachol displaced [3H]oxotremorine labeling in adult and neonatal membranes in a relatively similar manner (IC(50)=7-20 nM). The oxons all displaced [3H]oxotremorine binding in a concentration-dependent manner, with chlorpyrifos oxon being the most potent (IC(50): neonates, 15 nM; adults, 7 nM) and efficacious (maximum displacement: neonates, 42%; adults, 56%). Interestingly, methyl parathion was an extremely potent displacer of [3H]oxotremorine binding in adult tissues (IC(50)=0.5 nM, maximum displacement=37%) but had no effect in neonatal tissues. The displacement of [3H]oxotremorine binding by chlorpyrifos oxon (10 microM) was still apparent after washing the tissues, suggesting the oxon irreversibly blocked agonist binding to the receptor while interaction with MePS appeared reversible. As effective concentrations of the oxons were relatively similar to their anticholinesterase potencies, these findings suggest that direct interaction with cardiac muscarinic receptors by some organophosphorus agents may occur at relevant exposure levels and contribute to cardiac toxicity.

Aging↗
PubMed2002

Pharmacokinetics and pharmacodynamics of methyl parathion.

Methyl parathion and other organophosphorus insecticides are widely used in agriculture. Poisonings to this class of compounds are common and exerted primarily through inhibition of acetylcholinesterase. Methyl parathion became a major health concern when it was illegally sprayed in private homes. Since there are limited data with which to predict the long-term effects resulting from a pattern of exposure to methyl parathion that may have occurred in domestic settings, studies were performed to compare its pharmacokinetics and pharmacodynamics after intravenous, oral or dermal exposure. Methyl parathion was given to adult female rats as a single dose intravenously (2.5 mg/kg) through a femoral catheter, orally (2.5 mg/kg) by gavage, or dermally (< or = 50 mg/kg) by application to shaved skin at the nape of the neck. Blood (200 microl) was collected at increasing times from a separate catheter or from the retro-orbital sinus. Cholinesterase activity was measured in blood and normalized to hemoglobin content, whereas activities in brain and peripheral tissues were normalized to protein. Blood methyl parathion was quantitated by gas chromatography-electron capture. The pharmacokinetics of methyl parathion after intravenous exposure best fit a model in which it was distributed between two compartments and rapidly eliminated. Maximal concentrations of methyl parathion ranged from 200 to 350 ng/ml. The half-life of methyl parathion was 51 minutes, its volume of distribution was 10.1 L/kg, and clearance was 108 ml/min/kg. The kinetics of methyl parathion after single oral exposure contrasted with those after intravenous exposure. Despite a high absorption coefficient, oral bioavailability of methyl parathion was less than 5%, and concentrations in blood were 2% or less of those after intravenous exposure. After single dermal exposure (25 or 50 mg/kg), blood methyl parathion levels increased during the first 6 h and then remained constant for the next 42 h at about 150 ng/ml. Despite differences in its pharmacokinetics, methyl parathion caused similar time-dependent changes in blood and brain cholinesterase activities after intravenous or oral administration. Maximal inhibition of blood cholinesterase occurred within 15-60 min, and activities recovered within 30 - 48 h. In contrast, inhibition of blood cholinesterase caused by single dermal exposure (> or = 25 mg/kg) to methyl parathion developed gradually over 24 h, but was sustained. Cholinesterase inhibited by a lower dose (< or = 12 mg/kg) of methyl parathion required up to 21 days to recover fully. The pharmacokinetics and pharmacodynamics of methyl parathion are complex, and the complexity varies with the route of exposure. A significant 'first pass' effect for methyl parathion is seen with oral administration. Dermal exposure to methyl parathion, as likely occurred with the illegal spraying of private homes and businesses, may exacerbate toxicity and increase the potential for long-term adverse health effects.

Animals↗
PubMedDate not supplied

Biotransformation of the organophosphorus insecticides parathion and methyl parathion in male and female rat livers perfused in situ.

Although numerous previous reports have characterized the mammalian biotransformation of the organophosphorus insecticides parathion and methyl parathion, questions still remain regarding the toxicological significance of certain metabolic pathways in vivo. The present study utilized rat liver perfusions in order to better characterize the hepatic biotransformation of parathion and methyl parathion in intact liver. Single-pass liver perfusions with parathion and methyl parathion over a range of perfusate concentrations of 10-80 microM resulted in the appearance of paraoxon and methyl paraoxon, respectively, in effluent. Furthermore, rat blood did not have the capacity to prevent transport of paraoxon and methyl paraoxon to extrahepatic tissues, suggesting that oxon produced hepatically can distribute to extrahepatic tissues. In addition, striking sex differences were noted in the metabolite profile of parathion and methyl parathion in perfused livers. However, these differences could not account for the observation that females are more susceptible to parathion, but less susceptible to methyl parathion, compared to males. And finally, S-methyl glutathione or S-p-nitrophenyl glutathione could not be detected in effluent or bile of livers from either sex perfused with methyl parathion, suggesting that glutathione-dependent detoxification of this insecticide does not occur to any significant degree in intact rat liver.

Animals↗
PubMed2004

A study on the environmental degradation of pesticides azinphos methyl and parathion methyl.

The effect of environmental parameters (temperature and relative humidity) on the degradation rate of azinphos methyl and parathion methyl was studied. Proprietary emulsifiable concentrates were diluted and added to each of 90 glass Petri dishes for each pesticide and were left overnight to dry. Petri dishes were placed in 18 air-tight containers (9 for each pesticide) in which were created environments with relative humidity (RH) of 60, 82, and 96%. The containers were stored at 0, 20, and 40 degrees C. From the experimental results best fit curves, kinetic equations, rate constants, and half-lives were calculated. Half-lives of azinphos methyl for the RH studied were, from 124 to 267 days at 0 degrees C, from 89 to 231 days at 20 degrees C, and from 25 to 71 days at 40 degrees C. Corresponding half-lives for parathion methyl were from 48 to 57 days at 0 degrees C, from 9.2 to 10.5 days at 20 degrees C and from 1.3 to 1.5 days at 40 degrees C. The results were correlated with relevant results from the decomposition of the same or similar pesticides on apples both, on the trees and during refrigerated storage. These correlations are suggesting that biological factors strongly affected the decomposition rate of azinphos methyl. On the contrary the decomposition of parathion methyl was mainly affected by environmental rather than biological factors.

Azinphosmethyl↗
PubMed2007

Reductive transformation of parathion and methyl parathion by Bacillus sp.

Based on the results of phenotypic features, phylogenetic similarity of 16S rRNA gene sequences and BIOLOG test, a soil bacterium was identified as Bacillus sp. DM-1. Using either growing cells or a cell-free extract, it transformed parathion and methyl parathion to amino derivatives by reducing the nitro group. Pesticide transformation by a cell-free extract was specifically inhibited by three nitroreductase inhibitors, indicating the presence of nitroreductase activity. The nitroreductase activity was NAD(P)H-dependent, O(2)-insensitive, and exhibited the substrate specificity for parathion and methyl parathion. Reductive transformation significantly decreased the toxicity of pesticides.

Bacillus↗
PubMed1992

Prolonged toxicity with intermediate syndrome after combined parathion and methyl parathion poisoning.

A prolonged type of organophosphate toxicity, previously characterized as the Intermediate Syndrome, has been recognized in 6 out of 7 prospectively studied patients poisoned by insecticide containing parathion and methyl parathion in equal proportions. The clinical characteristics included respiratory paresis, weakness in the territories of several motor cranial nerves, neck flexors and proximal limb muscles, and depressed tendon reflexes, all lasting for several days or weeks. Electromyography in the early stages disclosed diverse types of impaired neuromuscular transmission. EMG normalization preceded clinical recovery. Severe plasma butyrylcholinesterase and erythrocyte acetylcholinesterase inhibition persisted along with the occurrence of Intermediate Syndrome-related symptoms. We conclude that combined parathion and methyl parathion poisoning is more likely to induce Intermediate Syndrome than parathion poisoning alone. The mechanisms underlying this difference remain obscure. The Intermediate Syndrome shows clinical and electromyographic hallmarks of combined postsynaptic impairment of neuromuscular transmission.

Adult↗
PubMed2006

Oxidative stress biomarkers in the freshwater characid fish, Brycon cephalus, exposed to organophosphorus insecticide Folisuper 600 (methyl parathion).

Methyl parathion (MP) is an organophosphorus insecticide used worldwide in agriculture and aquaculture due to its high activity against a broad spectrum of insect pests. The effect of a single exposure to 2 mg L(- 1) of a commercial formulation of MP (MPc: Folisuper 600(R), MP 600 g L(- 1)) on catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione S-transferase (GST), reduced glutathione (GSH) and lipid peroxidation (LPO) of the liver, white muscle and gills of Brycon cephalus was evaluated after 96 h of treatment. MPc exposure resulted in a significant induction of SOD, CAT and GST activity in all tissues. However, the GPx activity decreased significantly in white muscle and gills, whereas no alterations were observed in hepatic GPx activity. MPc also induced a significant increase in LPO values in the white muscle and gills, while hepatic LPO levels did not show any significant alteration. The current data suggest that MPc has oxidative-stress-inducing potential in fish, and that gills and white muscle are the most sensitive organs of B. cephalus, with poor antioxidant potentials. The various parameters studied in this investigation can also be used as biomarkers of exposure to MPc.

Animals↗
PubMed2005

Evaluation of potential adverse health effects resulting from chronic domestic exposure to the organophosphate insecticide methyl parathion.

Methyl parathion (MP) was used illegally to spray homes for insect control over approximately an 8-yr period. In an attempt to determine if there were any adverse health effects from this, health-screening evaluations were performed on 353 individuals living in homes that were illegally sprayed. The average subject spent 15.5 h a day in the home. Subjects from homes with high levels of MP (exposure group) were compared to controls that lived in homes with minimal or no MP. Subjects were aware of the levels of MP found in their homes and recall bias was likely. There were no significant differences in the symptoms reported or by the physician assessment of subacute or chronic toxicity between those in the exposure group and controls. No significant differences were found in growth and developmental evaluations. Three subjects were identified who most likely suffered acute toxicity from the initial exposure and were not appropriately diagnosed and treated. Cholinesterase determinations also did not differ between those in the exposure group and controls. When subjects from the exposure group were stratified by the level of MP in their home, those from homes with the highest levels appeared to have an increased likelihood of subacute toxicity and reported an increased number of neuropsychiatric symptoms (OR 2 for both evaluations).

Adolescent↗
PubMed2002

Urinary p-nitrophenol as a biomarker of household exposure to methyl parathion.

Methyl parathion (MP) is an organophosphate pesticide illegally applied to the interiors of many hundreds of homes throughout the United States by unlicensed pesticide applicators. Public health authorities developed a protocol for investigating contaminated homes and classifying their need for public health interventions. This protocol included environmental screening for MP contamination and 1-day biomonitoring (a.m. and p.m. spot urine samples) of household members for p-nitrophenol (PNP), a metabolite of MP. The variability of urinary PNP excretion under these exposure conditions was unknown. We collected a.m. and p.m. spot urine samples for 7 consecutive days from 75 individuals, who were members of 20 MP-contaminated households in the greater Chicago, Illinois, area, and analyzed them for PNP. We also assessed the ability of the 1-day sampling protocol to correctly classify exposed individuals and households according to their need for public health interventions, assuming that 1 week of sampling (14 urinary PNPs) represented their true exposure condition. The coefficient of variation of log urinary PNPs for individuals over the course of 7 days of a.m. and p.m. sampling averaged about 15%. Adjusting for urinary excretion of creatinine improved reproducibility of urinary PNPs among children but not among adults. The 1-day protocol correctly classified true risk category in 92% of individuals and 85% of households. The data contained in this study can be used to refine what is already a reasonable and effective approach to identifying MP-exposed households and determining the appropriate public health intervention.

Adolescent↗
PubMedDate not supplied

Rapid determination of methyl parathion and methyl paraoxon in milk by gas chromatography with solid-phase extraction and flame photometric detection.

Methyl parathion (MPT; O,O-dimethyl-O-4-nitrophenyl phosphorothioate) and its active metabolite, methyl paraoxon (MPO; O,O-dimethyl-O-4-nitrophenyl phosphate), were isolated from raw milk by solid-phase extraction (SPE) and determined by gas chromatography with flame photometric detection. The SPE method was compared with a traditional liquid-liquid extraction (LLE) procedure to determine whether SPE had suitable sensitivity and better efficiency in extracting MPT and MPO from milk of cows and goats. Method detection limits were higher for SPE, but the differences were not significant (t-test). Recoveries of MPT and MPO from raw milk samples spiked at 0.05, 0.5, and 5.0 micrograms/mL ranged from 80.0 to 118%, and the coefficients of variation were usually less than 10% for both methods. LLE required more organic solvents and was more time consuming compared with SPE.

Animals↗
PubMed1999

[Study on the analytical method of methyl-parathion and phoxim in methyl-parathion, phoxim and cypermethrin mixed formulation].

This paper describes an HPLC method to simultaneously determine methyl-parathion and phoxim in mixed formulation of methyl-parathion, phoxim and cypermethrin. A C8 column was used. The mobile phase was V(MeOH):V(H2O) = 70:30, Methyl-parathion and phoxim were monitored at 254 nm or 280 nm by UV detector. The average recoveries were 99.8% and 99.9% for methyl-parathion and phoxim respectively. The linearity of detector response vs concentration was calibrated in the concentration ranges from 0.1746 to 1.091 g/L for methyl-parathion and from 0.1927 to 1.205 g/L for phoxim.

English Abstract↗
PubMed1975

[Effect of methyl parathion and zineb administration on the activity of some hepatic enzymes in rats].

Male albinos rats were fed diets containing parathion-methyl or Zineb so that the average daily intake is 1/10 or 1/20 lethal dose 50, for a period of 4 or 8 weeks. The activity of hepatic microsomal enzymes, namely :aminopyrine N-demethylase, BHT oxidase, aniline hydroxylase, Butter Yellow & Amaranth reductases, NADPH-cyt. c reductase, G6P phosphatase, were measured. The activities of G6P & 6PG deshydrogenases were also determined. With the application of the parathion-methyl doses, the only effect showed is the lowering of the microsomal protein concentration.

Aminopyrine N-Demethylase↗