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PubMedDate not supplied

Mixtures of benomyl, pirimiphos-methyl, dimethoate, diazinon and azinphos-methyl affect protein synthesis in HL-60 cells differently.

Dimethoate, azinphos-methyl, diazinon and pirimiphos-methyl, widely used organophosphorous insecticides, and benomyl, a benzimidazole fungicide, induce different cytotoxic effects on the human leukemia cell line HL-60. Among the insecticides tested, only azinphos and diazinon induced a dose-related inhibition of protein synthesis in HL-60 cells at 24 h, at 60 and 40 micrograms/ml medium, respectively. Dimethoate and pirimiphos were not active up to 100 micrograms/ml. Benomyl strongly inhibited protein synthesis at 50 micrograms/ml and the polymerisation of actin to give cytoskeletal microfilaments (F-actin) at 30 micrograms/ml. Mixtures of benomyl-pirimiphos and dimethoate azinphos-diazinon were also investigated. Pirimiphos, when present in equal concentration, antagonized the inhibitory effect of benomyl on protein synthesis at 4 h, but not at 24 h. The effect of the other insecticide mixture on the same parameter was greater than that of the two active components, diazinon and azinphos given singly.

Actins↗
PubMed2005

Joint effects of dimethoate and heavy metals on metabolic responses in a grasshopper (Chorthippus brunneus) from a heavy metals pollution gradient.

We studied how an exposure to an additional stressing factor-dimethoate, might affect detoxifying ability of grasshoppers collected at 5 meadow sites located along a heavy metal pollution gradient. Activities of esterases and enzymes linked with glutathione (GSH) metabolism were assayed 24 h after topical treatment with 0.32 microg dimethoate per insect. Inhibition of acetylcholinesterase (AChE) reaches nearly 50% of the value stated in untreated insects, without significant site-dependent differences. The pesticide also caused a significant decrease in activities of glutathione peroxidase (GPx) followed by a decrease in GSH levels in grasshoppers from all assayed groups, demonstrating high sensitivity of glutathione-dependent metabolism to the additional stressing factor. In the case of glutathione reductase (GR) and carboxylesterases (CarE) the fall of activity was shown especially in insects from less polluted meadows and the reference site. Glutathione reductase (GR) activity in individuals treated with dimethoate did not decrease only in insects from the most contaminated site I. This might suggest the trade-off mechanisms adapting grasshoppers to life in seriously polluted environments.

Acetylcholinesterase↗
PubMed2005

Functional changes of nicotinic acetylcholine receptor in muscle and lymphocyte of myasthenic rats following acute dimethoate poisoning.

The mechanism underlying intermediate myasthenia syndrome (IMS) following acute organophosphate poisoning remains largely unknown. Previous studies indicated that the mechanism of myasthenia in rats and IMS patients is most likely due to a postsynaptic neurotransmission blocking at neuromuscular junctions (NMJ). Nicotinic acetylcholine receptor (nAChR) is a key postsynaptic component at NMJ. Whether functional changes of nAChR are related to the development of myasthenia has not been demonstrated and addressed in vivo so far. In this study, we attempted to investigate temporal and spatial changes of nAChR in the blood lymphocyte, muscle and brain of rats during the course of myasthenia after acute dimethoate poisoning by using radioligand-binding assay. We found that specific nAChR binding activity in the gastrocnemius muscle and blood lymphocytes of myasthenia rats was significantly increased at 48h after dimethoate poisoning. However, no changes of nAChR binding activity were found in the lymphocytes and muscle of non-myasthenia rats which were sacrificed at 1h after intoxication. Interestingly, no changes of nAChR and muscarinic acetylcholine receptor (mAChR) binding activity were found in the cerebrum and cerebellum of all rats after dimethoate intoxication either at 1 or 48h. The change of nAChR specific binding activity in the lymphocytes is parallel with that in the skeletal muscle during the development of myasthenia. This implied that the changes of nAChR receptor binding activity in the skeletal muscle and lymphocytes are highly associated with the development of myasthenia. The functional changes of nAChR at NMJ might play an important role in the paralysis of skeletal muscle following acute organophosphates (OPs) poisoning.

Animals↗
PubMed1997

Dimethoate inhibits extrathyroidal 5'-monodeiodination of thyroxine to 3,3',5-triiodothyronine in mice: the possible involvement of the lipid peroxidative process.

The effects of daily administration of dimethoate (2, 4 and 8 mg/kg body weight for 30 days) on thyroid function in mice were investigated. While serum triiodothyronine (T3) concentration was decreased significantly, serum thyroxine (T4) was increased in the medium and highest dose treated groups. However, the serum concentration of thyrotropin was unaltered. Hepatic type-I iodothyronine 5'-monodeiodinase (5'-D) enzyme activity was depressed by the two higher doses of dimethoate. These observations suggest that dimethoate-induced alterations in thyroid function are not mediated through the hypophyseal thyroid axis, but through the changes in extrathyroidal conversion of T4 to T3. To correlate the lipid peroxidation (LPO) with 5'-D activity, hepatic LPO and the activity of antioxidant enzymes, i.e. superoxide dismutase (SOD) and catalase (CAT), were studied. The pesticide increased the activity of SOD and CAT along with hepatic lipid peroxidation. The possible involvement of the lipoperoxidative process in the inhibition of 5'-D activity has been suggested.

Animals↗
PubMedDate not supplied

S-methylation of O,O-dialkyl phosphorodithioic acids: O,O,S-trimethyl phosphorodithioate and phosphorothiolate as metabolites of dimethoate in mice.

O,O,S-Trimethyl phosphorodithioate and phosphorothiolate [(MeO)2P(S)SMe and (MeO)2P-(O)SMe, respectively are known from earlier studies to be impurities, delayed toxicants, and detoxication inhibitors in several major O,O-dimethyl phosphorodithioate insecticides. Our recent studies show extensive S-methylation of mono- and dithiocarbamic acids in mice, suggesting the possibility that phosphorodithioic acids such as (MeO)2P(S)SH might also undergo S-methylation. This possibility was examined in ip-treated mice with emphasis on the metabolites of dimethoate [(MeO)2P(S)SCH2C(O)NHMe], one of the most important organophosphorus insecticides. The urinary metabolites of dimethoate, which contains no P-SMe substituent, were found to include four compounds with P-SMe moieties identified by 31P NMR spectroscopy as MeO(HS)P(O)SMe, MeO(HO)P(O)SMe, (MeO)2P(S)SMe, and (MeO)2P-(O)SMe; the latter two compounds are also established by GC-MS as dimethoate metabolites in mouse urine, liver, kidney, and lung. Several approaches verified unequivocally that the previously unknown P-SMe metabolites in urine and tissues are due to in vivo S-methylation rather than to impurities. Studies with other O,O-dimethyl and O,O-diethyl phosphorodithioate insecticides established the analogous S-methylation pathway for ethion, malathion, phenthoate, phosalone, and phosmet in mice. Thus, metabolism of O,O-dialkyl phosphorodithioate insecticides in mammals is shown here for the first time to yield S-methyl phosphorodithioates and phosphorothiolates from in vivo S-methylation of the intermediate O,O-dialkyl phosphorodithioic acids.

Animals↗
PubMed1998

Effects of the pesticides carbofuran, chlorpyrifos, dimethoate, lindane, triallate, trifluralin, 2,4-D, and pentachlorophenol on the metabolic endocrine and reproductive endocrine system in ewes.

Many pesticides are used in the agricultural environment, and some may have the potential to disrupt reproductive or endocrine function. Ewes, in separate groups of 6, received orally into their rumen either empty gelatin capsules or capsules containing chlorpyrifos (12.5 mg/kg), trifluralin (17.5 mg/kg), lindane (2.5 mg/kg), or pentachlorophenol (2 mg/kg) 2 times per week for 43 d. Dimethoate (0.2 mg/kg), carbofuran (0.30 mg/kg), 2,4-dichlorophenoxyacetic acid (10 mg/kg), or triallate (5 mg/kg) was given 3 times per week. After 36 d of treatment, blood samples were taken every 12 min for 6 h for hormone analysis. Ewes were euthanized at the end of the study for necropsy and histopathology. No overt signs of toxicity were seen, and body weight was not affected by treatment. Carbofuran caused a significant increase in serum concentrations of thyroxine compared to control ewes, but all other pesticides, except trifluralin, resulted in a marked decrease in thyroxine concentrations. Serum concentrations of cortisol were significantly increased by trifluralin and chlorpyrifos. Concentrations of insulin in serum were markedly increased in ewes given dimethoate, lindane, trifluralin, triallate, and pentachlorophenol, and concentrations of estradiol were also significantly increased in ewes given lindane and trifluralin. Mean serum concentrations of LH were markedly decreased by trifluralin, and basal LH concentrations were significantly decreased by lindane, dimethoate, and trifluralin but increased by triallate. Both pentachlorophenol and triallate caused a significant increase in severity of oviductal intraepithelial cysts in ewes. Data suggest that several currently used pesticides could influence serum concentrations of reproductive and metabolic hormones, particularly thyroxine, the major secretory product of the thyroid and a principal regulator of metabolism.

Agriculture↗
PubMed1984

Disappearance of dimethoate, methamidophos and pirimicarb in lettuce.

Foliar sprays of dimethoate at 150 or 300 g a.i./ha, methamidophos at 450 or 900 g a.i./ha and pirimicarb at 140 or 280 g a.i./ha were applied for control of the green peach aphid, Myzus pericae (Sulzer), and the lettuce aphid, Nasonovia ribisnigri ( Mosley ), about 2 weeks before the lettuce started heading, and again about 1 week from harvest. In lettuce, dimethoate partially oxidized to its oxon and pirimicarb converted to its methylamino- and/or formyl methylamino-analogues. Most residues were present in the outer leaves which were exposed directly to the sprays; only traces of residues were detected in samples of the inner head leaves. Total residues disappeared rapidly. Pirimicarb was the least persistent and only traces of residues (less than 0.01 ppm) were detected in marketable heads. Concentrations of dimethoate, including the oxon and of methamidophos were well below their respective tolerances of 2 and 1 ppm respectively.

Carbamates↗
PubMed1985

Teratogenic evaluation of the pesticides baygon, carbofuran, dimethoate and EPN.

Baygon was administered IG once daily to CD rats (5 to 50 mg/kg), on the 7th-19th day of gestation or to CD-1 mice (5 to 60 mg/kg) on days 6-16 of gestation. Baygon, at dose levels which were not maternally lethal, did not produce fetotoxicity, fetal lethality or malformations in the fetuses. Baygon was not teratogenic in the CD rat or CD-1 mouse at maternally nontoxic dose levels. Carbofuran was administered IG once daily to CD rats (0.05 to 5.0 mg/kg), on the 7th-19th day of gestation or to CD-1 mice (0.1 to 20 mg/kg) on days 6-16 of gestation. At dose levels which were not maternally lethal, carbofuran did not produce fetotoxicity, fetal lethality or malformations in the fetuses. Carbofuran was not teratogenic in the CD rat or CD-1 mouse at maternally nontoxic dose levels. Dimethoate was administered IG once daily to CD-1 mice (10 to 80 mg/kg), on the 6th-16th day of gestation. At dose levels which were not maternally lethal, dimethoate did not produce fetotoxicity, fetal lethality or malformations in the fetuses. Dimethoate was not teratogenic in the CD-1 mouse at maternally nontoxic dose levels. EPN was administered IG once daily to CD-1 mice (1.0 to 12.0 mg/kg) on the 6th-16th day of gestation. EPN, at dose levels up to those which were maternally lethal, did not produce fetotoxicity, fetal lethality or an increase in malformations. EPN was not teratogenic in the CD-1 mouse at maternally nontoxic dose levels.

Animals↗
PubMed1999

14C-dimethoate residues in olive oil during oil processing.

An olive tree was treated twice in the field with 14C-dimethoate (237.7 muCi, 2.4 g) and 14C residues were determined in the olive fruits at harvest. The fruits were crushed and pressed to extract the crude oil, then refined by neutralization, bleaching and deodorization. The crude oil contained 14.1% of the total 14C in the olive fruits. Neutralization resulted in a reduction of 14C by about 50% of the total 14C residues in oil. Bleaching and deodorization processes further reduced the 14C residues and the refined oil contained 31.6% (which corresponds to 4.4% of 14C residues of the total 14C in olive fruits) of the total 14C in the crude oil. Industrially extracted crude oil was fortified with 14C-dimethoate at 1.8 mg kg-1 (0.02 muCi) level and subjected to the same refining process. A sharp decrease in the amount of 14C was observed by neutralization and the amount of 14C remaining in the refined oil was about 7.3% of the total 14C in the crude fortified oil. The data suggest that the 14C residues in the aged and the fortified oil amples were not of the same nature. The terminal 14C residue in the refined oil obtained from the field experiment did not contain dimethoate and/or its oxon.

Carbon Radioisotopes↗
PubMedDate not supplied

Effects of dimethoate on snail B-esterase and growth as a function of dose, time and exposure route in a laboratory bioassay.

The aim was to study the effects of dimethoate on enzymatic targets and on the growth of Helix aspersa for different times and modes of exposure under laboratory conditions. Young snails were exposed to increasing dimethoate concentrations in the food (D.exp) or in an artificial substrate (S.exp) for 1, 2, 7 and 14 days. Both acetylcholinesterase (AChE) and carboxylesterase (CaE) activities were measured in the foot of the snails for each concentration and exposure time tested. Growth was evaluated after 7 days of exposure. AChE inhibition, dose-dependent for all lengths of exposure, was stronger in S.exp. AChE was more sensitive than CaE for both modes of exposure. IC50(-7) days was 38.3 micrograms g-1 in D.exp and 11.7 micrograms g-1 in S.exp for AChE and was higher than 150 micrograms g-1 in two exposure modes for CaE. AChE activity decreased from the first day to reach maximum inhibition after 7 days of exposure. As noted for B-esterase activities, growth inhibition was stronger in S.exp and was only significant for AChE inhibition of > 90%. The present results show that AChE activity could be used to give early warning of toxic effects of dimethoate in terrestrial gastropods.

Animals↗
PubMed1984

A comparative study of guanine N7-alkylation in mice in vivo by the organophosphorus insecticides trichlorphon, dimethoate, phosmet and bromophos.

Following intraperitoneal administration to male mice (strain AB Jena/Halle) of 14C-methyl-labelled trichlorphon, dimethoate, phosmet and bromophos, 10-20 Ci/mol, in dosages of 0.06-0.55 mmol/kg, DNA from liver and kidneys was analyzed for 14C in N-7 methylguanine (7-MeG). The extents of methylation were in the range of 5-10 mumol 7-MeG/mol guanine for trichlorphon and dimethoate and of 0.2-0.4 for phosmet and bromophos, for high doses, respectively Excretion half-lives of 7-MeG were differing between trichlorphon (5 hrs, high dose, and 15-17 hrs, low dose) and dimethoate (23-160 hrs, high dose). The extents of methylation at 0-6 of guanine were estimated to be around 0.01 mumol 0-6 MeG/mol guanine for high doses of organophosphates of sufficient water solubility. Factors associated with the partition of organophosphates in mammalian systems are useful for estimating DNA attack by organophosphates in mammals in vivo.

Alkylation↗
PubMed2001

Teratogenicity testing of BI 58 EC (38% dimethoate) in chicken embryos with special respect to degradation of the active ingredient.

The insecticide formulation BI 58 EC was tested for teratogenicity in chicken embryos, with particular reference to degradation of the active ingredient (dimethoate) after the treatment of embryonated eggs. The pesticide was diluted in water to a concentration level of 0.8%, and the emulsion was injected into the air space in a volume of 0.1 ml/egg, or hen's eggs were treated by the immersion technique. Residues of dimethoate were measured in the samples on days, 13, 15 and 19 of the incubation of chicken embryos, and morphological examinations were performed simultaneously. Analytical chemistry data indicated a slower degradation of dimethoate in embryos after the immersion of eggs, and cyllosis was remarkable in this group among the sporadic developmental anomalies. The liver tissues of both treated groups exhibited severe fatty infiltration.

Abnormalities, Drug-Induced↗
PubMed2002

[Dietary fat on the procreation of male rats induced by dimethoate].

The effect of dietary fat on the toxicity of dimethoate for the procreation of male rats was observed. Thirty two male rats were divided into 4 groups. 3 groups treated with dimethoate 12.5 mg/(kg.d) for 60 days were fed with high, moderate or low dietary fat respectively. The rats in control group were fed with water and moderate dietary fat. The results showed that serum testosterone(To) and LH and the activity of acid phosphatase and lactate dehydrogenase in testicle were higher in the high or low-fat diet groups than those in the moderate-fat diet group. It suggested that the highor low-fat diet could reduce the degree of harm in the testicle tissue of rats induced by dimethoate than that of moderate-fat diet.

Animals↗
PubMed2002

[The acute effects of dimethoate on the muscarinic-receptors of rat brains and the relationship between muscarinic-receptors and cholinesterase].

OBJECTIVE: To study the acute effects of dimethoate on the muscarinic-receptors(M1, M2) in the brain of rats. METHODS: 24 Sprague-Dawley rats were divided into 4 groups randomly. They were administered subcutaneously with 0, 25, 50, 100 mg/kg dimethoate, respectively. Brains were removed after 48 hours of administration. Radioligand binding assay was used to determine the density and affinity of M1 and M2 receptors. RESULTS: Rats in the treated group showed low density of M1 and M2 receptors compared with the control rats. The brain M1 receptor density of the rats in the highest dosage group was significantly lower than that in the control group while brain M2 receptors density had a decrease trend with increasing dosage, but the difference showed no significance. However, there were no differences of the affinity of both M1 and M2 among different treated groups. Correlation analysis showed there is positive relationship between cholinesterase activity and density of M1 receptors(r = 0.583, P < 0.01). CONCLUSION: M1 and M2 receptors density decreased with the increasing dosage of dimethoate. It is suggested that the alleviating of cholinergic symptoms may be due to the decrease of M1 and M2 receptors in rat brain.

Animals↗
PubMed1991

Toxic effect of dimethoate on the crosslinking of gingival and uteral collagen in female albino rats fed with normal and high protein diets.

The effect of dimethoate on gingival and uteral collagen crosslinking was studied in normal and high protein diets fed female albino rats. The gingival and uteral samples were collected from all the groups of rats and percent reversibility of neutral salt soluble collagen gel and the solubility of insoluble collagen in KCNS or urea were determined. The analysis of gingival and uteral samples showed alpha 1 and alpha 2 sub units of neutral salt soluble collagen appreciably increased beta chains and aldehyde content significantly decreased in dimethoate treated animals compared to controls. The results indicate that due to the effect of dimethoate, the crosslinking and maturation of collagen are impaired.

Animals↗
PubMed1990

[The effect of dimethoate and vibrations on the fetal development of the rat].

The influence of vibration and organophosphate insecticide dimethoate of rats (Rattus norvegicus Berkenhout) was examined by exposing pregnant dams to these influences on 12 d p.c. After exposures to vibrations for 12 h an increase of the rate of absorption could be ascertained. A dermal absorption of dimethoate (349 mg/kg) resulted in an increase of the rate of absorption, retardation and deformation. Combinations of exposure to vibrations and dimethoate show an intensifying effect.

Abnormalities, Drug-Induced↗
PubMed1997

Tricompartmental kinetics of the organophosphorous pesticide dimethoate.

We present a study on the distribution and persistence of the organophosphorous pesticide, dimethoate, in the Wistar rat. Dimethoate's levels in blood and tissues were determined using gas chromatography with a NPD detector. The toxicokinetic profile was estimated by non-linear regression using the software program PCNONLIN, which concluded that a tricompartmental model best described dimethoate's behavior in the rat body.

Adipose Tissue↗
PubMed2001

Protective effect of vitamin E in dimethoate and malathion induced oxidative stress in rat erythrocytes.

Organophosphate (OP) pesticides such as dimethoate and malathion intoxication has been shown to produce oxidative stress due to the generation of free radicals and alter the antioxidant defense system in erythrocytes. It is possible that vitamin E being present at the cell membrane site may prevent OP-induced oxidative damage. In the present study, rats were pretreated orally with vitamin E (250 mg/kg body wt, twice a week for 6 weeks) prior to oral administration of a single low dose of dimethoate and/or malathion (0.01% LD(50)). The result showed that treatment with OP increased lipid peroxidation (LPO) in erythrocytes, however, vitamin E pretreated rats administered OP's showed decreased LPO in erythrocytes. The increase in the activities of superoxide dismutase (SOD) and catalase (CAT) and total-SH content in erythrocytes from dimethoate and/or malathion treated rats as compared to control appears to be a response towards increased oxidative stress. Vitamin E pretreated animals administered OP's showed a lowering in these parameters as compared to OP treated rats which indicates that vitamin E provide protection against OP-induced oxidative stress. The glutathione-S-transferase (GST) activity in erythrocytes was inhibited in OP intoxicated rats which partially recovered in vitamin E pretreated animals administered OP's. Inhibition in erythrocyte and serum acetylcholinesterase (AChE) activity was not relieved in vitamin E pretreated rats administered OP's probably due to the competitive nature of enzyme inhibition by OP's. The results show that vitamin E may amelierate OP-induced oxidative stress by decreasing LPO and altering antioxidant defense system in erthrocytes.

Journal Article↗