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PubMed1991

In vitro effect of dimethoate on the activity of tryptophan pyrrolase in rat liver.

Total and holo-enzyme activities of tryptophan 2,3-dioxygenase were measured in vitro in the presence and absence of the organophosphorous insecticide, dimethoate. Addition of dimethoate to the reaction mixture decreased the activities of both total and holo-forms. Total and holo-enzyme activities were decreased by 34% and 26%, respectively, by 1 mM dimethoate. On the other hand, 5 mM dimethoate resulted in 56% and 34% inhibition to total and holo-enzyme activities, respectively. Lineweaver-Burk plot of the total-enzyme activity at different tryptophan concentration in the presence of 2 mM dimethoate gave uncompetitive type of inhibition.

Animals↗
PubMed2006

Acute and chronic effects of pulse exposure of Daphnia magna to dimethoate and pirimicarb.

Short-term (<48 h) and long-term (21 d) effects of dimethoate and pirimicarb were studied in Daphnia magna exposed to pulses of 0.5 to 8 h in duration. During a 21-d postexposure observation period, the following parameters were monitored: Mortality, mobility, day for first offspring, animal size, weight of offspring and adults, and number of offspring produced. In general, animals exposed to a single pulse of dimethoate or pirimicarb regained mobility after 24 to 48 h in clean media. Animals exposed to repeated pulses of dimethoate did not recover mobility during a 48-h postexposure observation period, and mortality was significantly increased. Animals exposed to two pulses of pirimicarb showed less recovery of mobility compared with those exposed to one pulse. Exposure of D. magna to 30 mg/L of dimethoate or 100 microg/L of pirimicarb for 2 to 6 h resulted in a significant reduction in the number of offspring and in the average weight of offspring. The average body length was reduced after pulse exposure to 30 mg/L of dimethoate for 3 h or 70 microg/L of pirimicarb for 4 h, and these exposure concentrations caused a delay in the day for first offspring at exposure durations of 2 to 6 h. The most important new findings in the present study are that short-term (<4 h) pulse exposure of neonates to acetylcholinesterase-inhibiting pesticides caused reproductive damage in D. magna and that repeated-pulse exposure significantly increased mortality in animals that apparently had recovered after a single-pulse exposure.

Aging↗
PubMed1992

Comparative response of nestling European starlings and red-winged blackbirds to an oral administration of either dimethoate or chlorpyrifos.

Red-winged blackbird (Agelaius phoeniceus; blackbird) and European starling (Sturnus vulgaris; starling) nestlings were dosed with either 2.0 mg/kg body mass chlorpyrifos, 50.0 mg/kg body mass dimethoate, or a propylene glycol carrier in situ. Four growth measurements (body mass, culmen, tarsus, wing) were recorded from nestlings to determine if these organophosphorus compounds caused perturbations in development at sublethal concentrations. Blackbird nestlings were more sensitive to chlorpyrifos than starling nestlings were more sensitive to dimethoate than blackbird nestlings. This was in contrast to reported adult LD50 values where the reverse was true. Blackbird nestlings were more tolerant of a substantially higher concentration of dimethoate than the adult LD50. The sensitivity of starling nestlings to dimethoate was similar to adults. In contrast, juveniles of both species were more sensitive to chlorpyrifos than adults. After the initial 24 hr, surviving nestlings dosed with either chemical recovered and continued their development. Exposure to dimethoate caused significant depression in starling body mass during the initial 24 hr period. Survivors obtain body mass equal to controls within 48 hr post dosing. The research presented here demonstrates that the simple supposition that passerine nestlings are typically more sensitive to toxins than adults does not always hold true. It also indicates that sensitivity relationships among adults do not necessarily apply to their nestlings.

Administration, Oral↗
PubMed1997

[Blocking effects of dimethoate on acetylcholine receptor channels].

The patch-clamp technique was used to study the inhibitory effect of dimethoate, an organophosphrous pesticide, on the membrane of embryoinc Xenopus musle cells in culture. Using whole-cell clamp and cell-attached clamp, we found that the direct inhibitory effects of dimethoate was evidenced on both miniature end-plate currents (MEPC) and single channel currents. Dimethoate increased the amplitude and frequency of MEPC at a lower concentration (21.6 mumol/L) while both decreased at a higher concentration (237 mumol/L). The dimethoate at a concentration of 146 mumol/L shortened the opening time and decreased the opening probability of the single channel. The results show that dimethoate is an AChR channel blocker.

Animals↗
PubMed1992

Toxic effects of different concentrations of dimethoate on lysosomal enzymes of female albino rats.

The effect of three different concentrations of dimethoate on the activity of certain lysosomal enzymes, viz. beta-glucuronidase, beta-N-acetylglucosaminidase, cathepsin B and cathepsin D in serum, skin, liver, kidney and spleen and the stability of liver and kidney lysosomes was studied in female albino rats. The activity of beta-glucuronidase, beta-N-acetylglucosaminidase, cathepsin D was found to increase in serum and tissues in higher concentration (2.25 mg/100 g body weight) of dimethoate treated rats. A significant increase in the rate of release of beta-glucuronidase was found in the liver and kidney of higher concentration of dimethoate treated rats compared to controls. The results demonstrate that the activity of lysosomal enzymes increased in higher concentration of dimethoate treated rats than the lower concentration (0.56 mg/100 g body weight) of dimethoate treated rats.

Animals↗
PubMedDate not supplied

Developmental neurotoxicological effects of lead and dimethoate in animal experiments.

Neurophysiological changes caused by parallel treatment with inorganic lead and dimethoate (a combination of possible health risk at population level) were investigated in different phases of the ontogenesis. Wistar rats were treated by gavage with lead (80.0 or 320.0 mg/kg); with dimethoate (7.0 or 28.0 mg/kg), or with their combination on days 5-15 of pregnancy, days 5-15 of pregnancy + days 2-28 of lactation (females of P generation), or days 5-15 of pregnancy + days 2-28 of lactation (females of P generation) + 8 weeks after weaning (males of F1 generation). Electrophysiological parameters (electrocorticogram, cortical evoked potentials) of the F1 male rats in the above groups were investigated at the age of 12 weeks. Both spontaneous and evoked electrophysiological phenomena showed dose-, treatment- and combination-dependent changes (e.g. significantly decreased mean amplitude and increased frequency of the electrocorticogram, lengthened latency and duration of the somatosensory, visual and auditory evoked potentials) which seemed to be more pronounced in the groups treated with the combination of lead and dimethoate than in the groups given lead or dimethoate alone. The results indicate that a simultaneous, pre- and postnatal exposure to the neurotoxicants, lead and dimethoate, considerably altered the functioning of the central nervous system.

Animals↗
PubMed1977

Bioassay of dimethoate for possible carcinogenicity.

A bioassay of the carcinogenicity of technical-grade dimethoate was conducted using Osborne-Mendel rats and B6C3F1 mice. The test material was administered in feed to groups of 50 rats of each sex at either of two concentrations for 80 weeks, followed by 35 weeks of observation. Initial doses were not well tolerated; therefore, they were reduced during the study. The "time-weighted average doses" for rats were 155 and 310 ppm for males and 192 and 384 ppm for females. All surviving rats were killed between 113 and 115 weeks. Dimethoate was administered in feed to groups of 50 male and 50 female mice at two concentrations. Female mice received diets containing 200 and 500 ppm of dimethoate for 80 weeks; male mice received the same dosage. However, high-dose males were returned to the control diet at 60 weeks, and low-dose males at 69 weeks. All surviving mice were killed between 93 and 94 weeks. Tremors and hyperexcitability, both indications of dimethoate toxicity, were observed in the treated animals. However, it is considered that the low-dose group of rats and both dose groups of mice survived long enough to permit an evaluation of carcinogenicity. Pathologic evaluation revealed no statistically significant increase in tumors associated with dimethoate treatment in either species of animal, and it is concluded that there was no carcinogenic effect under the conditions of the experiment.

Journal Article↗
PubMed2006

Developmental toxicity of orally administered technical dimethoate in rats.

BACKGROUND: Dimethoate (O,O-dimethyl-S-(N-methylcarbamoyl-methyl) phosphorodithioate), an organophosphate insecticide, was examined for its potential to produce developmental toxicity in rats after oral administration. METHODS: Pregnant Fischer 344 rats were given sublethal doses of 0 (corn oil), 7, 15, and 28 mg/kg/day dimethoate by gavage on gestation days (GD) 6-15. Maternal effects in 15 and 28 mg/kg/day dose groups included cholinergic signs such as tremors, diarrhea, weakness, and salivation, and depression in the maternal and fetal brain acetylcholinesterase (AChE) activities. Other maternal toxicity that included reduction in body weight and feed consumption was observed only in the treated group of 28 mg/kg/day. No maternal toxicity was apparent in the 7 mg/kg/day dose group. RESULTS: Maternal exposure to dimethoate during organogenesis significantly affected the number of live fetuses, early resorption, and mean fetal weight in the 28 mg/kg/day dose group. No external, visceral, and skeletal abnormalities were observed in any of the treated groups compared to the control. CONCLUSIONS: On the basis of the present results dimethoate can produce clinical signs of toxicity and significant inhibition of the maternal and fetal AChE activities in dose groups of 15 and 28 mg/kg/day and showed fetotoxicity without teratogenic effects at 28 mg/kg/day.

Abnormalities, Drug-Induced↗
PubMed1996

The effect of dimethoate on bone marrow cell chromosomes of rats in subchronic four-generation experiments.

The effect of the insecticide dimethoate (O,O-dimethyl S-/N-methylcarbamoylmethyl phosphorodithioate) on bone marrow cells of four generations of rats was investigated. Male and female Wistar rats were treated for 6 weeks with 5 treatments per week via gavage at doses of 7.0, 9.33, and 14.0 mg/kg (1/ 100, 1/75, and 1/50 of the LD50). Chromosomes of 10 of the treated males were prepared. Other males (6-8 males per dose) were paired with females (11-16 females per dose). This represented the first (P) generation. During pregnancy and lactation females were treated with adequate doses of dimethoate. In F1 (70 males and 56 females), F2 (71 males and 62 females), and F3 generations (62 males and 44 females) treatment with dimethoate and the preparation of chromosomes (40 males per generation) were the same as those in the P generation. Following treatment with dimethoate in P and F1 generations, the number of numerical chromosome aberrations increased significantly. No significant changes in chromosome aberrations were found in F2 and F3 generations compared to the control groups. The frequency of numerical chromosome aberrations decreased considerably compared to the P generation at the dose of 14.0 mg/kg (1/50 of LD50).

Animals↗
PubMed1996

Toxicity of dimethoate to some soil animal species in different soil types.

Toxicity of dimethoate (insecticide) to an earthworm (Aporrectodea caliginosa tuberculata), a collembola (Folsomia candida), and an enchytraeid worm (Enchytraeus crypticus/variatus) was studied in three different soil types (artificial soil, clayey soil, and humus sandy soil). Parameters measured were survival and biomass change of the earthworms and survival and reproduction of the collembolas and enchytraeids. The degradation of dimethoate was analyzed too. Toxic effects were observed at the concentrations of some mg/kg dry soil. The biomass reduction of the earthworms occurred at lower concentrations than reduction in survival. The collembolas were more susceptible to dimethoate than the enchytraeids. High organic matter content of the soil reduced the toxic effects. The degradation of dimethoate was rather slow in the soils and under conditions tested. Half-life varied between 41 and 84 days.

Analysis of Variance↗
PubMed1980

Studies on the action of dimethoate on the immune system.

The actions of the organophosphorous insecticide dimethoate (0.0-dimethyl S-(N-methylcarbamoylmethyl)phosphorodiothioate) on the immune response of mice and rats were studied. There was a decrease of lymphocytes to at 50% of normal. The weights of the thymus and spleen were diminished and the production of antibodies was reduced. 72 h after administration all the parameters measured had returned to normal. Histological examinations show a reduction of the cortex of the thymus and disruption of the thymocytes. The number of rosettes forming cells in rats was reduced after dimethoate. The actions seen after dimethoate administration are identical with the effects observed after glucocorticoid application. These results suggest an indirect depression of the immune system by dimethoate producing a release of glococorticoids.

Animals↗
PubMed1996

Behavioral effects of acute sublethal exposure to dimethoate on wood mice, Apodemus sylvaticus: II--Field studies on radio-tagged mice in a cereal ecosystem.

The effects of direct exposure to an organophosphate (OP) pesticide, dimethoate, were examined in free-living wood mice, Apodemus sylvaticus, in a wheat field. Male mice were radio-tagged at night and followed during 2-3-d periods, before and after an intraperitoneal injection of 50 mg/kg dimethoate which previous laboratory studies had demonstrated causes a maximum depression in brain acetylcholinesterase (AChE) activity of 75% relative to non-exposed mice. In subsequent weeks, survival was estimated by tracking and trapping data. Exposure to dimethoate significantly decreased locomotor activity in the first 6 h after administration resulting in a significant decrease in the area over which animals moved. These effects were limited to the night of treatment and disappeared 24 h later. The transient behavioral impairment of the dimethoate-treated animals appeared to have no effect on medium-term survival. Direct exposure to OPs sufficient to cause 75% depression of brain AChE is unlikely to be hazardous to wood mice if exposure is transient, as in the present study; it would be expected that sustained exposure sufficient to cause such behavioral effects would, however, be detrimental.

Animals↗
PubMed1983

Effect of dimethoate and O-demethyldimethoate on bone marrow cells of CFLP mice.

The organophosphorus pesticide dimethoate and its nonalkylating O-demethyl derivative were tested for their ability to induce chromosomal alterations in bone marrow cells of CFLP mice after ip administration. A single dose of 20 mg/kg dimethoate proved to be ineffective. However, doses of 60 mg/kg dimethoate or 69 mg/kg O-demethyldimethoate sodium salt significantly increased the aberration rates above those of the controls. The same effect was observed after a nontoxic dose of 690 mg/kg O-demethyldimethoate sodium salt. Considering the distribution of the several aberration types, these findings suggest that the alkylating properties of dimethoate only in part may be responsible for its cytogenetic activity.

Alkylation↗
PubMed1995

Carbohydrate metabolism in hepatic tissue of freshwater catfish Clarias batrachus L. during dimethoate exposure.

Clarias batrachus L., a freshwater catfish of commercial importance, was exposed to a sublethal concentration of dimethoate (Rogor). The acute effect of dimethoate on some aspects of carbohydrate metabolism of hepatic tissue was studied after 1, 2, 4 and 8 days. The glycogen content was depleted, whereas the lactate level was elevated throughout the experimental period and an increase in lactate dehydrogenase was observed. The activity levels of glycogen phosphorylase a and ab in the hepatic tissue were increased during dimethoate stress. The results suggest that carbohydrate metabolism was adversely affected in the hepatic tissue by the organophosphate insecticide dimethoate.

Animals↗
PubMed2002

Biochemical changes in primary culture of skeletal muscle cells following dimethoate exposure.

In order to investigate the cellular mechanism of muscular weakness in the Intermediate Myasthenia Syndrome (IMS) following acute organophosphate poisoning, we studied the cytotoxicity of dimethoate and its effects on the activity of acetylcholine esterase (AChE), Na+-K+-ATPase, succinate dehydrogenase (SDH), and Ca2+-ATPase in primary cultured skeletal muscle cells. The results showed that the activity of AChE was significantly inhibited in a dose and time-dependent manner when cells were exposed to dimethoate for 2 h, but the expression of heat-shock protein (HSP70) in muscle cells was significantly increased in a time-dependent manner following dimethoate exposure. Dimethoate can significantly increase the activity of Na+-K+-ATPase in the mitochondrial and cytoplasm fraction of muscle cells, and inhibit the activity of Ca2+-ATPase. This study suggests that the disruption of intracellular homeostasis and energy metabolism of the muscle cells may play a role in the etiology of IMS.

Acetylcholinesterase↗
PubMed2005

Life stage specific impact of dimethoate on the predatory mite Hypoaspis aculeifer canestrini (Gamasida: Laelapidae).

Toxicants may affect juveniles more than adults because of physiological and behavioral aspects. When developing toxicity tests, this issue is often not addressed, and the most sensitive end point may be ignored. The topic was raised by a European working group aiming to develop a standard toxicity test with the predatory mite, Hypoaspis (Geolaelaps) aculeifer Canestrini, as this species was included in the EU Guidance documentfortesting of pesticides. To assess whether the juvenile life stages are the most susceptible, we examined the acute toxicity of dimethoate on larvae, protonymphs, deutonymphs, males, and females of H. aculeifer. The mites were exposed to 0, 2, 4, and 6 mg dimethoate kg(-1) for 7 days in an OECD artificial soil (5% organic matter). Total juvenile biomass, reproduction, mortality, and population growth rate (pgr) lambda were assessed at the end of the test. A comparison of mortality ranked the sensitivity of the life stages: Larvae (LC50 = 3.8 mg kg(-1)) > protonymphs (LC50 = 5.3 mg kg(-1)) > males (LC50 = 5.6 mg kg(-1)) > deutonymphs (LC50 = 7.1 mg kg(-1)) > females (LC50 = 7.6 mg kg(-1)). Effects on reproduction and pgr were significant at 2 mg dimethoate kg(-1), with population decline starting at this concentration. Thus, a test system with H. aculeifer including reproduction as end point is a rational approach, as reproduction will encompass juvenile mortality, at least with respect to dimethoate. Moreover, we suggest that pgr should be included in chronic standard tests because of high ecological relevance and the feasibility of applying it.

Animals↗
PubMed2003

Three-year study of fenthion and dimethoate pesticides in olive oil from organic and conventional cultivation.

Residues of fenthion and dimethoate pesticides were determined in organic and conventional olive oils by liquid-liquid and solid-phase extractions with subsequent gas chromatography and mass spectrometric analysis. The olive oil samples were collected from Crete during 1997-99. The average concentrations of fenthion in conventional olive oils were 0.1222, 0.145 and 0.1702 mg x kg(-1), and for dimethoate were 0.0226, 0.0264 and 0.0271 mg x kg(-1) for 1997, 1998 and 1999, respectively. The average concentrations of fenthion in organic olive oils were 0.0215, 0.0099 and 0.0035 mg x kg(-1) for 1997, 1998 and 1999, while for dimethoate they were 0.0098, 0.0038 and 0.0010 mg x kg(-1), respectively. All the olive oils contained residue levels lower than the maximum residue levels according to the FAO/WHO Codex Alimentarius. The organic olive oil contained significantly lower concentrations of the two pesticides. The levels of fenthion and dimethoate in organic olive oils exhibited a decreasing trend following the implementation of the new cultivation method. We propose procedures that should be established in the organic cultivation in order to maximize its effectiveness.

Dimethoate↗
PubMed1988

In vivo chronic effect of dimethoate and deltamethrin on rabbits.

The in vivo effect of dimethoate and deltamethrin on body and organ weights, serum proteins and on plasma acetylcholinesterase (AChE), aromatic esterase and ATPase were examined in growing male rabbits throughout five months period. Both compounds had no significant effect on body weight; however, adrenal, testis & pituitary weights decreased (P less than 0.01); the liver and spleen weights increased (P less than 0.01) in a dose dependent manner. Serum total proteins and globulin decreased (P less than 0.01) in a dose dependent trend, while serum albumin was not greatly affected. AChE activity was increased (P less than 0.01) after 1 month of treatment with the two doses of dimethoate and deltamethrin; thereafter, AChE activity showed 40% inhibition of the control level. The activity of aromatic esterase increased markedly after the first month, then declined gradually until the fifth month. High dose of dimethoate markedly inhibited this enzyme particularly after the 5th month of treatment. Both doses of deltamethrin increased ATPase activity after the first month of treatment, then the ATPase activity was normal. Dimethoate inhibited ATPase particularly at the end of treatment in a dose dependent manner.

Acetylcholinesterase↗