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PubMed2000

Biochemical characterization of dichlorvos-induced delayed neurotoxicity in rat.

In vitro and in vivo studies were carried out to assess the delayed neurotoxicity potential of dichlorvos. In vitro, dichlorvos caused a concentration and time-dependent decrease in the activity of neuropathy target esterase (NTE). The Ki of dichlorvos for NTE was calculated to be 1.28 x 10(3) M-1 min-1. In vitro reactivation and ageing studies revealed that dichlorvos-inhibited NTE became refractory to activation by potassium fluoride after 5 min in the ageing medium, thus indicating the formation of an aged complex between dichlorvos and NTE. In vivo also, dichlorvos (200 mg/kg body wt) given as a single subcutaneous dose inhibited NTE in brain at various intervals after exposure (24 h, 10 days, and 21 days). The delayed neurotoxicity potential of dichlorvos was finally confirmed by the rota rod test, which revealed severe motor deficit in all the exposed animals.

Animals↗
PubMed1994

Investigations of the genotoxicity and cell proliferative activity of dichlorvos in mouse forestomach.

This study investigated the possible mechanism by which dichlorvos may have caused forestomach tumours in mice in a chronic corn oil gavage cancer bioassay [NTP (1989) Toxicology and carcinogenesis studies of dichlorvos in F344/N rats and B6C3F1 mice (gavage studies). National Toxicology Program Technical Report 342, NIH Publ. No 89-2598]. For this purpose, a method has been developed to assess the genotoxicity of irritant substances on mouse forestomach epithelium. Groups of five B6C3F1 mice were given a single oral dose of dichlorvos, the genotoxic forestomach carcinogen 1-methyl-3-nitro-1-nitrosoguanidine (MNNG) or the irritant, non-genotoxic forestomach carcinogen butylated hydroxyanisole (BHA). After periods of 2-48 h, three parameters were assessed: unscheduled DNA synthesis (UDS) by autoradiography of tissue sections, replicative DNA synthesis (RDS) also by autoradiography of incorporated [3H]thymidine, and histopathological changes, including hyperplasia. MNNG induced UDS but not RDS or hyperplasia in forestomach epithelium, consistent with its genotoxic mode of action. BHA and dichlorvos did not induce UDS, consistent with absence of genotoxic activity in the forestomach after in vivo exposure. In contrast, BHA and dichlorvos induced RDS and subsequent hyperplasia, which is likely to result from irritant damage. These data suggest that the chronic effects of dichlorvos on mouse forestomach epithelium in the oral gavage bioassay were mediated via enforced cell proliferation, rather than by a genotoxic mechanism.

Animals↗
PubMed1998

Biochemical and behavioral deficits in adult rat following chronic dichlorvos exposure.

The present study was carried out to assess the biochemical and behavioral sequelae of chronic dichlorvos (6 mg/kg b.wt/day for 8 weeks) exposure in rats. Dichlorvos administration significantly decreased the activities of neuropathy target esterase and other carboxylesterase viz., paraoxon resistant and mipafox and paraoxon resistant esterases. The acetylcholinesterase activity was also appreciably decreased following dichlorvos exposure. The alterations in biochemical parameters were also reflected in the behavioral patterns of dichlorvos-treated animals. Dichlorvos administration caused a marked decrease in both the ambulatory and stereotypic components of spontaneous locomotor activity of rats. The muscle strength and coordination of the dichlorvos-treated animals was also significantly impaired. Besides, a marked deterioration in the memory function assessed in terms of the conditioned avoidance response was discernible at the end of the treatment schedule in the experimental animals.

Aggression↗
PubMed2006

Atmospheric fate of dichlorvos: photolysis and OH-initiated oxidation studies.

The OH-initiated oxidation of dichlorvos (a widely used insecticide) has been investigated under atmospheric conditions at the large outdoor European photoreactor (EUPHORE) in Valencia, Spain. The rate constant of OH reaction with dichlorvos, k, was measured by using a conventional relative rate technique where 1,3,5-trimethylbenzene (TMB) and cyclohexane were taken as references. With the use of the rate constants of 5.67 x 10(-11) and of 6.97 x 10(-12) cm3 molecule(-1) s(-1) for the reactions OH + TMB and OH + cyclohexane, respectively, the resulting value of the OH reaction rate constant with dichlorvos was derived to be k = (2.6 +/- 0.3) x 10(-11) cm3 molecule(-1) s(-1). The tropospheric lifetime of dichlorvos with respect to reaction with OH radical has been estimated to be around 11 h. The major carbon-containing products observed for the OH reaction with dichlorvos in air under sunlight condition were phosgene and carbon monoxide. The formation of a very stable toxic primary product such as phosgene associated with the relatively short lifetime of dichlorvos may make the use of this pesticide even more toxic for humans when released into the atmosphere.

Atmosphere↗
PubMed2006

Kinetics and mechanism of degradation of dichlorvos in aqueous solutions containing reduced sulfur species.

Reactions of dichlorvos with five reduced sulfur species (hydrogen sulfide, bisulfide, thiosulfate, thiophenol, and thiophenolate) were examined in well-defined anoxic aqueous solutions to investigate their role in its degradation. Reactions were monitored at varying concentrations of reduced sulfur species over pH range to obtain the second-order reaction rate constants. Experiments at 25 degrees C demonstrated that degradation of dichlorvos promoted by bisufide, thiosulfate, and thiophenolate were of much greater importance than hydrolysis under the experimental conditions in our study. In contrast, hydrogen sulfide and thiophenol were not effective in the degradation of dichlorvos. The activation parameters of the reaction of dichlorvos with bisulfide, thiosulfate, and thiophenolate were also determined from the measured second-order rate constants over a temperature range of 12-50 degrees C. The relative reactivity of the reduced sulfur species decreases in the following order: PhS- > HS- approximately equal to S2O3(2-). When the second-order rate constants at 25 degrees C are multiplied by the environmentally relevant concentration of the reduced sulfur species, predicted half-lives of dichlorvos ranged from hours to days. The results indicated that reduced sulfur species could play a very important role in the chemical fate of dichlorvos in coastal marine environments.

Dichlorvos↗
PubMedDate not supplied

Effect of high-fat and high-protein diets on toxicity of parathion and dichlorvos.

Growing male rats that weighed 120 +/- 5 g were kept for 30 days on the following synthetic diets: high protein diet (HPD), 59% casein; high fat diet (HFD), 50% saturated fat; and normal diet (ND), 19% casein, 10% saturated fat, and 60% sucrose. Other essential dietary ingredients were included in all the diets. All animals were injected at the end of the 30-day period with parathion [10 mg/kg intraperitoneal (ip) injection as a single dose] or dichlorvos (30 mg/kg ip as a single dose) to compare the effect of dietary pretreatments on mortality from parathion and dichlorvos. A lower dose of parathion (7.5 mg/kg) and dichlorvos (20 mg/kg) was employed in another set of experiments to compare the spontaneous regeneration of plasma and red blood cell (RBC) cholinesterase (ChE) activity at 2 hr, 1 day, 3 days, and 5 days after administration of parathion or dichlorvos. The effect of these diets on hepatic microsomal oxidases was also determined. Results showed that diets per se did not affect initial plasma and RBC ChE activity. The HPD and HFD significantly protected against mortality from parathion but not from dichlorvos. Hepatic microsomal cytochrome P-450 and aminopyrine demethylase activity were unchanged, but aniline hydroxylase activity was increased significantly by HPD and HFD. Parathion oxidase in hepatic microsomes was significantly increased in rats fed HFD only. For the HPD, spontaneous regeneration of ChE diminished in RBCs in parathion-intoxicated rats and in plasma and RBCs of dichlorvos-intoxicated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Memantine alleviates toxicity induced by dichlorvos in rats.

The changes of N-methyl-D-aspartate (NMDA) receptor and protective efficacy of memantine (MEM) in rats poisoned with dichlorvos were studied. Dichlorvos evoked down-regulation of the affinity and density of [(3)H]MK-801 binding to NMDA receptor in the brain of rats receiving dichlorvos (15 and 25 mg/kg bw, i.p.). The binding capacity of NMDA receptor and acetylcholinesterase activity were determined at 4 h, 8 h, 16 h, 24 h and 48 h after treatment. When rats were given a different doses of MEM (5, 15 and 45 mg/kg bw) after poisoning (dichlorvos 25 mg/kg bw), the latency of onset of signs was postponed and the magnitude of muscular fasciculation was alleviated as the dose of MEM increased. The lower doses of MEM (5 and 15 mg/kg bw) could antagonize the dichlorvos-evoked down-regulation of NMDA receptor, while the highest dose (45 mg/kg bw) decreased the Bmax and Kd values of NMDA receptors. These results show the dichlorvos-evoked down-regulation of NMDA receptor might be self-regulation by the body to protect the central nervous system. MEM could antagonize the down-regulation of NMDA receptors, and alleviated signs of poisoning, especially reducing the magnitude of muscular fasciculation. We suggest that the role of NMDA receptor in organophosphates (OP) poisoning should receive more attention, and, that MEM treatment in acute OP poisoning, as a supplement to atropine and oxime, should be considered.

Acetylcholinesterase↗
PubMedDate not supplied

Brain hypoplasia caused by exposure to trichlorfon and dichlorvos during development can be ascribed to DNA alkylation damage and inhibition of DNA alkyltransferase repair.

Treatment of pregnant guinea pigs with trichlorfon causes cerebellar hypoplasia in offspring. The most sensitive period for treatment is days 42-47 of gestation, which coincides with the rapid brain growth spurt and with the development of cerebellar granule cells. When rat granule cells were exposed in vitro to trichlorfon and dichlorvos for 24 hours they died, whereas trichloroethanol had no effect. When the cells were exposed to trichlorfon and dichlorvos for 3 hours, only dichlorvos was lethal indicating that the metabolite dichlorvos was more potent than trichlorfon itself. Cultured cerebellar granule cells were also found to be quite sensitive to other DNA-alkylating agents such as methylazoxymethanol and methylmethane sulphonate and to O6-benzylguanine; a potent and specific inhibitor of the DNA alkyltransferase involved in the repair of DNA alkylation damage. The organophosphorous compounds were also found to cause inhibition of the alkyltransferase and the lethal effects of the tested compounds on granule cell culture correlated well with the potency of inhibition. In a bacterial test system for monitoring alkylation effects on the DNA, dichlorvos was demonstrated to have a strong DNA alkylation effect. These results suggest that alkylation of DNA and inhibition of its repair can contribute to the brain hypoplasia observed after exposure to trichlorfon and dichlorvos during brain development.

Alkyl and Aryl Transferases↗
PubMed1992

The influence of single topical application of dichlorvos on blood esterases and toxicity in male calves.

The effect of dichlorvos on inducing changes in blood esterase activities and systemic toxicity was investigated following single topical applications of 1, 3 or 6% dichlorvos concentrations to male calves. Dichlorvos at 1% concentration did not produce any signs of toxicity, whereas 3 and 6% concentrations induced mild to severe toxicity characteristic of anticholinesterase poisoning. Dichlorvos at all concentrations significantly inhibited erythrocyte cholinesterase (25-75%), plasma cholinesterase (30-85%), and serum carboxylesterase (15-51%) activities in male calves. The dose-dependent inhibition was maximum 12 h after insecticide exposure. The extent of inactivation of blood esterases was not correlated with the severity of toxicity. Inhibition of blood cholinesterases by the 6% dichlorvos was still present 21 d after the dichlorvos exposure.

Administration, Cutaneous↗
PubMed1983

Interaction of dichlorvos-crotoxyphos insecticide with phenothiazine anthelmintic in sheep with or without Haemonchus and Trichostrongylus infections.

The temporal interaction of an emulsifiable mixture of 2.3% dichlorvos and 10% crotoxyphos with phenothiazine anthelmintic was studied in 8 groups of 5 lambs each, free from or parasitized with Haemonchus and Trichostrongylus spp. Each lamb in 1 of 3 parasitized groups and 1 of 3 nonparasitized groups was treated with phenothiazine orally (12.5 g initially and 4 days later with 6.25 g every 3 days for 9 treatments) and/or the mixture of dichlorvos and crotoxyphos dermally (1,550 ml of 0.25% emulsion sprayed every 2 weeks for 3 applications). Two groups served as controls. Onset of clinical signs of toxicosis, lethality, and erythrocyte acetylcholinesterase (EACE) activity were monitored. After each dichlorvos-crotoxyphos mixture spray, clinical signs of toxicosis were seen within 40 minutes in parasitized and nonparasitized lambs regardless of concurrent phenothiazine treatment. Phenothiazine alone was not toxic and did not inhibit EACE activity. The EACE activities of dichlorvos-crotoxyphos mixture-sprayed lambs were significantly (P less than 0.05) depressed regardless of parasitism or concurrent phenothiazine treatments. The severity of inhibition increased with each dichlorvos-crotoxyphos mixture spray, but EACE activity recovered within 48 hours after each spray although base-line values were never attained. There was no apparent potentiation of the toxic effects of the dichlorvos-crotoxyphos mixture by phenothiazine.

Animals↗
PubMed1997

Prevention and treatment of dichlorvos-induced toxicosis in mice by diphenhydramine.

Dosing male mice with 125 mg dichlorvos/kg orally produced cholinergic overstimulation and death in up to 100% of the animals. Administration of 20 or 30 mg diphenhydramine HCl/kg s.c. 15 min before dichlorvos dosing significantly reduced the development of toxicity and increased 24-h survival rates to 87 and 100% respectively. Diphenhydramine was less effective when given immediately after dichlorvos dosing; however, repetitive treatments of 20 mg diphenhydramine/kg s.c. increased the survival rate to 75%. The administration of a single injection of 30 mg diphenhydramine/kg s.c. 15 min before dichlorvos dosing or as multiple s.c. or i.p. doses after dichlorvos increased the 24-h oral dichlorvos LD50 by 30, 50 or 70%, respectively. The anticholinergic effects of diphenhydramine protects and effectively treats mice poisoned with dichlorvos.

Animals↗
PubMed1979

The chemical and biochemical reactivity of dichlorvos.

The chemical structure, reactivity and metabolic fate of the insecticide dichlorvos (2,2-dichlorovinyl dimethyl phosphate) are discussed in relation to the possible genotoxicity of this and other methyl phosphate triesters. Recent attempts to demonstrate the methylation of DNA following exposure of bacteria and animals to dichlorvos are reviewed. On the basis of comparative data relating mutagenesis to methylation reactions, it seems entirely appropriate to conclude that the mutagenicity of dichlorvos to bacteria is due solely to methylation of the bacterial DNA under the conditions of these tests. However, the methylation of mammalian DNA could not be demonstrated under realistic exposure conditions (when the alkylating mutagen methyl methanesulphonate afforded clearly measurable methylation). The failure to detect methylation by dichlorvos in vivo is attributed to the operation of highly efficient enzyme-catalysed biotransformations which rely largely on the phosphorylating reactivity of dichlorvos. The biotransformation pathways, characterised mostly in the rat, appear to be common also to pig, mouse, hamster, and man.

Animals↗
PubMed1991

The therapeutic effects of 2,3-butanedione monoxime and atropine in severe dichlorvos intoxication in buffalo calves.

2,3-Butanedione monoxime and atropine alone or in combination were evaluated for their ability to alleviate the toxicity and to reverse the biochemical changes induced by dichlorvos in the blood of buffalo calves. Treatment with 2,3-butanedione monoxime plus atropine 30 min after oral administration of dichlorvos (160 mg/kg) eliminated the apparent toxic signs within 10-15 min, completely prevented lethality, and reversed the dichlorvos-induced alterations in the concentrations of serum carboxylesterase, total plasma proteins, blood glucose and plasma cholinesterase within 2, 4, 12 and 168 h, respectively. Treatment with either 2,3-butanedione monoxime or atropine alone was less effective but the former was the more potent of the two in counteracting the biochemical effects of dichlorvos. These antidotal studies suggest that 2,3-butanedione monoxime in conjunction with atropine would provide effective therapy against severe dichlorvos intoxication in buffalo.

Animals↗
PubMed1996

Metrifonate induces cholinesterase inhibition exclusively via slow release of dichlorvos.

Metrifonate, a long-acting cholinesterase (ChE) inhibitor with very low toxicity in warm-blooded animals, inhibits rat brain and serum cholinesterase (ChE) in vitro through its hydrolytic degradation product, dichlorvos. This conclusion is based on the finding that metrifonate-induced ChE inhibition showed the same pH dependence as its reported dehydrochlorination to dichlorvos. The ChE inhibition induced by dichlorvos was not pH dependent. It was mediated by a competitive drug interaction with the catalytic site of the enzyme, which led to irreversible inhibition within several minutes of incubation. After this time, addition of further substrate to the inhibited enzyme was not able to promote drug dissociation and hence enzyme reactivation. Similar characteristics of inhibition, i.e. interaction with the substrate binding site and time-dependent switch to non-competitive inhibition were observed with the reference compound, physostigmine. However, the physostigmine-induced inhibition of ChE could be readily reversed by further substrate addition. Another reference compound, tetrahydroaminoacridine (THA), also induced a reversible inhibition of rat brain and serum cholinesterase, but with a mechanism of action different from that of both dichlorvos and physostigmine in that enzyme inhibition occurred rapidly upon drug addition at an allosteric site on the enzyme surface. It is suggested that the unique slow release plus the slow inhibition of ChE by dichlorvos is responsible for the lower toxicity of metrifonate compared to that of directly acting ChE inhibitors.

Animals↗
PubMed2006

Dissipation of endosulfan and dichlorvos residues in/on cauliflower curds.

Dissipation behaviour of endosulfan and dichlorvos in/on cauliflower, variety Snowball-16, was studied during rabi season (Sep.-March) 2003-2004. Endosulfan and dichlorvos were sprayed @ 350 and 110g a.i. with 115 g a.i., respectively, 80 days after transplanting. Samples were taken at the interval of 0 (1h after spray), 3, 5, 7, and 10 days after spray (DAS) in triplicate and residues were estimated on GC-ECD system equipped with capillary column. The initial deposits of 3.452 and 0.295microg g(-1) of endosulfan and dichlorvos dissipated to 0.084 (97.56%) and 0.009 (96.95%), respectively after 10 DAS. Residues of endosulfan reached below maximum residue limit of 2microg g(-1) one day after spray and of dichlorvos were below MRL value of 0.5microg g(-1) even on 0 day. Dissipation pattern followed first order kinetics for both the insecticides with half life periods of 1.81 and 2.08 days for endosulfan and dichlorvos, respectively.

Brassica↗
PubMed1978

Mutagenicity of dichlorvos and other structurally related pesticides in Salmonella and Streptomyces.

The following pesticides: azinphosmethyl, diallate, dichlorvos, EPTC, fenchlorphos, mevinphos, monocrotophos, noruron, parathionmethyl, triallate, trichlorphon and vegadex were tested for the ability to induce his+ revertants in four histidines requiring strains of Salmonella typhimurium--TAI 535(missense), TAI 536, TAI 537 and TAI 538 (frame-shift)- and resistance to low levels of streptomycin in Streptomyces coelicolor. Dichlorvos, which is a phosphoric ester with a dichlorovinyl group as side chain, and trichlorphon, which is known for its spontaneous conversion in dichlorvos, are both mutagenic in Salmonella (strain TAI535) and Streptomyces. Five organophosphorus pesticides similar to dichlorvos but devoid of the vinyl group are not mutagenic. Three carbamates, diallate, triallate and vegadex, which contain a chloroallyl group similar to the vinyl group of dichlorvos are mutagenic in Streptomyes; triallate and vegadex are powerful mutagens also in Salmonella (strain TAI535); two other carbamates devoid of the chlorinated group are not mutagenic. The results suggest that the presence of a vinyl chloride or allyl chloride group in the molecule of these pesticides is responsible for the ability to induce point mutations in Salmonella and Streptomyces.

Animals↗
PubMed1992

Neurotoxicity of dichlorvos: effect on antioxidant defense system in the rat central nervous system.

The effect of dichlorvos exposure (5 mg kg-1 body wt, ip) on lipid peroxidation and antioxidant defense system in different regions of the rat central nervous system was studied. In the present paper an inhibition of acetylcholinesterase activity was used as an index of dichlorvos neurotoxicity. We observed significant increases in the activities of the antioxidant enzymes superoxide dismutase (SOD) and catalase which were accompanied by a decrease in the values of lipid peroxidation. Dichlorvos exposure also resulted in a significant decrease in glutathione peroxidase activity. The decreased levels of both reduced and oxidized glutathione as observed on dichlorvos exposure affected the GSH/GSSG ratio. These results indicate that the enzymes SOD and catalase may enhance the disposal of potentially toxic radicals. Furthermore, the decrease in GSH levels may be a mechanism for the detoxification of dichlorvos in the brain.

Acetylcholinesterase↗
PubMedDate not supplied

Latent dichlorvos neurotoxicity detected by vagal tone monitoring in dogs.

Dichlorvos (dimethyl 2,2-dichlorovinyl phosphate) was administered orally to German Shorthair Pointer dogs at approximately 60 mg/kg (twice the usual clinical dose). Plasma and erythrocyte cholinesterase (ChE) was monitored prior to, 90 min, and 180 min post-ingestion. 2-PAM (20 mg/kg IV) and atropine sulfate (0.022 mg/kg IM) were administered 90 min after the dichlorvos to paired treated and control dogs. The telemetered electrocardiographic (ECG) signal was analyzed by a Vagal Tone Monitor (VTM) to yield mean heart period (msec) and an estimate of the amplitude of respiratory sinus arrhythmia (V in natural log values of msec2) for five min intervals. Dichlorvos did not cause cholinomimetic symptoms even though blood cholinesterase was significantly inhibited (plasma -51.3% and erythrocyte -43.7%). The atropine sulfate treatment resulted in the expected vagolytic effects in both the control and the dichlorvos treated dogs, but the atropine effects were attenuated in the latter dogs. Three weeks later, ChE activity was not significantly depressed in the dichlorvos treated dogs, and their V responses to atropine were more similar to the responses in control dogs.

Animals↗