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PubMed1996

A study of the aneugenic activity of trichlorfon detected by centromere-specific probes in human lymphoblastoid cell lines.

The potential of the pesticide trichlorfon to induce mitotic aneuploidy has been investigated in genetically engineered human lymphoblastoid cell lines. Trichlorfon failed to induce micronuclei in the AHH-1 and MCL-5 cell lines when treated in media at normal cell culture pH (pH 7.3). Under a treatment pH of 5.5, trichlorfon exposures resulted in the induction of both chromosome loss and chromosome non-disjunction as measured by fluorescence in situ hybridisation (FISH) using a pan-centromeric probe for all human centromeres and centromere probes specific for chromosomes 2, 7 and 18. At treatment concentrations greater than 20 micrograms/ml trichlorfon also induced structural chromosome damage resulting in the production of centromere negative micronuclei.

Aneuploidy↗
PubMed2002

Effect of a treatment with eprinomectin or trichlorfon on the yield and quality of milk produced by multiparous dairy cows.

The effects of a strategic antiparasitic treatment against Hypoderma species and other parasites on the milk yield, composition, and somatic cell counts of 742 multiparous dairy cattle were investigated on 79 farms in a Hypoderma species-endemic area in western Switzerland; 357 of the cows were treated with eprinomectin, 252 with trichlorfon, and 133 were left untreated. The treatments were given between October and early December 1998, on average 53 days before calving. Milk yield, fat, protein and somatic cell counts were measured once a month until the end of lactation. Eprinomectin and trichlorfon significantly increased milk yield during the first month after treatment compared with the control cows by 2.14 (P < 0.001) and 2.50 kg per day (P < 0.001), respectively. Initially, the difference between the eprinomectin- and trichlorfon-treated animals was not significant, but the effect of eprinomectin on milk yield was persistent, whereas the effect of trichlorfon decreased significantly by 0.12 kg per day per month (P < 0.05). The somatic cell counts increased significantly slower in the treated cows than in the control cows (P < 0.05). Milk composition was not affected by the treatments.

Animals↗
PubMed1984

An acute and subacute neurotoxicity assessment of trichlorfon.

The toxicity of trichlorfon (O,O-dimethyl-2,2,2,-trichloro-1-hydroxyethylphosphonate, Dipterex, Dylox), reported to elicit delayed neurotoxicity in man and chickens, was studied by administering single subcutaneous doses of 100 or 300 mg/kg to adult White Leghorn hens. At 24 h posttreatment, the birds were observed for visible signs of neurotoxicity, were euthanized, and samples of blood plasma, brain, and spinal cord (cervical and thoracic regions) were obtained for quantification of cholinesterase and neurotoxic esterase (NTE) activities. In subacute studies, hens were dosed with trichlorfon (100 mg/kg) every 72 h for a total of six doses. Seventy-two hours after the final dose the hens were euthanized, the brains, spinal cords, and distal sciatic nerves were removed for enzymatic and (or) histological examination. Parallel acute and subacute studies were conducted using diisopropyl phosphorofluoridate (DFP), a known neurotoxic agent, at subcutaneous dosages of 1.0 mg/kg. In the acute studies, both DFP and trichlorfon markedly inhibited tissue cholinesterase activities but only DFP elicited a significant inhibition of NTE. In the subacute studies, DFP produced a characteristic central-peripheral distal axonopathy in the 18-day period of study which was confirmed by clinical and morphological evidence and by marked inhibition of neuronal NTE. Trichlorfon caused little or no obvious neurotoxicity, an observation that was supported by minimal morphological changes and impairment of walking ability and no inhibition of brain or spinal cord NTE.

Animals↗
PubMed1991

Utilization of dichlorvos and trichlorfon in salmonid farming in Norway during 1981-1988.

The main objectives of this investigation were to quantify the use of dichlorvos and trichlorfon in the treatment of salmon lice infestations, to evaluate the prescribing of these drugs, and to estimate possible changes in the salmon lice problem by use of drug statistics. This study has shown that the use of trichlorfon increased from 4.9 tons in 1981 to 28.3 tons in 1985. This figure declined to 3.2 tons in 1988. The use of dichlorvos increased from 0.3 tons in 1986 to 3.2 tons in 1988. The change in the prescribing from trichlorfon to dichlorvos has dramatically reduced the pollution caused by these substances in the marine environment. Moreover, if necessary safety rules are observed, this change reduces the exposure of the workers on fish farms to these drugs, and also reduces the possibilities of intoxications of the fish during the treatment procedure. The sales figures of dichlorvos and trichlorfon, related to the calculated biomass of farmed salmonids in the sea, indicate a dramatic increase in the salmon lice problem.

Agriculture↗
PubMed1989

Cardiovascular effects recorded in horses during anaesthesia after treatment with trichlorfon.

Five horses were anaesthetised twice with thiopentone sodium, guaifenesin and halothane. The second anaesthesia was 16 days after the first and two days following oral administration of trichlorfon. Heart rate, carotid arterial, pulmonary arterial and right atrial pressures, cardiac output and blood temperature were measured every 15 minutes for 120 minutes. Heart rate, carotid arterial pressure and cardiac output were similar on both occasions. Pulmonary arterial and right atrial pressures were highest during anaesthesia after treatment with trichlorfon when compared with values obtained before treatment. Pulmonary vascular resistance was significantly decreased at four measurement times during anaesthesia after treatment with trichlorfon. All cardiovascular measurements were within ranges accepted as normal for halothane anaesthesia in horses. In a second experiment, four ponies were anaesthetised with xylazine and ketamine on two occasions one week apart. Two ponies received trichlorfon two days before the second anaesthesia. Heart rate, arterial pressure and respiratory rate recorded during anaesthesia were not different in ponies after organophosphate treatment. The time to standing after the second anaesthesia was significantly increased in all ponies.

Anesthesia, General↗
PubMed2002

A case of fatal trichlorfon and methidathion poisoning.

A 50-year-old man, suspected of ingesting organophosphorus insecticides, was found dead in a graveyard. In the gas chromatography-mass spectrometric screening, trichlorfon and methidathion were detected in his gastric contents. The quantitative analysis for trichlorfon and methidathion was carried out by high-performance liquid chromatography. The concentrations (microg/ml or microg/g) of trichlorfon and methidathion were 409 and 1.9 in the heart blood, 281 and 0.4 in the femoral vein blood, 430 and 5.8 in the cerebrum, 385 and 5.1 in the brain stem, 256 and 2.8 in the right apex of lung, 449 and 15.1 in the left basal of lung, 856 and 131.0 in the liver, 460 and 1.6 in the right kidney, 390 and 1.9 in the left kidney, 524 and 3.4 in the spleen, 152 and 0.6 in the thigh muscle, 207 and 0.9 in the urine, 20,000 and 19,400 in the gastric contents, respectively. According to the autopsy finding and toxicological analysis, the cause of death was judged to be acute trichlorfon and methidathion poisoning.

Journal Article↗
PubMed1982

Activity of organophosphorus insecticides in bacterial tests for mutagenicity and DNA repair--direct alkylation vs. metabolic activation and breakdown. I. Butonate, vinylbutonate, trichlorfon, dichlorvos, demethyl dichlorvos and demethyl vinylbutonate.

The following organophosphates were tested for their ability to induce DNA damage in a rec-type repair test with Proteus mirabilis strains PG713 (rec- hcr-) and PG273 (wild type) and point mutations in his- strain TA100 of Salmonella typhimurium--butonate: O,O-dimethyl-(1-n-butyryloxy-2,2,2-trichloroethyl)-phosphonate; vinylbutonate: O,O-dimethyl-(n-butyryloxy-2,2-dichlorovinyl)-phosphonate; trichlorfon: O,O-dimethyl-(1-hydroxy-2,2,2-trichloroethyl)-phosphonate; dichlorvos: O,O-dimethyl-O-(2,2-dichlorovinyl)-phosphate; the demethylated derivatives--demethyldichlorvos: O-methyl-O-(2,2-dichlorovinyl)-phosphoric acid; demethyl vinylbutonate: O-methyl-(1-n-butyryloxy-2,2-dichlorovinyl)phosphonic acid. Of the six compounds tested, dichlorvos and trichlorfon induced base pair substitutions and DNA damage. No mutagenicity and DNA damage were found in experiments with butonate, vinylbutonate, demethyl vinylbutonate and demethyl dichlorvos. Genotoxic activity for dichlorvos and the absence of both mutagenic and RNA damaging properties for its non-alkylating demethyl derivative favors the hypothesis that alkylation of DNA is the essential step for mutation induction by this organophosphate. Furthermore, the absence of genetic effects after treatment with vinylbutonate and demethyl dichlorvos does not support a crucial role of vinyl or allyl groups in side chains of organophosphates for genetic activity. Microsomal enzymes decreased genetic activity of dichlorvos and trichlorfon in vitro. No evidence for a role of metabolic activation in the mutagenic activity of any of these compounds was found.

Alkylating Agents↗
PubMed2002

Organophosphate induced delayed neuropathy in genetically dissimilar chickens: studies with tri-ortho-cresyl phosphate (TOCP) and trichlorfon.

Measurements of plasma cholinesterase (pl.ChE), brain cholinesterase (Br.ChE) and brain Neuropathy Target Esterase (Br.NTE) were made in three different lineages of chickens. All birds received toxicants through gavage in a single oral dose between 08:00 and 09:00 h, after overnight fast. Babcock chickens were treated with 800 mg/kg tri-ortho-cresyl phosphate (TOCP) or 80 mg/kg trichlorfon. The TOCP group had 82% Br.NTE inhibition, when compared to the control group, and no birds displayed symptoms of clinical organophosphate-induced delayed neuropathy (OPIDN). Hy-line w36 lineage chickens were given 1600 mg/kg TOCP and despite this higher dose, Br.NTE inhibition was similar that presented by Babcock chickens. Isabrown chickens were given 1600 mg/kg TOCP or 80 mg/kg trichlorfon. At 36 h all trichlorfon treated birds had from 80 to 90% inhibition of Pl.ChE and Br.ChE, when compared to controls. However, Br.NTE was inhibited less than 20%, and there were no clinical signs of OPIDN. All TOCP treated isabrown chickens had more than 80% Br.NTE inhibition while one of them exhibited just light signs of OPIDN, two chickens became totally paralyzed. This finding suggested that chicken strain was important in the appearance of OPIDN. In addition, 70-80% of NTE inhibition was necessary but was not sufficient to produce OPIDN in chickens, since babcock and hy-line w36 chickens exhibited NTE inhibition in the range of 70-80% without clinical signs of OPIDN.

Animals↗
PubMed1991

Mutagenic evaluation of trichlorfon using different assay methods with Salmonella typhimurium.

Evaluation of the mutagenicity of trichlorfon pesticide was carried out with strains TA1535, TA100, TA97, TA98 and TA104 of Salmonella typhimurium by means of several assay methods: (i) spot test; (ii) standard plate incorporation test; (iii) plate incorporation test with preincubation; (iv) fluctuation test and (v) fluctuation test with preincubation, with and without post-mitochondrial liver fraction (S9) from Wistar rats pretreated with phenobarbital and 5,6-benzoflavone as a metabolic activation system. Trichlorfon induced base-pair substitution mutations, and its mutagenic activity was decreased by the addition of S9 mix. The fluctuation test and fluctuation test with preincubation were the most sensitive assay methods for detecting the mutagenicity of trichlorfon.

Animals↗
PubMed1986

Efficacy of an oxibendazole-trichlorfon paste formulation against third stage larvae of Gasterophilus intestinalis and its safety in horses.

A paste formulation containing 14.3 per cent of oxibendazole and 44 per cent of trichlorfon was administered to 33 ponies and horses. The dose rate used was equivalent to 10 mg and 30 mg/kg bodyweight, of oxibendazole and trichlorfon respectively. After treatment 25 animals passed between one and 82 third stage larvae of Gasterophilus intestinalis in their faeces. Dosing with 0.2 mg ivermectin/kg bodyweight three weeks later resulted in six animals expelling between one and four bots. The efficacy of the oxibendazole-trichlorfon paste was on average 96.2 per cent. This drug combination given to 52 ponies and horses at the indicated dose rate and to six ponies at twice that dose was tolerated without side effects except transient softening of the faeces in several animals and mild symptoms of colic in two horses.

Administration, Oral↗
PubMed1992

The effects of iodinated glycerol, trichlorfon, and acetaminophen on tumor progression in a Fischer rat leukemia transplant model.

Sixty-day bioassays of iodinated glycerol, trichlorfon, and acetaminophen were conducted using a leukemia transplant model in 6- to 8-week-old F344 rats to investigate the potential of these chemicals to affect tumor progression. The chemicals were administered in the drinking water at doses that approximated those used in previously conducted 2-year carcinogenesis studies. Simultaneous with dose administration, half of a group of young, healthy, syngeneic rats were given subcutaneous transplants of mononuclear cells derived from spleens of leukemic donors. Variables used to quantitate tumor progression included body weight, spleen weight, white blood cell (WBC) and red blood cell (RBC) counts, packed cell volume, hemoglobin concentration, and platelet counts. Iodinated glycerol at 1.25 or 2.5 mg/ml caused a greater increase in leukocytosis in dosed transplant recipients in comparison to that experienced by undosed recipients: trichlorfon at 2.5 or 5.0 mg/ml enhanced splenomegaly and induced greater reductions in RBC parameters in dosed recipients in comparison to that experienced by undosed recipients. Acetaminophen at 3.0 and 6.0 mg/ml resulted in insignificant but dose-related increases in spleen weight and leukocytosis only in the female rat transplant recipients, as was observed in 2-year studies. Based on results from the short-term leukemia transplant model, data from 2-year carcinogenicity studies, and structure-activity considerations, exposure to iodinated glycerol and trichlorfon was more strongly associated with the expression of leukemia than exposure to acetaminophen. The potential carcinogenicity of each of these chemicals should be taken into consideration when calculating estimates of risk and decisions for their use.

Acetaminophen↗
PubMedDate not supplied

Direct gas chromatographic analysis of trichlorfon for its decomposition products.

The analysis of trichlorfon by direct gas chromatography is discussed. A procedure is described for the determination of impurities in trichlorfon by using a fused silica capillary column and cold on-column injection. Attempts at quantitating trichlorfon using this system were unsuccessful due to problems with irreproducibility of the peak area. Although no derivatization was performed, there was no decomposition of the analyte as confirmed by mass spectrometry.

Chromatography, Gas↗
PubMed1978

Critical tests of the anthelmintic febantel in the horse: activity of a paste formulation alone or with a trichlorfon paste.

Critical tests were carried out in 10 horses to evaluate the antiparasitic activity of febantel given alone or with trichlorfon. Paste formulations were administered intraorally at dose levels of 6 mg of febantel (active ingredient)/kg and 35 mg of trichlorfon (active ingredient)/kg. In 5 tests with febantel alone, removal of 100% was recorded for mature or immature Parascaris equorum from 2 infected horses. Strongylus vulgaris from 4 infected horses, S edentatus from 5 infected horses, and mature Oxyuris equi from 1 infected horse; and removal of 96% was recorded for small strogyles from 1 horse tested, and bots in 5 infected horses were not affected. In 5 horses treated with both compounds, removal of 100% was recorded for mature P equorum from 2 infected horses, immature P equorum from 1 infected horse, S vulgaris from 5 infected horses, Sedentatus from 5 infected horses, mature O equi from 2 infected horses, immature O equi from 1 horse tested, 2nd Gasterophilus intestin-equi from 1 infected horse, 2nd-instar C nasalis from 1 infected horse, and 3rd-instar C nasalis from 4 infected horses. Removal of 98% was recorded for small strongyles from 1 horse tested, and removal of 65% to 100% for 3rd-instar C intestinalis from 5 infected horses. In the aggregate, removal of 3rd-instar C intestinalis was 99%. Untoward effects of treatment were quite limited. Only a transient softening of feces in 1 of 5 horses given the trichlorfon paste plus the febantel paste was recorded.

Acetanilides↗
PubMed1981

Membrane-bound and soluble esterase activities in various hen brain regions after diisopropyl phosphorofluoridate and trichlorfon treatment.

Acetylcholinesterase, neurotoxic esterase, and nonspecific esterase activities were studied in subcellular fractions obtained from homogenates of forebrain, cerebellum, and brainstem areas of hen brain. The hens were given a single, oral dose (1.0 mg/kg of Dyflos (diisopropyl phosphorofluoridate) or 100 mg/kg of trichlorfon (dimethyl -2,2,2-trichloro-1-hydroxyethylphosphonate). The animals were killed 24 hr after dosing. The level of neurotoxic esterase and soluble nonspecific esterase activities were consistent from region to region; however, acetylcholinesterase activity among the brain regions varied significantly. Both organophosphorus compounds produced definite inhibition of acetylcholinesterase. The cerebellar acetylcholinesterase activity was the most susceptible to organophosphorus ester-induced inhibition. A marked inhibition of neurotoxic esterase (70-80%) was produced by diisopropyl phosphorofluoridate in all areas. Trichlorfon produced little or no inhibition of neurotoxic esterase (0-10%). Little variation in soluble nonspecific esterase activity (alpha -naphthyl acetate) was noted between the three brain regions studied. Both diisopropyl phosphorofluoridate and trichlorfon failed to significantly alter soluble nonspecific esterase activity among the brain regions.

Acetylcholinesterase↗
PubMed1980

[Use of trichlorfon as an anthelmintic in horses (author's transl)].

The use of trichlorfon as an anthelmintic in horses has increased since it was combined with mebendazole and febantel, and became commercially available as Telmin-trichlorfon and Rintal-plus respectively. Field studies showed that these combined preparations frequently gave rise to cases of poisoning. Mild to severe colic was observed up to six hours after treatment, diarrhoea and/or anorexia continuing to be present for one to six days after administration. The 'horse weight measurer' introduced by Janssen Pharmaceutica is not sufficiently accurate to prevent overdosage. It is advisable only to use trichlorfon when the body weight can be estimated by a reliable method.

Animals↗
PubMed1983

Activity of organophosphorus insecticides in bacterial tests for mutagenicity and DNA repair--direct alkylation versus metabolic activation and breakdown. II. O,O-dimethyl-O-(1,2-dibromo-2,2-dichloroethyl)-phosphate and two O-ether derivatives of trichlorfon.

The following organophosphates were tested for their ability to induce DNA damage in a rec-type repair test with Proteus mirabilis strains PG713 (rec- hcr-) and PG273 (wild-type) and point mutations in the his- strain TA100 of Salmonella typhimurium: O,O-dimethyl-O-(1,2-dibromo-2,2-dichloroethyl)-phosphate (NALED); trichlorfon-O-methyl ether (TCP-O-ME), O,O-dimethyl-(1-methoxy-2,2,2-trichlorethyl)-phosphonate; trichlorfon-O-methyl ether vinyl derivative (TCP-O-MEVD), O,O-dimethyl-(1-methoxy-2,2-dichlorovinyl)-phosphonate. All compounds were negative in the repair test but induced base pair substitutions in S. typhimurium. The mutagenicity of NALED is due to the direct alkylating ability of the parental molecule and to mutagenic metabolites generated by enzymatic splitting of the side chain. Glutathion-dependent enzymes in the S9-mix eliminate the mutagenic activity of NALED completely. Mutation induction by TCP-O-ME and TCP-O-MEVD is predominantly caused by the reactive O-methyl ether configuration of the side chain and is resistant to metabolic inactivation by NADPH- or glutathion-dependent enzymatic pathways in the S9-mix of mice.

Animals↗
PubMed1992

Hepatotoxicity of trichlorfon and dichlorvos in isolated rat hepatocytes.

Hepatotoxicity of organophosphorus insecticides, trichlorofon and dichlorvos, a dechlorinated form of the former, was examined in isolated hepatocytes from untreated control and phenobarbital-pretreated (80 mg/kg, i.p., for 3 days) rats. These compounds produced toxic effects on hepatocytes as evidenced by malondialdehyde production and lactate dehydrogenase leakage in a dose-dependent manner up to the concentration of 2 mM, dichlorvos being more toxic than trichlorfon. Hepatocytes from phenobarbital-pretreated rats were more sensitive to these organophosphates than those from control rats. Dichloroacetaldehyde and dichloroacetic acid, metabolites of dichlorvos, did not injure hepatocytes. The toxic effects of dichlorvos on hepatocytes were enhanced by increasing oxygen concentration during the incubation, or by addition of glycolytic substrates (pyruvate, lactate or fructose) to the incubation mixtures. On the other hand, addition of antioxidants (diethyldithiocarbamate or N,N'-diphenyl-p-phenylenediamine), or cytochrome P-450 inhibitors (SKF-525A or metyrapone) to the incubation mixtures attenuated malondialdehyde production caused by dichlorvos and protected cells from death. Addition of dichlorvos to the incubation mixtures of hepatic microsomes stimulated lipid peroxidation in the presence of NADPH, which was inhibited by further addition of superoxide dismutase but not catalase. These results suggest that hepatotoxicity of trichlorfon and dichlorvos are related to their peroxidative property in microsomes which is accelerated by oxygen.

Animals↗
PubMed1984

Critical tests of morantel-trichlorfon paste formulation against internal parasites of the horse.

Critical tests were completed on six horses to evaluate the antiparasitic activity of a paste formulation mixture of morantel citrate and trichlorfon, administered intraorally at the dose rate of 6 mg morantel base kg-1 and trichlorfon at 30 mg kg-1. Aggregate average removals were: 78% for two horses infected with 2nd instar Gasterophilus intestinalis; 100% for one infected with 2nd instar G. nasalis; 96% for six infected with 3rd instar G. intestinalis; 100% for four infected with 3rd instar G. nasalis; 100% for five infected with Parascaris equorum; 100% for one infected with mature Oxyuris equi; 100% for five infected with Strongylus vulgaris; 72% for five infected with S. edentatus; and partial removal (25%) of Anoplocephala perfoliata infection from one infected animal. Pre- and post-treatment EPG and LPG data indicated a reduction of 97% of the mature small strongyle infections. Evidence of toxicosis was not observed in any of the horses.

Animals↗