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At least 109 records · Page 6Linked to original sources
PubMed1988

The bradycardic and mydriatic effects of chlordimeform and its demethylated analogs in the rat: antagonism by idazoxan but not by prazosin.

Pupillary and cardiac responses to i.v. injections of chlordimeform (CDM, 0.3-10 mg/kg), a formamidine insecticide, and its metabolites demethylchlordimeform (DCDM, 0.03-1 mg/kg) and didemethylchlordimeform (DDCDM, 0.1-3 mg/kg) were studied in rats anesthetized with pentobarbital. Both CDM and DCDM induced a dose-dependent mydriasis and bradycardia and DCDM was 10 times more potent than CDM in causing these effects. In contrast, DDCDM did not induce a mydriasis or bradycardia. The alpha 2-adrenoreceptor antagonist, idazoxan (0.2 mg/kg, i.v.) abolished or reduced CDM- and DCDM-induced mydriasis and bradycardia, whereas the alpha 1-adrenoreceptor antagonist, prazosin (1.5 mg/kg, i.v.) did not change these effects of CDM and DCDM. SKF 525-A (50 mg/kg, i.p.), an inhibitor of enzymatic demethylation, administered 10 min before the first dose of CDM, failed to reduce the effects of CDM. The results suggested: 1) the mydriatic and bradycardic effects of CDM and DCDM are mediated by alpha 2-adrenoreceptors, 2) the monodemethylation of CDM increases its alpha 2-adrenoreceptor agonistic activities, but the didemethylation of CDM abolishes these activities, and 3) CDM can exert alpha 2-adrenoreceptor agonistic activities without undergoing a demethylation process.

Amidines↗
PubMed1996

Genotoxicity of 4-chloro-o-toluidine in Salmonella typhimurium, human lymphocytes and V79 cells.

In the absence of a metabolizing system (S9 mix) 4-chloro-o-toluidine (4-COT) was found to be ineffective in a combination of assays for gene mutations in Salmonella typhimurium, for chromosome aberrations and sister chromatide exchanges in human lymphocytes, and for the induction of spindle disturbances in V79 Chinese hamster cells. In the presence of S9, 4-COT was also ineffective in producing structural or numerical changes in mammalian cells, but the yields of 4-COT induced revertants in S. typhimurium strains TA 100 and TA 98 were about 2-fold higher than those in controls.

Animals↗
PubMed1998

Identification of the binding site for a low-molecular-weight inhibitor of plasminogen activator inhibitor type 1 by site-directed mutagenesis.

A novel low-molecular-weight inhibitor, AR-H029953XX, was developed from a known fibrinolytic compound, flufenamic acid, which prevented complex formation of human plasminogen activator inhibitor type 1 (PAI-1) with tissue plasminogen activator (tPA) by inhibition of PAI-1. To explore the binding site for AR-H029953XX, mutants of human PAI-1 were constructed by site-directed mutagenesis and were then expressed in CHO cells, purified, activated, and characterized. (1) PAI-1 with mutations in the reactive center loop: L1-PAI-1 (P10, Ser337Glu) had stability and activity similar to those of wild-type PAI-1 (wt-PAI-1), and L2-PAI-1 (P12, Ala335Glu) was highly stable but was a substrate for tPA. (2) PAI-1 with mutations near the binding epitope for the strongly inhibiting monoclonal antibody CLB-2C8: C1-PAI-1 (Phe114Glu), C2-PAI-1 (Val121Phe), C3-PAI-1 (Arg76Glu/Arg115Glu/Arg118Glu), and C4-PAI-1 (Arg115Glu) were all comparable in activity and stability to wt-PAI-1. AR-H029953XX (Ki = 25 microM) prevented complex formation between tPA and active wt-PAI-1 as well as that with mutants L1-, L2-, C1-, C2-, and C4-PAI-1. AR-H029953XX also inhibited binding of these PAI-1 variants to the antibody CLB-2C8, as measured by surface plasmon resonance. In contrast, AR-H029953XX had almost no inhibitory effect on the complex formation of tPA with C3-PAI-1. Moreover, AR-H029953XX had no effect on the binding rate of CLB-2C8 to C3-PAI-1, or on the binding to latent PAI-1 or to cleaved L2-PAI-1. The binding site of AR-H029953XX thus appears to be located in the neighborhood of the postulated epitope for CLB-2C8, near residues Arg76 and/or Arg118. This specific domain of the PAI-1 molecule might thus also be important for the mechanism of inhibitory activity toward tPA. Moreover, the structure of this region in active PAI-1 has to be different from the corresponding regions in latent and cleaved PAI-1.

Animals↗
PubMed1980

Action of formamidine pesticides on octopamine receptors.

The formamidines are a structurally novel group of pesticides of growing importance in the control of mites, cattle ticks and certain orders of insects which have become resistant to conventional acaricides and insecticides. Their mode of action is complex with dose-dependent lethal and subletahal effects. At sublethal levels they cause behavioural changes in the target pest species (for example in feeding and in mating behaviours), changes which are responsible for the protective effects on crops and livestock. Although many suggestions have been made for the underlying biochemical mechanism, including inhibition of monoamine oxidase activity, uncoupling of respiration and blockade of neuromuscular transmission, no direct evidence has been presented. Another possibility is interaction with octopamine receptors in the central nervous system. We report here that the formamidine acaricide/insecticide, chlordimeform (CDM), and its demethylated deivative can mimic the actions of octopamine at the locust neuromuscular junctions. This gives the clearest evidence to date of the site of action of the formamidines and indicates a novel mode of action for these pesticides.

Amidines↗
PubMed1991

[Acute hemorrhagic cystitis following chlordimeform poisoning ].

A 19-year-old and a 50-year-old man who together had cleaned a water-tank as part of their duties in a tank protection and cleaning firm developed that same evening lower abdominal pain, dysuria and haematuria. Cystoscopy revealed haemorrhagic cystitis in both patients, a finding confirmed by bladder mucosa biopsy. 4-chlor-2 methylaniline (concentration less than 1 mg/l) was found in hydrolysed serum of both. This metabolite of the pesticide chlordimeform was also found in the urine of the 51-year-old patient (16 mg/l). The haematuria regressed within two days of the patients having increased their fluid intake. Dysuria improved within a week. It is likely that chlordimeform had previously been transported in the water-tank. In case of haemorrhagic cystitis possibly caused by occupational or other poisoning, serum and urine should always be obtained for toxicological tests.

Acute Disease↗
PubMed1976

Multiple infection with Toxocara canis. Influence of antihistamines and corticosteroids on the histopathological response.

The histopathology of the tissues of mice infected with ten doses of 100 embryonated eggs of Toxocara canis and the influence of antihistamines and corticosteroids on these findings is described. The main lesions were confined to the liver and lungs. In infected but untreated control mice hepatic lesions consisted of periportal infiltrates, widespread foci of liver cell necrosis and polymorphonuclear and mononuclear accumulation and a few fibrotic granulomata. Treatment with antihistamines did not change these findings significantly, but corticosteroids decreased the amount of cellular infiltration and the size of the lesions. Pulmonary lesions consisted mostly of confluent infiltrates of polymorphonuclears, eosinophils and mononuclear cells with some macrophage proliferation. Neither drug seemed to affect the lung involvement.

Amidines↗
PubMed1980

Human health effects of selected pesticides, chloroaniline derivatives.

The health effects of two pesticides, chlordimeform and propanil, are discussed. Chlordimeform and 2-methyl-4-chloroaniline, a major metabolite of chlordimeform, cause severe hemorrhagic cystitis in humans. In cats, however, only a mild effect on the bladder was noted. The herbicide propanil has produced chloracne in humans, and along with 3,4-dichloroaniline, hyperkeratosis in rabbits. The contaminants 3,4,3',4'-tetrachloroazobenzene and 3,4,3',4'-tetrachloroazoxybenzene are responsible for the chloracnegenic characteristics of propanil, 3,4-dichloroaniline, and methazole.

Acne Vulgaris↗
PubMed1984

Evaluation of chlordimeform and degradation products for mutagenic and DNA-damaging activity in Salmonella typhimurium and Escherichia coli.

The mutagenic activity of chlordimeform and two of its breakdown products, 4-chloro-o-toludine and 4-chloro-N-formyl-o-toluidine were determined with five histidine dependent strains of Salmonella typhimurium (TA1535, TA1537, TA1538, TA98, TA100) and five tryptophan dependent strains of E. coli WP2 (WP2, WP2uvrA, WP67, CM611, CM571) with and without rat liver microsomal enzymes. 4-chloro-o-toluidine increased the number of the reversions of the S. typhimurium strain TA1535 more than two fold over spontaneous at the concentration of 400 micrograms/plate. The results of the DNA repair tests in the Salmonella TA1538/TA1978 and E. coli multirepair deficient systems showed that both breakdown products were active in inducing damage not repaired in at least one repair deficient strain while chlordimeform itself was inactive.

Amidines↗
PubMed1977

Lack of involvement of monoamine oxidase inhibition in the lethality of acute poisoning by chlordimeform.

Depletion of serotonin or norepinephrine in male rats by pretreatment with p-chlorophenylalanine or DL-alpha-methyl-p-tyrosine, respectively, failed to reduce the lethality of the monoamine oxidase-inhibiting acaricide, chlordimeform. Administration of phenylephrine, a directly acting alpha-adrenergic agonist, with chlordimeform did not increase the lethality of chlordimeform. Thus, monoamine oxidase inhibition by chlordimeform does not seem to contribute to its lethality.

Amidines↗
PubMed1984

The effects of dieldrin and chlordimeform on learning and memory in the cockroach, Periplaneta americana: a study in behavioral toxicology.

A one-session T-maze training procedure for cockroaches in which animals were trained to turn right or left to avoid a shock was utilized to investigate the effects of dieldrin and chlordimeform (two neurotoxic pesticides) on learning and memory. These animals were trained and then tested for retention 5 h later. Three behavioral measures were recorded: choice behavior or direction turned, the time taken to proceed down the runway (runway time), and the time taken to proceed from the runway to either choice arm (choice point time). In control animals the number of correct choices, the runway time, and the choice point time increased with succeeding trials during training. Furthermore, control animals showed retention of correct choice behavior from training to testing. A nontoxic dose (no overt behavioral signs) of dieldrin was injected 2 h before training or 15 min after training. Pretraining injections of dieldrin eliminated correct-choice learning but did not alter the increase with training in runway or choice point times. Posttraining dieldrin administration did not interfere with retention of correct-choice behavior upon testing. These findings indicate that dieldrin induces behavioral alterations in a low acute dose and that detrimental effects are more likely with more complex behavior. Furthermore, behavioral disruption is more likely the closer exposure is to the initial learning of a task. Nontoxic doses of chlordimeform injected 1 h before training eliminated correct-choice learning and facilitated an increase in runway times during training.

Amidines↗
PubMed1985

Suppression of the antibody response by a formamidine pesticide: dependence on the route of exposure.

These studies investigated the effects of exposure to chlordimeform (CDM), a formamidine pesticide, on selected in vivo immune parameters in the random bred CD-1 mouse. Further studies were done on the effects of this compound on the in vitro PFC response in C57BL/6 mice. Acute and 14-d exposure to CDM via the i.p. route resulted in a decrease in IgM antibody-forming (plaque-forming) cells (PFC) directed at the sheep red blood cell (sRBC) antigen when measured 4 d after i.p. immunization. This suppression was seen at doses as low as 20 mg/kg . d for 14 d. These same doses of CDM did not result in any alteration of cell-mediated immunity as measured by the delayed hypersensitivity response (DHR) to both keyhole limpet hemocyanin (KLH) and sRBC. Lymphocyte blastogenesis was increased in spleen cells from mice exposed to 40 mg/kg . d CDM in response to media alone, concanavalin A (Con A), and lipopolysaccharide (LPS). The in vitro PFC response by C57BL/6 mice was utilized to determine if CDM could suppress the antibody response due to a direct effect on the immune cells. CDM suppressed the in vitro PFC response only at concentrations that were directly cytolytic. A direct cytolytic effect was considered unlikely following exposure in the whole animal, since the suppression of the antibody response occurred in the absence of any effects on spleen cell number or spleen weight. To determine if route of exposure was a factor in the suppressive effects of CDM, 14-d studies were conducted administering CDM orally at doses up to 120 mg/kg . d. Both the CD-1 and C57BL/6 mouse were used to verify that a strain difference was not a factor. There was no effect on either the d 4 or d 5 antibody response, even though 43% of the mice exposed to 120 mg/kg died from the acute toxicity that can characterize this chemical. From an operational standpoint, these results indicate that the route of exposure of a compound relative to the route of administration of an antigen is an important consideration when determining the effects of that compound on an immune response. From an environmental standpoint, these results indicate that relatively high doses of chlordimeform do not result in consistent immunotoxicity as determined by the assays utilized.

Administration, Oral↗