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At least 811 records · Page 45Linked to original sources
PubMed2006

Intensive insecticide spraying for fly control after mass antibiotic treatment for trachoma in a hyperendemic setting: a randomised trial.

BACKGROUND: There are no data on the cumulative effect of fly control and antibiotic distribution on trachoma in hyperendemic communities. We sought to determine whether insecticide spray intervention after mass antibiotic treatment could reduce trachoma and ocular infection with Chlamydia trachomatis in hyperendemic neighbourhoods in Tanzania. METHODS: We did a single-blind, randomised clinical trial in 16 neighbourhoods (balozi) in Kongwa, Tanzania. All children aged 1-7 years were enrolled, with 119 children in the eight balozi of the intervention group and 183 in the eight control balozi. Children were examined at baseline, 6 months, and 1 year for clinical trachoma and ocular C trachomatis infection. One dose of azithromycin was offered to all residents of both intervention and control balozi after the baseline survey. Households (and surrounding areas) in the intervention group were then sprayed with insecticide throughout the ensuing year and monitored for reductions in fly counts. This study is registered at ClinicalTrials.gov, number NCT00347763. FINDINGS: The intervention balozi had significantly lower fly counts than controls at all monitored weeks (p<0.05), apart from weeks 7-9. The trachoma rate did not differ significantly in the intervention and control balozi at 6 months post-treatment (20%vs 33%, p=0.07), nor did it at 1 year (43%vs 44%, p=0.90). Infection with C trachomatis did not differ between groups at 6 months post-treatment (9%vs 7%, p=0.45). INTERPRETATION: Intensive insecticide spraying reduced flies in the environment, but our results suggest that fly reduction after mass antibiotic treatment has no added benefit on reduction of trachoma.

Anti-Bacterial Agents↗
PubMed2002

Effects of pyrethroid insecticides and estrogen on WNT10B proto-oncogene expression.

Breast cancer is a serious illness affecting approximately one in nine women in the United States. Although an actual cause for breast cancer is unknown, genetic and environmental factors have been associated with its onset. Elevated levels of estrogen and heightened expression of the WNT10B proto-oncogene have been implicated in the development of human malignant breast tumors because they enhance the proliferation of mammary tissue. Two pyrethroid insecticides, sumithrin and fenvalerate, have been shown to mimic estrogenic activity in MCF-7 human breast carcinoma cells by inducing pS2 expression whereas two other pyrethroids, permethrin and d-trans allethrin do not have the same capability. To investigate if estrogen and these four pyrethroid insecticides could affect the expression of a gene related to mammary gland development, WNT10B expression in pyrethroid-treated MCF-7 cells was examined. MCF-7 cells under normal growth conditions do not express WNT10B. Reverse-transcriptase polymerase chain reaction (RT-PCR), nested PCR and Southern hybridization were employed to detect WNT10B expression. As controls, cells were treated with either ethanol, corn oil, or Vista LPA solvent. When compared to the solvent-treated controls, sumithrin, fenvalerate and estrogen treated MCF-7 cells all had increased levels of WNT10B expression. The non-estrogenic pyrethroids, d-trans allethrin and permethrin, demonstrated a similar elevation of WNT10B expression at a lower concentration, but not at the higher concentration. The results suggest that pyrethroid insecticides and estrogen can enhance the expression of the WNT10B proto-oncogene. However, since both the estrogenic and non-estrogenic substances amplified Wnt10B expression, the mechanism likely involves multiple distinct pathways.

Breast Neoplasms↗
PubMed2001

Striatal dopaminergic pathways as a target for the insecticides permethrin and chlorpyrifos.

Because insecticide exposure has been linked to both Parkinsons disease and Gulf War illness, the neurotoxic actions of pyrethroid and organophosphate insecticides on behavior and striatal dopaminergic pathways were investigated in C57BL/6 mice treated with permethrin (three i.p. doses at 0.2-200 mg/kg) or chlorpyrifos (three s.c. doses at 25-100 mg/kg) over a 2-week period. Permethrin altered maximal [3H]dopamine uptake in striatal synaptosomes from treated mice, with changes in Vmax displaying a bell-shaped curve. Uptake was increased to 134% of control at a dose of 1.5 mg/kg. At higher doses of PM (25 mg/kg), dopamine uptake declined to a level significantly below that of control (50% of control at 200 mg/kg, P < 0.01). We also observed a small, but statistically significant decrease in [3H]dopamine uptake by chlorpyrifos, when given at a dose of 100 mg/kg. There was no significant effect on the Km for dopamine transport. Evidence of cell stress was observed in measures of mitochondrialfunction, which were reduced in mice given high-end doses of chlorpyrifos and permethrin. Although cytotoxicity was not reflected in decreased levels of striatal dopamine in either 200 mg/kg PM or 100 mg/kg CPF treatment groups, an increase in dopamine turnover at 100 mg/kg CPF was indicated by a significant increase in titers of the dopamine metabolite, 3,4-dihydroxyphenylacetic acid. Both permethrin and chlorpyrifos caused a decrease in open field behavior at the highest doses tested. Although frank Parkinsonism was not observed, these findings confirm that dopaminergic neurotransmission is affected by exposure to pyrethroid and organophosphorus insecticides, and may contribute to the overall spectrum of neurotoxicity caused by these compounds.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2001

Point mutations in homology domain II modify the sensitivity of rat Nav1.8 sodium channels to the pyrethroid insecticide cismethrin.

Two point mutations in homology domain II of the housefly Vsscl voltage-sensitive sodium channel subunit, M918T and L1014F are associated with resistance to pyrethroid insecticides and reduce the pyrethroid sensitivity of Vsscl sodium channels expressed in Xenopus laevis oocytes. To assess the impact of these residues as determinants of pyrethroid sensitivity in another sequence context, we mutated the corresponding positions of the rat pyrethroid-sensitive, TTX-resistant peripheral nerve sodium channel (rNav1.8; also called SNS or PN3) and determined the sensitivity of native and mutated channels expressed in Xenopus oocytes to the pyrethroid insecticide cismethrin. The rNav1.8 channel, like other vertebrate sodium channel isoforms, contains a conserved isoleucine residue at sequence position 780 that aligns with the conserved methionine at position 918 of Vsscl and other insect sodium channels. Channels mutated to contain methionine at position 780 (1780M) exhibited enhanced sensitivity to cismethrin and larger decay constants for pyrethroid-modified channel states. In contrast, the mutation corresponding to M918Tin the Vssc1 channel (1780T) profoundly decreased the cismethrin sensitivity of expressed channels. Insertion of the mutation corresponding to L1014F (L879F in rNav1.8) reduced the cismethrin sensitivity of channels having either isoleucine or methionine at position 780, whereas channels containing the 1780T/L879F double mutation were insensitive to this insecticide. Mutations at Ile780 and Leu879 also modified the voltage dependence of rNav1.8 channels, but these effects were not related to changes in pyrethroid sensitivity. These results confirm the importance of residues in homology domain II as fundamental determinants of the pyrethroid sensitivity of sodium channels.

Animals↗
PubMed2003

Voltage-dependent block of sodium channels in mammalian neurons by the oxadiazine insecticide indoxacarb and its metabolite DCJW.

Indoxacarb is a newly developed insecticide with high insecticidal activity and low toxicity to non-target organisms. Its metabolite, DCJW, is known to block compound action potentials in insect nerves and to inhibit sodium currents in cultured insect neurons. However, little is known about the effects of these compounds on the sodium channels of mammalian neurons. We compared the effects of indoxacarb and DCJW on tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) sodium channels in rat dorsal root ganglion neurons by using the whole-cell patch clamp technique. Indoxacarb and DCJW at 1-10 microM slowly and irreversibly blocked both TTX-S and TTX-R sodium channels in a voltage-dependent manner. The sodium channel activation kinetics were not significantly modified by 1 microM indoxacarb or 1 microM DCJW. The steady-state fast and slow inactivation curves were shifted in the hyperpolarization direction by 1 microM indoxacarb or 1 microM DCJW indicating a higher affinity of the inactivated sodium channels for these insecticides. These shifts resulted in an enhanced block at more depolarized potentials, thus explaining voltage-dependent block, and an apparent difference in the sensitivity of TTX-R and TTX-S channels to indoxacarb and DCJW near the resting potential. Indoxacarb and its metabolite DCJW cause toxicity through their action on the sodium channels.

Action Potentials↗
PubMed1998

The actions of the H2-blocker cimetidine on the toxicity and biotransformation of the phosphorothioate insecticide parathion.

Parathion, like most organophosphorus insecticides currently in use, must undergo cytochrome P450(P450)-dependent activation in order to exert its acute mammalian toxicity (cholinergic crisis). Since P450 isoforms play such an important role in mediating the toxicity of parathion and related insecticides, factors which significantly alter P450 activities, such as exposure to certain xenobiotics, can also be expected to affect the toxicity of these potentially hazardous insecticides. Cimetidine is a H2-histamine antagonist that has been shown to inhibit several P450-isoforms. In addition, administration of cimetidine has been reported to result in clinically significant pharmacokinetic interactions with a wide variety of drugs. In the present study coexposure to cimetidine and parathion resulted in a moderate increase in the toxicity of this pesticide. However, coexposure to cimetidine and paraoxon did not alter the toxicity of the organophosphate, indicating that cimetidine likely affected P450-dependent formation of paraoxon from parathion. In vitro incubations of mouse hepatic microsomes demonstrated that, in addition to reducing the velocity of P450-dependent metabolism of parathion, cimetidine increased the proportion of paraoxon formed (activation). and decreased the proportion of p-nitrophenol formed (detoxification). Since parathion is not eliminated significantly by other routes in the mouse, the bulk of parathion in vivo was metabolized by P450 (although more slowly) in the presence of cimetidine, leading to a greater amount of paraoxon produced, and therefore greater toxicity. Incubations with individual P450 isoforms suggested that cimetidine could act by inhibition of P450 isoforms that detoxify parathion to a greater degree than cimetidine-resistant isoforms, and/or cimetidine could alter the proportions of detoxification versus activation of certain individual isoforms.

Animals↗
PubMed2001

Comparative efficacy of several insecticides for control of cattle lice (Mallophaga: Trichodectidae and Anoplura: Haematopinidae).

Several insecticides were applied to cattle at various rates, mixtures, application methods and numbers of treatments and evaluated for control of cattle lice. The insecticides included permethrin at various rates as a pour-on with and without the synergist piperonyl butoxide (PBO), and also at various rates as a spray with and without PBO. Pirimiphos-methyl was evaluated as a pour-on at various rates and with one or two applications. Lambda cyhalothrin in microencapsulated formulation was compared to a non-microencapsulated formulation. Rabon(R) was applied as a pour-on at two rates and at one or two treatments for each rate. Dimilin(R) was applied as a pour-on at two rates and mixed with permethrin and applied at two rates. Five endectocides, Eprinex(R), Ivomec(R), Dectomax(R), Cydectin(R) and Phoenectin(R) were all applied at the same rate. The cattle utilized in this research were all infested with a mixture of lice species. The species included: Bovicola (Damalinia) bovis (L.), Haematopinus eurysternus (Nitzsch), Linognthus vituli (L.) and Solenoptes capillatus (Enderlein). Most of the cattle were infested with at least two species and some had three or all four species present. All of the treatments except permethrin 1.0%+5% PBO, at a rate of 3ml/45.4kgwt. provided acceptable lice control with one application. Data indicated that applying the insecticides in early January should provide enough control to render the need for a second treatment unnecessary.

Animals↗
PubMed2003

Insecticidal action of the polyphenolic rich fractions from the stem bark of Streblus asper on Dysdercus cingulatus.

Extracts from the stem bark of Streblus asper possess insecticidal activity against the fifth instar of Dysdercus cingulatus. Methanolic extract showed an LC(50) value of 5.56 microg/insect. Partition with chloroform increased the insecticidal activity (LC(50) 2.01 microg/insect). Three polyphenolic rich fractions were obtained from silica-gel column chromatography of the chloroform fraction and found to have noteworthy insecticidal activity (LC(50): 1.82 microg, 2.70 microg, 2.26 microg/insect) by topical application. This may provide a useful beginning for the development of biopesticides.

Animals↗
PubMed2001

Evaluation of in vitro methods for detecting the effects of various chemicals on the human progesterone receptor, with a focus on pyrethroid insecticides.

The progesterone receptor (PR) is associated with physiological events such as implantation and the maintenance of pregnancy. Recently, it has become a social concern that chemicals may exert agonistic or antagonistic effects on hormone receptors. Therefore, we examined the effects of various chemicals on the human PR, with a focus on pyrethroid insecticides, using three in vitro methods. Eight pyrethroid insecticides (fenvalerate, d-allethrin, d-phenothrin, prallethrin, empenthrin, permethrin, cypermethrin and imiprothrin), examples of environmental pollutants and positive control chemicals were subjected to a reporter gene assay (luciferase assay) using human breast cancer T-47D cells, a two-hybrid assay and a binding assay using the same whole cells or receptors (cell-free). In none of these did the eight pyrethroid insecticides show any binding to the PR, agonistic or antagonistic effects.

Binding, Competitive↗
PubMed1998

Cytotoxic effects and induction of cytochromes P450 1A1/2 by insecticides, in hepatic or epidermal cells: binding capability to the Ah receptor.

Insecticides deserve particular attention since the general population is potentially exposed to such chemicals through many routes. We therefore tested the comparative acute and chronic toxicity of chemicals belonging to the major insecticides families (DDT, malathion and tetrachlorvinphos, carbaryl, cypermethrin, diflubenzuron), in hepatocytes, HepG2 and HaCaT cell lines. Two kinds of end-points were used: cytotoxicity parameters and CYP1A1 induction. Except for cypermethrin and diflubenzuron, all these chemicals exerted a cytotoxic effect in hepatocytes and HaCaT, but not in HepG2 cells. However, the induction of the EROD activity appeared more sensitive since a response was detected at lower concentrations. Significant differences were observed between the cell types and the insecticides. Furthermore, these chemicals were unable to displace [3H]TCDD from its binding sites, suggesting that they would not be a ligand of the Ah receptor. The experimental approach used herein may be a good means for predicting the acute and chronic toxicity of pesticides.

Animals↗
PubMed2001

Insecticidal properties of volatile extracts of orange peels.

Statistical studies using the randomised complete block design with four replicates showed that volatile extracts of two species of orange peel--Citrus sinensis (sweet orange) and Citrus aurantifolia (lime) had insecticidal activity against mosquito, cockroach and housefly. Insecticidal activity was better after 60 min than at 30 min spraying of rooms. Volatile extracts of C. sinensis showed greater insecticidal potency, while the cockroach was the most susceptible to the orange peels among the three insects studied.

Animals↗
PubMed2002

Synergistic interaction between two cockroach sodium channel mutations and a tobacco budworm sodium channel mutation in reducing channel sensitivity to a pyrethroid insecticide.

Pyrethroid insecticide resistance due to reduced nerve sensitivity, known as knockdown resistance (kdr or kdr-type), is linked to multiple point mutations in the para-homologous sodium channel genes. Previously we demonstrated that two mutations (E434K and C764R) in the German cockroach sodium channel greatly enhanced the ability of the L993F mutation (a known kdr -type mutation) to reduce sodium channel sensitivity to deltamethrin, a pyrethroid insecticide. Neither E434K nor C764R alone, however, altered sodium channel sensitivity. To examine whether E434K and C764R also enhance the effect of pyrethroid resistance-associated sodium channel mutations identified in other insects, we introduced a V to M mutation (V409M) into the cockroach sodium channel protein at the position that corresponds to the V421M mutation in the Heliothis virescens sodium channel protein. We found that the V409M mutation alone modified the gating properties of the sodium channel and reduced channel sensitivity to deltamethrin by 10-fold. Combining the V409M mutation with either the E434K or C764K alone did not reduce the V409M channel sensitivity to deltamethrin further. However, the triple mutation combination (V409M, E434K and C764R) dramatically reduced channel sensitivity by 100-fold compared with the wild-type channel. These results suggest that the E434K and C764R mutations are important modifiers of sodium channel sensitivity to pyrethroid insecticides.

Animals↗
PubMed2003

The house fly aliesterase gene (MdalphaE7) is not associated with insecticide resistance or P450 expression in three strains of house fly.

It was recently proposed that a mutation (G137D) in the MdalphaE7 gene was responsible for increasing transcription of a P450 (CYP6A1) resulting in resistance to diazinon. To examine if MdalphaE7 had a role in resistance in other strains we sequenced a fragment (approximately 700 bp) of the MdalphaE7 gene from individual flies of two insecticide susceptible and three insecticide resistant (due to increased monooxygenase-mediated detoxification) strains. Five unique alleles were discovered. While all of the susceptible strains had Gly137, so did the resistant LPR and NG98 strains. Of the two alleles in the YPER strain one had the G137D substitution and the other did not. Based on the lack of correlation between the presence of the 'mutant' MdalphaE7 and resistance (or P450 levels), we conclude that the G137D mutation in MdalphaE7 is not involved in transcriptional control of the P450s involved in resistance in the LPR, NG98 or YPER strains. The relationship between MdalphaE7 alleles and insecticide resistance is discussed in light of these findings.

Amino Acid Sequence↗
PubMed1997

A single amino acid change in the para sodium channel protein is associated with knockdown-resistance (kdr) to pyrethroid insecticides in German cockroach.

Previous genetic and pharmacological studies suggest that knockdown-resistance (kdr) to pyrethroid insecticides likely results from a mutation(s) in the para sodium channel gene. In this study, para sodium channel genes from an insecticide-susceptible German cockroach strain, CSMA, and a kdr-type German cockroach strain, Ectiban-R, were cloned and sequenced. Comparison of the nucleotide sequences of paraCSMA and paraEctiban-R revealed two nucleotide differences at nt 1491 and nt 2979, respectively. Only the difference at nt 2979 (G in paraCSMA and C in paraEctiban-R) resulted in an amino acid change (Leu993 in CSMA and Phe993 in Ectiban-R). Leu993/Phe993 is located in the highly conserved membrane-spanning segment 6 of domain II (IIS6). Furthermore, reverse transcription-polymerase chain reaction (RT-PCR) sequence analysis using another two insecticide-susceptible and one kdr German cockroach strain, revealed that C2979 was specifically associated with kdr resistant strains, whereas only G2979 was present in all susceptible strains. These results suggest that a single amino acid change from Leu993 to Phe993 is responsible for the kdr-type resistance in German cockroach.

Amino Acid Sequence↗
PubMed2003

Synthesis and insecticidal activity of novel dihydropyrrole derivatives with N-sulfanyl, sulfinyl, and sulfonyl moieties.

This paper reports the synthesis and insecticidal activity of a new type of dihydropyrrole derivatives with sulfur moieties such as sulfanyl, sulfinyl, and sulfonyl groups at the 1-position. These derivatives exhibited high insecticidal potency against Nilaparvata lugens and Nephotettix cincticeps. Investigation of the structure-activity relationships revealed that the alkoxycarbonyloxy groups at the 4-position tended to increase the systemic insecticidal activity.

Animals↗
PubMed1999

Photorhabdus toxins: novel biological insecticides.

Following concerns over the potential for insect resistance to insecticidal Bacillus thuringiensis toxins expressed in transgenic plants, there has been recent interest in novel biological insecticides. Over the past year there has been considerable progress in the cloning of several alternative toxin genes from the bacteria Photorhabdus luminescens and Xenorhabdus nematophilus. These genes encode large insecticidal toxin complexes with little homology to other known toxins.

Amino Acid Sequence↗
PubMed1999

In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues.

Malathion [S-(1,2-dicarboethoxyethyl)O,O-dimethyl phosphorodithioate] is a commonly used organophosphorus insecticide reported to be genotoxic both in vivo and in vitro, but the reports are conflicting. In order to elucidate the genotoxic potency of the main compounds present in commercial preparations of malathion, the DNA-damaging effect of this insecticide, its major metabolite malaoxon [S-(1,2-dicarboethoxyethyl)O,O-dimethyl phosphorothiolate] and its isomer isomalathion [S-(1,2-dicarboethoxyethyl)O,S-dimethyl phosphorodithioate], all at purity of at least 99.8%, was investigated by use of the alkaline single cell gel electrophoresis (comet assay). Freshly isolated human peripheral blood lymphocytes were incubated with 25, 75 and 200 microM of the chemicals for 1 h at 37 degrees C. The concentrations used are comparable to those found in blood following various non-lethal human exposures to pesticides. Malathion did not cause any significant changes in the comet length of the lymphocytes, throughout the range of concentrations tested. Malaoxon and isomalathion introduced damage to DNA in a dose-dependent manner. The effect induced by malaoxon was more pronounced than that caused by isomalathion. Treated cells were able to recover within a 60-min incubation in insecticide-free medium at 37 degrees C except the lymphocytes exposed to malaoxon at 200 microM, which did not show measurable DNA repair. The latter result suggests a considerable cytotoxic effect (cell death) of malaoxon at the highest concentration used. The reported genotoxicity of malathion might, therefore, be a consequence of its metabolic biotransformation to malaoxon or the presence of malaoxon and/or isomalathion as well as other unspecified impurities in commercial formulations of malathion. In this regard, the results of our study clearly indicate that malathion used as commercial product, i.e., containing malaoxon and isomalathion, can be considered as a genotoxic substance in vitro. This means that it may also produce DNA disturbances in vivo, such as DNA breakage at sites of oncogenes or tumor suppressor genes, thus playing a role in the induction of malignancies in individuals exposed to this agent. Therefore, malathion can be regarded as a potential mutagen/carcinogen and requires further investigation.

Cells, Cultured↗
PubMed2001

On-column trace enrichment by sequential frontal and elution electrochromatography. 1. Application to carbamate insecticides.

An on-column trace enrichment method for CEC of dilute samples is presented. The method involves on-line preconcentration by frontal electrochromatography under conditions of strong solute binding to the stationary phase followed by a step-gradient elution electrochromatography with a mobile phase of high eluting strength. This method is tested with dilute samples of carbamate insecticides using capillary columns of 100-microm i.d. packed with a 5-microm octadecyl silica (ODS) stationary phase. The effectiveness of on-line preconcentration (i.e., zone narrowing) depends on the retention factor, k', of the analyte in the injection solvent as well as in the eluting mobile phase (i.e., the organic solvent content), the applied voltage during sample introduction, and elution and length of the introduced sample plug. Under optimal frontal and elution electrochromatography conditions, a 500-fold sensitivity increase is achieved for carbofuran (a carbamate insecticide) with a UV detector. The method is demonstrated with deionized and tap water samples spiked with carbamate insecticides.

Carbamates↗