Sorption of tetrachlorvinphos insecticide (Gardona) to the hemolymph of Periplaneta americana

Tetrachlorvinphos insecticide (Gardona, SI) 8447) sorbs to the hemolymph of the American cockroach via noncovalent bonding. The amount sorbed is dependent upon both the concentration of hemolymph and tetrachlorvinphos used. Acrylamide disc gel electrophoresis and Sephadex column chromatography of the complex revealed that tetrachlorvinphos binds to a variety of proteins in the hemolymph. No one protein serves as a specific carrier.These studies show that 80% of the LD₅₀ dose of tetrachlorvinphos can bind to the hemolymph contained in a single roach. The observed LD₅₀ value could then be considered as an inflated value, since the hemolymph can sorb large quantities of tetrachlorvinphos and thereby reduce the concentration of free compound available for inducing a toxic event. An alternative possibility, however, should not be overlooked. The binding of tetrachlorvinphos to hemolymph can be looked upon as a transport mechanism, whereby the compound is transported throughout the roach, to dissociate from the “carrier” proteins, and to penetrate into or through the cell membrane at the appropriate time. This would have the effect of actually enhancing the toxicity of the compound.     

Toxicological studies with the 1,3,5-triazine herbicide cyanazine

Acute and long-term mammalian toxicity studies were carried out with the 1,3,5-triazine herbicide cyanazine (I) and its two major plant and soil metabolites DW 43 85 (II) and DW 4394 (III). Depending upon the species used, the acute oral LD50 values for cyanazine ranged from 140-750 mg/kg, the values in any one species not being influenced by formulation. The acute, percutaneous LD50 values were greater than 1000 mg/kg, the maximum dose which could be administered. Cyanazine was non-irritant to eyes and skin and a non-sensitiser to skin. The acute oral LD50 in rats for (II) was 789 mg/kg and for (III) was >2000 mg/kg. In 13-week studies on cyanazine, reduced growth rates and organ weight changes were the most sensitive criteria of exposure, 25 parts/million in the diet of rats and 5 mg/kg orally dosed to dogs being considered to be without toxicological effect. In two year studies 12 parts/million in the diet of rats and 1.25 mg/kg, orally dosed to dogs produced no changes of toxicological significance. In 13-week studies with (II) and (III), intakes of up to 10 000 parts/million in the diet failed to produce any toxicologically significant changes.     

Further studies of the degradation of the pyrethroid insecticide cypermethrin in soils

Studies of the degradation of the pyrethroid insecticide cypermethrin (NRDC 149) and its cis- and trans-isomers (NRDC 160 and NRDC 159, respectively), have been extended. In soils stored in the laboratory for up to 52 weeks, cypermethrin continued to be degraded by hydrolysis and oxidation. A previously unidentified product has now been identified as the dicarboxylic acid 3-(2, 2-dichlorovinyl)-1-methylcyclopropane-1, 2-dicarboxylic acid. Comparative experiments carried out under indoor and outdoor conditions showed that essentially the same products were formed under these different conditions. However, α-carboxy-3-phenoxybenzyl 3-(2, 2-dichlorovinyl)-2, 2-dimethyl-cyclopropanecarboxylate was one minor product detected only under outdoor conditions. Evidence is presented for the further degradation of bound residues arising in soil from cypermethrin treatments. There was limited uptake of the radiolabel into wheat grown in soil containing radiolabelled bound residues.     

Fitness costs associated with insecticide resistance

Insects are exposed to a variety of stress factors in their environment, and, in many cases for insect pests to agriculture, those factors include toxic chemical insecticides. Coping with the toxicity of insecticides can be costly and requires energy and resource allocation for adaptation and survival. Several behavioural, physiological and genetic mechanisms are used by insects to handle toxic insecticides, sometimes leading to resistance by constitutive overexpression of detoxification enzymes or inducing mutations in the target sites. Such actions are costly and may affect reproduction, impair dispersal ability and have several other effects on the insect's fitness. Fitness costs resulting from resistance to insecticides has been reported in many insects from different orders, and several examples are given in this mini‐review. Copyright © 2012 Society of Chemical Industry     

The biochemistry of insecticide resistance in Anopheles sacharovi: Comparative studies with a range of insecticide susceptible and resistant Anopheles and Culex species

Fourth instar larvae, the progeny from wild-caught Anopheles sacharovi females, were subjected to a number of biochemical tests and the results were compared to those from similar tests on laboratory insecticide resistant and susceptible strains of anopheline and culicine mosquitoes. DDT resistance in An. sacharovi is associated with the ability to rapidly metabolise DDT to DDE. The organophosphorus and carbamate resistance was not associated with quantitative changes in esterases, multifunction oxidases, or glutathione S-transferase. The acetylcholinesterase was less sensitive to malaoxon and propoxur than laboratory susceptible An. albimanus, and plots of inhibition suggest that the population was polymorphic for more than one form of acetylcholinesterase. Metabolism studies on malathion and pirimiphos methyl did not indicate resistance due to increased metabolism. There was no evidence of penetration barriers contributing to resistance to either DDT or malathion, and there was no indication of any resistance to pirimiphos methyl in our tests.     

Studies on the performance of laying hens and broiler chickens fed low doses of tetrachlorvinphos

The effects of moderate to low doses of tetrachlorvinphos (TCVP) on egg production in hens and growth in broiler chickens have been studied. Dietary levels of 0, 50 and 500 mg TCVP/kg were fed to laying hens for 12 or 13 weeks. Adverse effects of the treatment on egg production, egg and yolk weight, egg hatchability, shell thickness, bird weight or food consumption were not observed. In an 8-week study on broiler chickens fed dietary concentrations of 0,2,5,50,100 and 150 mg TCVP/kg growth and food conversion were not significantly affected.     

Resistance to cyfluthrin and tetrachlorvinphos in the lesser mealworm, Alphitobius diaperinus, collected from the eastern United States

The lesser mealworm, Alphitobius diaperinus (Panzer), is an important pest in poultry facilities. The toxicity of cyfluthrin and tetrachlorvinphos to five strains of the lesser mealworm was compared with the toxicity to a susceptible laboratory strain. Bioassays were carried out with both larvae and adults. For the susceptible strain, cyfluthrin and tetrachlorvinphos had similar toxicity to adults, but cyfluthrin was 5 times more toxic to larvae when compared with tetrachlorvinphos. High levels of resistance to tetrachlorvinphos in two beetle strains were detected in both larvae and adults, although these strains were heterogeneous and still contained susceptible individuals. Resistance to cyfluthrin ranged from 1.7- to 9.5-fold for adults and from 0.5- to 29-fold for larvae at the LC(95). Overall, the patterns of resistance did not mirror the insecticide use patterns reported at these facilities. The implications of these results to management of the lesser mealworms are discussed.     

A comparative study of insecticide resistance assays with the German cockroach

Females of a diazinon-resistant strain of German cockroach exhibiting cross resistance to propoxur were evaluated for resistance to diazinon and propoxur by six assays: LD₅₀s for topical application and injection; LC₅₀, KT₅₀ and LT₅₀ for deposits on wood and KT₅₀ for deposits on glass. Also investigated were certain variables in the topical application technique and the experimental conditions for topical synergism studies. Among all assays, diazinon resistance ratios (resistant:susceptible) ranged from 3- to 145-fold; propoxur varied from 1- to 14-fold. Resistance ratios based on KT₅₀ data were consistently low (<4x) for both insecticides. Resistance to diazinon was 13x when applied topically and 6x when injected. Resistance to propoxur was 14x by injection compared to 8x for topical application. The LC₅₀ assay exhibited the greatest difference in resistance to the two insecticides: namely, 145x to diazinon and 1x(no resistance) to propoxur. By LT₅₀ analysis, resistance to propoxur was 10x compared with 100x resistance to diazinon. Thus, the method used had a significant effect on the final value of the resistance ratio. Even though resistance ratios may vary widely among different techniques, the final choice of a method depends upon many factors. The LT₅₀ method may provide a more realistic appraisal of resistance in wild populations of German cockroaches especially when experimental residues are similar to those used in control programmes.     

转基因植物农药的毒理学评价

本文从现有农药分类入手,介绍了生物农药的一般概念,特别是植物农药（Plant-Incorporated-Protectants,PIPs）的概念及其安全性评价原则。并以B.t10转基因玉米为例,详细解析了PIPs农药毒理学安全性评价的靶标——蛋白及相关遗传物质如蛋白编码基因、标志基因、报告基因;一般资料要求,如毒性、致敏性、抗药性和非预期效应;评价原则和决策依据,为今后评价此类农药奠定基础。     

Photodegradation of the carbamate insecticide ethiofencarb

In order to study the photoreactivity and possible photodegradation pathways of ethiofencarb (2-ethylthiomethylphenyl methylcarbamate) on plant surfaces, model experiments in the presence of cyclohexane, cyclohexene methylcarbamate)onand iso-propanol were performed. Both artificial light (λ > 280 nm) and natural sunlight were used. Half-lives of the ethiofencarb photodegradation were in the order cyclohexane < isopropanol < cyclohexene and ranged from 75 min to more than 20 h. Depending on the solvent and the light source chosen, different photo-products were obtained. When ethiofencarb was irradiated in the presence of cyclohexane, photo-oxidation to the corresponding sulfoxide was the main degradation pathway, followed by a cyclization reaction. In the case of isopropanol as model solvent, numerous photoproducts were detected as a result of photo-oxidation, hydrolysis and the addition to ethiofencarb of the solvent molecule.     

Toxicological and mechanistic studies on neonicotinoid cross resistance in Q-type Bemisia tabaci (Hemiptera: Aleyrodidae)

The tobacco whitefly, Bemisia tabaci Gennadius (Homoptera: Aleyrodidae) is a serious pest in numerous cropping systems and has developed a high degree of resistance against several chemical classes of insecticides. One of the latest group of insecticides introduced to the market were the neonicotinoids (chloronicotinyls), acting agonistically on insect nicotinic acetylcholine receptors. Resistance to neonicotinoid insecticides has recently been shown to occur, especially in Q-type B tabaci in some places in Almeria, Spain, whereas control of B-type B tabaci in many other intense cropping systems worldwide has remained on high levels. Our study revealed that neonicotinoid-resistant Q-type strains from Almeria were often more than 100-fold less susceptible to thiamethoxam, acetamiprid and imidacloprid when tested in discontinuous systemic laboratory bioassays. The resistance factors were generally 2- to 3-fold lower in leaf-dip bioassays. In addition to the Spanish strains, we obtained two other highly neonicotinoid-cross-resistant B tabaci greenhouse populations, one from Italy (December 1999) and one from Germany (June 2001). A molecular diagnostic analysis revealed that both strains also belong to the (Spanish) subtype Q of the B tabaci species complex. The resistance levels of Q-type whitefly strains derived from Almeria greenhouses in 1999 remained stable for at least two years, even when maintained in the laboratory without any selection pressure. The biochemical mechanisms conferring resistance to neonicotinoids have not yet been elucidated in detail, but synergist studies suggested a possible involvement of microsomal monooxygenases. Furthermore, we checked two Almerian strains of B tabaci isolated in 1998 and 1999 and demonstrated that neonicotinoid resistance is not due to an altered [3H]imidacloprid binding site of nicotinic acetylcholine receptors.     

Toxicological significance of acetylcholinesterase of the housefly thorax

Polyacrylamide gel electrophoresis of the 100,000g supernatant fraction of thoracic homogenates from the DDT/S housefly strain separated five bands having acetylcholinesterase activity. Ferguson plots indicated that the three bands of slowest mobility constituted members of the heterologous-size isomer family described for the head enzyme. The two faster migrating bands appeared as electrophoretic artifacts of juxtaposition with a 3.6 S nonacetylcholinesterase component; in the absence of juxtaposition, a single form was characterized with identical molecular properties to the 5.3 S fundamental unit of head acetylcholinesterase. The kinetic properties of isolated forms were consonant with the molecular data and no major differences in K_m values for acetylthiocholine were discovered between the thoracic and head enzymes. We suggest the preferential in vivo inhibition of thoracic acetylcholinesterase by organophosphate pesticides is unlikely the consequence of biochemical differences between the enzymes from the two regions.     

Biochemistry of insecticide resistance

After briefly summarizing various resistance mechanisms and their effects on certain types of insecticides, attention is focused on gaps in the understanding of resistance. Most resistance mechanisms consist either of a change in sensitivity of the site of action or an increased capacity for detoxication. In both cases such changes could theoretically be due to quantitative changes of an enzyme (more sites of action or more detoxication enzyme) or to qualitative changes (less-sensitive site of action or more efficient detoxication enzyme). Examples have now been found for each of these possible causes of resistance to insecticides, except for an increased amount of sites of action. Whereas examples of the latter mechanism are known for cell lines resistant to anti-cancer chemicals, so far they have not been found in resistance to insecticides. The impact of the different mechanisms on development and stability of resistance is discussed.     

The interaction of insecticide synergists with nonenzymatic model oxidation systems

Insecticide synergists such as the 1,3-benzodioxoles, the 1,2,3-benzothiadiazoles and the phenyl-2-propynyl ethers inhibit the epoxidation of aldrin to dieldrin by a modified Fenton's reagent (H₂O₂, Fe²⁺, EDTA and bovine serum albumin). Inhibition appears to result from the ability of the synergists to compete with aldrin for the OH· radicals generated by the system, and as a result of this interaction the synergists are themselves chemically modified. In the case of the 1,3-benzodioxoles the reaction results in the formation of the corresponding catechols and the rate at which this occurs correlates favorably with the ability of the synergist to inhibit aldrin epoxidation in the system. Although a number of nonenzymatic systems generating radical species other than OH· are also capable of aldrin epoxidation, these are not affected by the presence of insecticide synergists and the synergists are not themselves modified by these systems. The possible relevance of these results to the mode of action of synergists is discussed.     

Phototransformation of the insecticide hydramethylnon in aqueous systems

Sunlight irradiation of hydramethylnon in aqueous media of different pH values resulted in 80-94% transformation within 10h. The rate of disappearance of the insecticide was affected marginally by the initial pH of the reaction medium. After 10 h irradiation, eight photoproducts were formed. Three products were isolated as pure crystalline substances and the structures of two of these (I & III) were characterised by mass and NMR spectroscopy. The reaction mechanisms involved in the formation of photoproducts are discussed.     

Dermal pharmacokinetics of the insecticide furathiocarb in rats

The pharmacokinetics of furathiocarb were studied in vivo in male Sprague-Dawley rats following dermal treatment. HPLC and post-column derivatization were used for the analysis of furathiocarb and its metabolites (carbofuran, 3-hydroxycarbofuran and 3-ketocarbofuran). Carbofuran and 3-hydroxycarbofuran were detected in plasma and urine rather than furathiocarb. 3-Ketocarbofuran, another potential metabolite, was not observed in any sample. The concentration of carbofuran was higher than that of 3-hydroxycarbofuran in plasma, but the reverse was the case in urine. The corresponding area under the plasma concentration-time curve, Tmax, and Cmax values of carbofuran and 3-hydroxycarbofuran for 1500 mg kg-1 doses were 2.4-8.0 mg equiv hml-1, 12 h and 0.1-0.4 mg equiv ml-1, respectively. T1/2 was calculated only for 3-hydroxycarbofuran (28 h). Two metabolites were excreted in a dose-dependent manner without saturation.     

Climate change and the genetics of insecticide resistance

Changes in global temperature and humidity as a result of climate change are producing rapid evolutionary changes in many animal species, including agricultural pests and disease vectors, leading to changes in allele frequencies of genes involved in thermotolerance and desiccation resistance. As some of these genes have pleiotropic effects on insecticide resistance, climate change is likely to affect insecticide resistance in the field. In this review, we discuss how the interactions between adaptation to climate change and resistance to insecticides can affect insecticide resistance in the field using examples in phytophagous and hematophagous pest insects, focusing on the effects of increased temperature and increased aridity. We then use detailed genetic and mechanistic studies in the model insect, Drosophila melanogaster, to explain the mechanisms underlying this phenomenon. We suggest that tradeoffs or facilitation between adaptation to climate change and resistance to insecticides can alter insecticide resistance allele frequencies in the field. The dynamics of these interactions will need to be considered when managing agricultural pests and disease vectors in a changing climate. © 2019 Society of Chemical Industry     

Esterase-inhibiting photo-oxidation products from the organophosphorus insecticide pyrimithate

Pyrimithate (2-dimethylamino-6-methylpyrimidin-4-yl diethyl phosphorothio-nate) decomposes when exposed to u.v. light in the presence of air to a complex mixture of products, some of which inhibit esterases directly or indirectly. Separation of the mixture by thin-layer and liquid chromatography gave five pure components in sufficient quantity for spectroscopic identification. A sixth was tentatively identified. The structures ( II-VII ) show that oxidative attack occurs at the dimethylamino group and at the sulphur atom.