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Insecticides mechanism of action

Brooks, G.T. (1992). Progress in structure-activity smdies on cage convnlsants and related GABA receptor chloride ionophore antagonists. In D. Otto and B. Weber (Eds.) Insecticides Mechanism of Action and Resistance. Newcastle npon Tyne, UK Intercept Press, 237-242. [Pg.340]

Eto, M. and Kuwano, K. 1992. Prenyl imidazoles and related compounds controlling hormonal development processes of insects. In Insecticides Mechanism of Action and Resistance, Otto, D. and Weber, B., Eds. Intercept Ltd., Andover, U.K. pp. 155-165. [Pg.252]

Otto, D. and Weber, B. 1992. Insecticides Mechanism of Action and Resistance. Intercept, Andover, U.K. 499 pp. [Pg.258]

Sterk, G. In Insecticides Mechanism of Action and Retistance (D. Otto,... [Pg.908]

Mechanism of action can be an important factor determining selectivity. In the extreme case, one group of organisms has a site of action that is not present in another group. Thus, most of the insecticides that are neurotoxic have very little phytotoxicity indeed, some of them (e.g., the OPs dimethoate, disyston, and demeton-5 -methyl) are good systemic insecticides. Most herbicides that act upon photosynthesis (e.g., triaz-ines and substituted ureas) have very low toxicity to animals (Table 2.7). The resistance of certain strains of insects to insecticides is due to their possessing a mutant form of the site of action, which is insensitive to the pesticide. Examples include certain strains of housefly with knockdown resistance (mutant form of Na+ channel that is insensitive to DDT and pyrethroids) and strains of several species of insects that are resistant to OPs because they have mutant forms of acetylcholinesterase. These... [Pg.59]

Hodgson, E. and Kuhr, R.J. (1990). A multiauthor work with a wealth of information on the mechanism of action of insecticides. [Pg.65]

Eldefrawi, M.E. and Eldefrawi, A.T. (1991). Nervous-System-Based Insecticides—Describes the mechanisms of action of a wide range of neurotoxic compounds, both human-made and naturally occurring. [Pg.317]

Neonicotinoids are potent broad-spectrum insecticides that exhibit contact, stomach and systemic activity. Acetamiprid, imidacloprid, nitenpyram, thiamethoxam and thiacloprid are representatives of the neonicotinoid insecticides (Figure 1). The mechanism of action is similar to that of nicotine, acting on the central nervous system causing irreversible blocking of postsynaptic nicotinic acetylcholine receptors (nAChR). Neonicotinoid insecticides are often categorized as antagonists of the... [Pg.1128]

Dinitrophenol is a member of the aromatic family of pesticides, many of which exhibit insecticide and fungicide activity. DNP is considered to be highly toxic to humans, with a lethal oral dose of 14 to 43mg/kg. Environmental exposure to DNP occurs primarily from pesticide runoff to water. DNP is used as a pesticide, wood preservative, and in the manufacture of dyes. DNP is an uncoupler, or has the ability to separate the flow of electrons and the pumping of ions for ATP synthesis. This means that the energy from electron transfer cannot be used for ATP synthesis [75,77]. The mechanism of action of DNP is believed to inhibit the formation of ATP by uncoupling oxidative phosphorylation. [Pg.662]

Even though all OP insecticides have a common mechanism of action, differences occur among individual compounds. OP insecticides can be grouped into direct and indirect ACHE inhibitors. Direct inhibitors are effective without any metabolic modification, while indirect inhibitors require biotransformation to be effective. Moreover, some OP pesticides inhibit ACHE more than PCHE, while others do the opposite. For example, malathion, diazinon, and dichlorvos are earlier inhibitors of PCHE than of ACHE. In these cases, PCHE is a more sensitive indicator of exposure, even though it is not correlated with symptoms or signs of toxicity. [Pg.4]

Hirohara, H. and Nishizawa, M. (1998) Biochemical synthesis of several chemical insecticide intermediates and mechanism of action of relevant enzymes. Bioscience, Biotechnology, and Biochemistry, 62, 1-9. [Pg.101]

Taylor, K.S., G.D. Waller, and L.A. Crowder. 1987. Impairment of a classical conditioned response of the honey bee (Apis mellifera L.) by sublethal doses of synthetic pyrethroid insecticides. Apidologie 18 243-252. Theophilidis, G., M. Benaki, and E. Papadopoulu-Mourkidou. 1997. Neurotoxic action of six pyrethroid insecticides on the isolated sciatic nerve of a frog (Rana ridibunda). Comp. Biochem. Physiol. 118C 97-103. Tippe, A. 1987. Evidence for different mechanisms of action of the three pyrethroids, deltamethrin, cypermethrin, and fenvalerate, on the excitation threshold of myelinated nerve. Pestic. Biochem. Physiol. 28 67-74. [Pg.1133]

Clark JM (1995) Effects and mechanisms of action of pyrethrins and pyrethroid insecticides. In Chang LW, Dyer RS (eds) Handbook of neurotoxicity. Marcel Dekker, New York, NY, pp 511-546... [Pg.69]

Fukuto TR (1990) Mechanism of action of organophosphorus and carbamate insecticides. Environ Health Perspect 87 245-254... [Pg.199]

Although some steroids have been reported to reduce the toxic effects of some insecticides, the steroid ethylestrenol decreased the rate of recovery of depressed cholinesterase activity in disulfoton- pretreated rats (Robinson et al. 1978). The exact mechanism of this interaction was not determined. Ethylestrenol alone caused a small decrease in cholinesterase activity, and, therefore, resulted in an additive effect. Rats excreted less adrenaline and more noradrenaline when given simultaneous treatments of atropine and disulfoton compared with rats given disulfoton alone (Brzezinski 1973). The mechanism of action of disulfoton on catecholamine levels may depend on acetylcholine accumulation. In the presence of atropine, the acetylcholine effect on these receptors increases the ability of atropine to liberate catecholamines. [Pg.125]

Herbicides, used to kill or damage a plant, are the most rapidly growing segment of pesticides. Prior to the 1930s, herbicides were non-specific and often very toxic to humans as well as other animals. In the 1930s, in parallel with the development of new insecticides, researchers discovered several chemicals that selectively killed plants. These chemicals are now widely used to increase food production and have been used in warfare. Herbicides come in a variety of chemical structures and mechanisms of action, so they will be discussed in only general terms. Interested readers are referred to the many web sites and extensive literature on herbicides (see below and the presentation). [Pg.78]

Organophosphate insecticides such as parathion may lead to a variety of symptoms in mammals poisoned by them. List five such symptoms and explain these in terms of the mechanism of action. [Pg.401]

Most of the examples published deal with the interaction of anesthetics with membranes, but calcium channel openers, [l-blockers, antimalarial drugs, anticancer drugs, antibiotics, and insecticides have also been examined. The NMR resonance signals of atoms and groups within the lipid, and of drag molecules, have been followed and described as a function of the interaction. For the interaction of anesthetics and the involved mechanism of action, the reader s attention is directed to a review [112],... [Pg.92]


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Mechanism insecticides

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