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Mode of action
MOA Insektisida
Acetylcholinesterase (AChE) inhibitors GABA-gated chloride channel antagonists Sodium channel modulators Nicotinic acetylcholine receptor (nAChR) agonists Nicotinic acetylcholine receptor (nAChR) allosteric activators Chloride channel activators Juvenile hormone mimics Miscellaneous nonspecific (multi-site) inhibitors Mite growth inhibitors
Microbial disruptors of insect midgut membranes Inhibitors of mitochondrial ATP synthase Uncouplers of oxidative phosphorylation via disruption of the proton gradient Nicotinic acetylcholine receptor (nAChR) channel blockers Inhibitors of chitin biosynthesis, type 0 Inhibitors of chitin biosynthesis, type 1 Moulting disruptor, Dipteran Ecdysone receptor agonists Octopamine receptor agonists Mitochondrial complex III electron transport inhibitors
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Mitochondrial complex I electron transport inhibitors Voltage-dependent sodium channel blockers Inhibitors of acetyl CoA carboxylase. Mitochondrial complex IV electron transport inhibitors Mitochondrial complex II electron transport inhibitors Ryanodine receptor modulators Compounds of unknown or uncertain MoA2
MOA Fungisida
RNA polymerase I adenosin-deaminase DNA topoisomerase type II (gyrase) -tubuline assembly in mitosis cell division delocalisation of spectrin-like proteins
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respiration
complex I NADH Oxido-reductase complex II: succinate-dehydro-genase complex III: cytochrome bc1 (ubiquinol oxidase) at Qo site
(cyt b gene)
complex III: cytochrome bc1(ubiquinone reductase) at Qi site uncouplers of oxidative phosphorylation inhibitors of oxidative phosphorylation, ATP synthase ATP production complex III: cytochrome bc1 (ubiquinone reductase) at Q x (unknown) site
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gene)
protein synthesis MAP/Histidine- Kinase in osmotic signal transduction MAP/Histidine- Kinase in osmotic signal transduction
signal transduction
phospholipid biosynthesis, methyltrans-ferase lipid peroxidation (proposed) cell membrane permeability, fatty acids (proposed) microbial disrupters of pathogen cell membranes cell membrane disruption (proposed)
C14- demethylase in sterol biosynthesis 14-reductase and 87- isomerase in sterol biosynthesis 3-keto reduc-tase, C4- de-methylation squalene-epoxidase in sterol biosynthesis
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AChEase is the enzyme responsible for the breakdown of the neurotransmitter acetylcholine (ACh). Organophosphate compounds are irreversible inhibitors of AChEase while carbamate compounds are reversible inhibitors of AChEase.
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The reaction between an organophosphate and the active site on AChEase (a serine hydroxyl group) results in the formation of an intermediate that undergoes partial hydroylsis with the loss of the "Z" group, leaving a stable, phosphorylated, permanently inhibited enzyme. Signs and symptoms are prolonged and persistent. Without intervention, the toxicity will persist until sufficient amounts of "new" AChEase are synthesized in 20 to 30 days.
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Carbamate compounds attach to the serine hydroxyl group, the "X" group is removed by hydrolysis forming a carbamylated enzyme, and then decarbamylation occurs regenerating free, active AChEase.
Both are mimic Agonists often mimic the action of a naturally occurring substance (GABA). Whereas an agonist causes an action, an antagonist blocks the action of the agonist and an inverse agonist causes an action opposite to that of the agonist.
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Chloride channels display a variety of important physiological and cellular roles that include regulation of pH, volume homeostasis, organic solute transport, cell migration, cell proliferation and differentiation
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Prolonged Repolarization
alters the Na+ channels, they open normally but are closed (inactivated) slowly. All of these factors reduce the rate at which repolarization occurs and increase the sensitivity of the neurons to small stimuli that would not elicit a response in a fully repolarized neuron.
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Other MOA????
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Contact * Translocated *
Inhibit protein synthesis, photosynthesis, or growth
Repellants *
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Kills eggs