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Nerve poisons

Carbon disulphide. When working with this solvent, its toxicity (it is a blood and nerve poison) and particularly its high inflammability should be home in mind. Distillation of appreciable quantities of carbon disulphide should be carried out in a water bath at 55-65° it has been known to ignite from being overheated on a steam bath. [Pg.175]

The effects of DDT on nerve action potential are illustrated in Figure 16.1. In nerves poisoned by the insecticide, there is a prolongation of the sodium current and a consequent delay in returning to the resting potential. This can result in the... [Pg.303]

Miyamoto J, Kaneko H, Tsuji R et al (1995) Pyrethroids, nerve poisons how their risk to human health should be assessed. Toxicol Lett 82(83) 933-940... [Pg.105]

We synthesized EPMP, by the method of Fukuto and Metcalf ( ) by reacting diethyl methylphosphonate with phosphorus penta-chlorlde, followed by reaction with sodium -nltrophenolate. EPMP was purified by distillation at reduced pressure. Analysis for C9H12NO5P. Calculated % C, 44.1 % H, 4.93 % N, 5.71. Found % C, 43.9 % H, 4.77 % N, 4.59. [Caution EPMP Is a VERY TOXIC NERVE POISON the subcutaneous lethal dose (LD50) In mice is 350 pg/kg (R. Howd, R. Kenley, unpublished), and the material should be handled with extreme care at all times.]... [Pg.212]

Nicotine is a potent nerve poison, and is included in many insecticide preparations. In lower concentrations, nicotine is a stimulant, i.e. it increases activity, alertness and memory, and this is one of the main factors that contribute to the dependence-forming properties of tobacco smoking. Nicotine increases heart-rate and blood pressure, and reduces appetite. In higher doses, nicotine acts as a depressant. In large doses, it can cause nausea and vomiting. The main symptoms of the withdrawal of nicotine intake include irritability, headaches, anxiety, cognitive disturbances and sleep disruption. [Pg.292]

Inorganic phosphates are relatively harmless P4 and PH3 are very toxic in mammals and fish. Phosphate esters are used as Insecticides (nerve poisons)-Elemental sulfur is highly -toxic to most bacteria and fungi, relatively harmless to higher organisms. is highly toxic to mammals S02 is highly toxk. [Pg.484]

Among the most deadly of simple compounds is sodium fluoroacetate. The LD50 (the dose lethal for 50% of animals receiving it) is only 0.2 mg/kg for rats, over tenfold less than that of the nerve poison diisopropylphosphofluoridate (Chapter 12).a b Popular, but controversial, as the rodent poison "1080," fluoroacetate is also found in the leaves of several poisonous plants in Africa, Australia, and South America. Surprisingly, difluoroacetate HCF2-COO is nontoxic and biochemical studies reveal that monofluoroacetate has no toxic effect on cells until it is converted metabolically in a "lethal synthesis" to 2R,3R-2-fluorocitrate, which is a competitive inhibitor of aconitase (aconitate hydratase, Eq. 13-17).b This fact was difficult to understand since citrate formed by the reaction of fluorooxalo-acetate and acetyl-CoA has only weak inhibitory activity toward the same enzyme. Yet, it is the fluorocitrate formed from fluorooxaloacetate that contains a fluorine atom at a site that is attacked by aconitase in the citric acid cycle. [Pg.957]

The thujones are found in true wormwood, Artemisia ahsinthum, a species of mug wort native to Europe and Asia. This plant was once a source for absinthe, a greenish, bitter-tasting alcoholic beverage that has since been banned because of the toxicity of the thujones. The compounds have a peppcrmint-like odor and act as nerve poisons that can be the cause of epileptic fits. Nevertheless, they still find some application in homeopathic medicine... [Pg.111]

Another example of a natural product that we synthesised using a ROM-RCM sequence are tetraponerines.23 Tetraponerines (T1-T8) (Figure 6) were isolated from the venom of the New Guinean ant Tetraponera sp.24 These alkaloids represent the major constituents of the contact poison and contaminated enemies immediately show symptoms of nerve poisoning. [Pg.323]

When working with this solvent, its toxicity (it is a blood and nerve poison) and particularly its high flammability should be borne in mind. Distillation of... [Pg.411]

Symmetrically substituted cydopentanones have proven to be very good substrates in allylic substitution chemistry [98]. This chemistry is elegantly exploited by Blechert and co-workers for the synthesis of the nerve poisoning tetraponerine... [Pg.377]

DDT acts as a nerve poison on insects and mammals. Symptoms of... [Pg.319]

Organochlorine pesticides are nerve poisons in both insects and mammals. Action mechanisms are complex and not yet fully understood. They have been shown to have estrogen-like effects (ref. 84a), to inhibit testicular growth and secondary sex characteristics in cockerels and mice (DDT), to induce persistent estrus in rats, and to affect fertility, gestation, lactation and survival times. [Pg.407]

Toxicity The acute oral LD50 and dermal LD50 toxicity of toxaphene in rats are 40 and 600 mg/kg, respectively. Toxaphene is an active nerve poison and interferes with fluxes of cations across nerve cell membranes, which increases neuronal irritability and results in convulsions and seizures. Toxaphene also has been found to damage the lungs, liver, and kidney of animals and humans. Although the dermal adsorption efficiency of toxaphene is less than that of other organochlorines, its absorption is enhanced by fat and fat solvents. Toxaphene has been shown to cause cancer in pregnant animals and to induce birth defects.68... [Pg.116]

Some pyrethroids have as many as eight different isomers, and there are several different types. Acute toxicity of a mixture of two isomers depends on the ratio of the amounts of isomers in the formulation. For example, the female rat s acute oral LD50 of permethrin increases from 224 mg/kg to 6,000 mg/kg as the proportion of transisomer increases from 20% to 80%. The route of exposure also is critical in assessing the acute toxicity of a synthetic pyrethroid. Like DDT and many other registered insecticides, naturally occurring pyrethrins and the synthetic pyrethroids are nerve poisons. [Pg.199]

The synthetic pyrethroid principal mechanism of action is believed to be the disruption of the permeability of nerve membranes to sodium atoms.3 Organo-phosphates and carbamates also are nerve poisons, but they do not attack the human peripheral (in addition to our central) nervous system, as do DDT and synthetic pyrethroids. The half-life of pyrethroids in soils ranges from 1 day to 16 weeks. (It is amazing that people apply them annually for termite control, even though permethrin is supposedly effective against termites in the very same soil for 1 to 5 years). [Pg.199]

There is a vast chemistry of organophosphorus compounds, and even for arsenic, antimony, and bismuth, the literature is voluminous. Consequently only a few topics can be discussed here. It must also be noted that we discuss only the compounds that have P—C bonds. Many compounds sometimes referred to as organophosphorus compounds that are widely used as insecticides, nerve poisons, and so on, as a result of their anticholinesterase activity, do not, in general, contain P—C bonds. They are usually organic esters of phosphates or thiophosphates examples are the well-known malathion and parathion, (EtO)2Pv(S)(0C6H4NO2). Compounds with P—C bonds are almost entirely synthetic, though a few rare examples occur in Nature. [Pg.420]

B. F., Casida, J.E. (2005). A brain detoxifying enzyme for organophosphorus nerve poisons. Proc. Natl Acad. Sci. USA 102 6195-200. [Pg.89]

Each category has distinct advantages and disadvantages. Digestive poisons present a lower environmental hazard than nerve poisons, but are not as effective against some pests such as the brown honse moth. Nerve poisons are nsnally more rapidly biodegraded than digestive poisons, but also exhibit less durability. [Pg.176]

Agricultural pesticides were found to be effective insect resist agents when applied in emulsion form to wool dyebaths. Dieldrin (Fig. 16.2a), one of the original nerve poisons, is also highly toxic to mammals and aquatic life and its use has been banned in most countries. Products based on permethrin (Fig. 16.2b), a synthetic pyrethroid, are very effective against moth larvae, but have less effect on Anthrenus beetles. To overcome this disadvantage, combination products of permethrin and hexahydropyrimidine derivatives (Fig. 16.2c) have been introduced. [Pg.177]

Nerve poisons used as insect resist finishes. [Pg.177]

In terms of their mode of action, insecticides fall into seven classes physical toxicants, protoplasmic poisons, nerve poisons, metabolic inhibitors, cytolytic toxins, muscle poisons, and alkylating agents. [Pg.143]

DDT or 1,1-(2,2,2-trichloroethylidene)bis [4-chlorobenzene] Organochlorine Nerve poison, affecting sodium balance of nerve membranes, nonsystemic contact and stomach action Mosquito control for malaria eradication for crop use replaced by less persistent products 11-21... [Pg.393]


See other pages where Nerve poisons is mentioned: [Pg.95]    [Pg.397]    [Pg.298]    [Pg.27]    [Pg.247]    [Pg.132]    [Pg.180]    [Pg.736]    [Pg.95]    [Pg.63]    [Pg.402]    [Pg.123]    [Pg.1954]    [Pg.286]    [Pg.262]    [Pg.1209]    [Pg.175]    [Pg.736]    [Pg.470]    [Pg.480]    [Pg.567]   
See also in sourсe #XX -- [ Pg.295 ]

See also in sourсe #XX -- [ Pg.177 ]

See also in sourсe #XX -- [ Pg.115 ]




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