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Carboxylesterases , nerve

A few OPs have been shown to cause OPIDN, a retrograde degeneration of long and large nerve fibers in the spinal cord and peripheral nerves of humans and experimental animals. Some OPs, such as GB, chlorpyrifos, and isofenphos, require very high doses to be acutely neuropathic (WHO 1986 Lotti 1991). Inhibition of approximately 70% or more of the carboxylesterase NTE often is associated with the disorder (WHO 1986 Lotti 1991). Onset of OPIDN is usually 10 days to several weeks after exposure. It is not clear whether OPIDN can occur after long-term exposure to low concentrations of OPs. [Pg.315]

Role of Carboxylesterases in Therapeutic Intervention of Nerve Gas Poisoning... [Pg.1033]

Sterri, S.H. (1989). The importance of carboxylesterase detoxification of nerve agents. In FOA Report C 40266-4.6,4.7 Proceedings of the Third International Symposium on Protection against Chemical Warfare Agents, pp. 235 0. FOA ABC-skydd, Umea. [Pg.1040]

See also A-Esterases Anticholinergics Carbamate Pesticides Carboxylesterases Neurotoxicity Nerve Agents Organophosphate Poisoning, Intermediate Syndrome Organophosphates Pesticides Veterinary Toxicology. [Pg.599]

On the above view, NLSD is primarily a disease of defective phospholipid metabohsm and the TAG-derived route of phospholipid biosynthesis is essential for the normal functioning of skin, muscle, liver, and the central nervous system. Further studies on the fatty hver dystrophic mouse which bears a close resemblance to human NLSD [103] may identify fhe defective gene. Defective neutral phospholipid metabolism in this mouse model is reflected by a decreased phosphohpid content of peripheral nerve myelin [109]. The nature of the hpase(s) involved in normal TAG-to-phospholipid acyltransfer has not been characterized, but may be similar to a previously described microsomal neutral hpase [110] or to a carboxylesterase [111]. [Pg.242]

The current human estimates for nerve agent vapor and aerosol toxicity are based upon data from animal models. Rodents are popular animal models in that they are readily available, cheap, and convenient to handle. Additionally, there is a great amount of background data on rodents available in the literature for comparison to many biological endpoints. However, nonrodent models are preferred for studies of prophylactic and therapeutic efficacy associated with nerve agent exposure due to the protective buffering impact of relatively high blood carboxylesterase levels in... [Pg.242]

Maxwell, D.M., Nerve agent specificity of scavenger protection by carboxylesterase, Proceedings of the Third International Symposium on Protection Against Chemical Warfare Agents, Umee, Sweden, 175-182,1989. [Pg.269]

Clinically, the most important effects of OP nerve agents are anticholinesterase actions. However, it should not be forgotten that OPs bind to a variety of enzymes, including esterases other than acetylcholinesterase, e.g. carboxylesterase, (long-chain fatty acid hydrolase), serine... [Pg.202]

Bovine chromaffin cells in primary culture possess carboxylcstcrase activities, 73% of w-hich is NTE the NTE component is resistant to inhibition by paraoxon and sensitive to mipafox and is localized to the particulate fraction of cell culture homogenates. Results suggest that bovine chromaffin cells may be a useful model for NTE studies because they possess a higher ratio of NTE/carboxylesterase than adrenal medulla tissue homogenates, brain tissue, or nerv e. [Pg.324]

Mo.st OP pesticides react preferentially with BuChE. In contrast, most OP nerve agents react preferentially with AChE. Carboxylesterase is also highly reactive with most OPs. This complicate.s the comparison of studies on rodents with studie,s on monkeys and humans because rodenhs have very high concentrations of carboxylesterase in plasma, whereas monkeys and humans have no carboxylesterase in plasma. On the other hand, albumin has esterase activity (Means and Wu, 1979), and this is sometimes mistaken for carboxylesterase activity in human plasma. [Pg.706]

The nerve gases are powerful inhibitors of the enzyme acetylcholinesterase (AChE), which causes rapid hydrolysis of acetylcholine. They are also inhibitors of butyryl-choUnesterase and carboxylesterase. Acetylcholine is the chemical that is released to transmit nerve impulses in the central nervous system and also at several peripheral locations. Once the impulse is transmitted, acetylcholine must be removed instantaneously for proper functioning of the nervous system. Such removal is done by the enzyme AChE, which is found extensively in nervous system and many non-nervous tissues. Nerve gases and other organophosphorus compounds bind... [Pg.674]


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Carboxylesterase

Carboxylesterases

Carboxylesterases , nerve agent effects

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