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Soman carboxylesterase

Maxwell, D.M., K.M. Brecht and D.E. Lenz. 1987b. Effect of carboxylesterase inhibition on carbamate protection against soman toxicity. Proc. Sixth Chem. Def. Biosci. Rev., pp. 17—24. (cited in Somani et al., 1992)... [Pg.209]

Maxwell, D.M., Brecht, K.M., O Neill, B.M. (1987). The effect of carboxylesterase inhibition on interspecies differences in soman toxicity. Toxicol. Lett. 39 35-42. [Pg.64]

Jokanovic, M. (1989). Role of carboxylesterase in soman, sarin and tabun poisoning in rats. Pharmacol. Toxicol. 65 181-4. [Pg.809]

Sterri, S.H., Fonnum, F. (1987). Carboxylesterases in guinea-pig plasma and liver tissue specific reactivation by diacetylmonoxime after soman inhibition in vitro. Biochem. Pharmacol. 36 3937-42. [Pg.1040]

Toxicity of organophosphates can be potentiated 15-20-fold in rats and mice by pretreatment with a metabolite of tri-O-cresylphosphate, CBDP (2-0-cresyl)-4H-l,3,2-benzodioxa-phosphorin-2-oxide), which is an irreversible inhibitor of CarbEs. In similar studies, tetraisopropylpyrophosphoramide (iso-OMPA), or mipafox, an organophosphate-irreversible inhibitor of CarbEs, potentiates three-to fivefold the toxicity of several OPs (soman, DFP, and methylparathion) and carbamates (carbofuran, aldicarb, propoxur, and carbaryl). Inhibition of CarbEs by CBDP, iso-OMPA, or mipafox pretreatment, particularly in plasma, liver, heart, brain, and skeletal muscles, is a major contributory factor in the potentiation of toxicity of organophosphates and carbamates. Thus, the toxicity of any drug, pesticide, or other type of agent that is normally detoxified by CarbEs, could be potentiated by pre-exposure to an organophosphorus or other carboxylesterase inhibitor. [Pg.434]

Maxwell DM and Koplovitz I (1990) Effect of endogenous carboxylesterase on HI-6 protection against soman toxicity. The Journal of Pharmacology and Experimental Therapeutics 254 440—444. [Pg.435]

Maxwell, D.M. and Brecht, K.M. The role of carboxylesterase in species variation of oxime protection against soman, Neurosci. Biobehav. Rev., 15, 135, 1991. [Pg.171]

Sterri S and Fonnum F (1989). Carboxylesterase - the soman scavenger in rodents heterogeneity and hormonal influence. In Enzymes Hydrolysing Organophosphorous Compounds (E Reiner, WN Aldridge and FCG Hoskinn, eds), pp. 155-164. Chichester, UK Ellis Harwood. [Pg.353]

S.L., The use of carboxylesterase inhibitors to develop an improved rodent model of soman toxicity, Soc. Neurosci. Abstr., 16, 1114A, 1990. [Pg.126]

An oral dose of 0.01 mg/kg in humans could be fatal. In animals, soman toxicity varied among species the LD50 values by subcutaneous administration were 20, 28, and 126 pg/kg for rabbits, guinea pigs, and rats, respectively (Maxwell et al. 1988). Exposure to a concentration of 21 mg/m soman caused a large inhibition of the activities of the enzyme carboxylesterase [9016-08-5] in bronchi, lungs, and blood tissues in rats (Aas... [Pg.679]

Certain oximes, such as bispyridinium oxime HI 6 and 2-PAM, have been reported to protect against soman toxicity. Pretreatment with HI 6 (50 mg/kg) together with atropine (10 mg/kg) increased the LC50 (LC50 X time) in rats by a factor of 7 (Schoene et al. 1985). HI 6 is an effective reactivator of soman-inhibited acetylcholinesterase. Its protective action was found to be greater in mice than in guinea pigs (Maxwell and Koplovitz 1990). In addition to reactivation of the enzyme acetylcholinesterase inhibited by soman, HI 6 produced an effect on carboxylesterase that... [Pg.680]


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See also in sourсe #XX -- [ Pg.1035 , Pg.1036 ]

See also in sourсe #XX -- [ Pg.261 , Pg.262 ]




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