The Influence of 2-/o-cresyl/-4 H-1 ∶ 3 ∶ 2-benzodioxa-phosphorin-2-oxide (CBDP) on organophosphate poisoning and its therapy

Bošković, Bogdan

doi:10.1007/bf00353713

Cited by 83 publications

(32 citation statements)

References 24 publications

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“…Chemicals that provoke induction of the enzymes involved in activation of OPCs can make them more toxic, as well as the chemicals that inhibit enzymes included in the detoxification phase and vice versa. 40,[42][43][44] However, clinical impact of interactions due to inhibition/induction of enzymes involved in detoxification or activation is difficult to predict because they often produce effects on several enzyme systems.…”

Section: Molecular Mechanisms Of Organophosphate Toxicitymentioning

confidence: 99%

Unequal Efficacy of Pyridinium Oximes in Acute Organophosphate Poisoning

Antonijević¹,

Stojiljković²

2007

Clinical Medicine & Research

215

159

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Section: Molecular Mechanisms Of Organophosphate Toxicitymentioning

confidence: 99%

Unequal Efficacy of Pyridinium Oximes in Acute Organophosphate Poisoning

Antonijević¹,

Stojiljković²

2007

Clinical Medicine & Research

215

159

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“…With the compound bound to serum carboxylesterase it is not free to be distributed to and thus inhibit target enzyme(s) in other tissues. An inverse relationship exists between the activity of serum carboxylesterase and the acute toxicity of an organophosphate such as soman (Boskovic 1979;Clement 1984a, c;Maxwell et al 1988;Jimmerson et al 1989). In addition, carboxylesterase inhibition altered the biodisposition of a subsequen@ administered anticholinesterase (Clement 1984a).…”

Section: Resultsmentioning

confidence: 97%

Serum carboxylesterase activity in various strains of rats: sensitivity to inhibition by CBDP (2-/o-cresyl/4H∶1∶3∶2-benzodioxaphosphorin-2-oxide)

Clement¹,

Erhardt²

1990

Arch Toxicol

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Rodents are relatively insensitive to the neurotoxic effects of various organophosphorus compounds. The purpose of this investigation was to determine if differences in inactivation of CBDP could explain the strain differences in the sensitivity to neurotoxicity following administration of TOCP (tri-o-cresyl phosphate) observed by Carrington and Abou-Donia (1988). Serum carboxylesterase but not cholinesterase is an important detoxification route for organophosphates. Serum carboxylesterase and cholinesterase activity were significantly different (p less than 0.05) among the various strains of rats. The rank order of carboxylesterase activity was Sprague Dawley (6158 nmole/ml serum/min) greater than Long Evans (5589) greater than Fischer 344 (5010) whereas the rank order for cholinesterase activity was Fischer 344 greater than Sprague Dawley greater than Long Evans. TOCP is metabolized to the active neurotoxicant CBDP (2-/o-cresyl/4H:1:3:2-benzodioxaphosphorin-2-oxide). The ED50 for CBDP inhibition of serum carboxylesterase activity was found to vary considerably for the various strains of rats. The rank order of CBDP ED50 concentration in the various strains was Fischer 344 (437 microM) greater than Long Evans (339 microM) greater than Sprague Dawley (78 microM), indicating that there was a difference between the carboxylesterase of the various strains with regard to interaction with CBDP. It is suggested that the differences in the quantity of serum carboxylesterase combined with the differences in the interaction of the inhibitor with the enzyme(s) may be responsible for the strain differences observed by Carrington and Abou-Donia (1988).

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“…This correlates well with the previously reported findings of OP potentiation through 2-(o-cresyl)-4H-1 : 3 : 2-benzodioxaphosphorin-2-oxide (CBDP), tetraisopropylpyrophosphoramide (iso-OMPA), mipafox, or TOCP pretreatment. All these potentiating compounds bind to serine-active sites such as the CarbE, and inhibit its activity in plasma, liver, brain, muscle, and heart (Boskovic, 1979;Clement, 1984b;Dettbarn and Gupta, 1989;Grubic et al, 1988;Gupta and Kadel, 1990a, b;Gupta et al, 1985Gupta et al, , 1986Gupta et al, , 2000Maxwell et al, 1988). The degree of potentiation may vary with the activity of the CarbE and susceptibility to the given OP or CM insecticides and thus could explain the variations between species (Maxwell, 1992;Maxwell et al, 1987;Wallace and Kemp, 1991).…”

Section: Interaction Between Che Inhibitors and Non-che Inhibitorsmentioning

confidence: 99%