Effect of chlorpromazine pre-treatment on the inhibition of total cholinesterases and butyryl-cholinesterase in brain of rats poisoned by physostigmine or dichlorvos

Michałek, Hanna; Stavinoha, W. B.

doi:10.1016/0300-483x(78)90003-3

Cited by 12 publications

(2 citation statements)

References 15 publications

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“…Studies on the nerve gases, soman, sarin, tabun, and DFP did not show differential inhibition of AChE in the brain regions (Gupta et al, 1987 a,b;Lim et al, 1987;Misulis et al, 1987). Differential inhibition in the brain regions was also not seen in the case of the OPs, parathion, paraoxon, and physostigmine (Michalek and Stavinoha, 1978;Costa et al, 1990;Chambers and Carr, 1993). However, dosedependent inhibition in some of the brain regions by soman in rats (Jimmerson et al, 1989) and sarin in mice (Tripathi and Dewey, 1989) has been reported.…”

Section: Discussionmentioning

confidence: 97%

Neurotoxicity and Pattern of Acetylcholinesterase Inhibition in the Brain Regions of Rat by Bromophos and Ethylbromophos

Santhoshkumar

1996

Fundamental and Applied Toxicology

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Bromophos (Bp) and ethylbromophos (EBp) are two structurally homologous organophosphorus (OP) insecticides which show wide differences in their toxicity as well as neurotoxic symptoms in the laboratory rat. EBp is 24-fold more toxic (LD50 = 91 +/- 14 mg/kg body wt) than Bp (LD50 = 2218 +/- 195 mg/kg body wt) and only EBp produced characteristic tremors and lacrimation. In vivo cholinesterase inhibition was in the order plasma > erythrocytes > brain. Experiments with equitoxic and equimolar doses showed that EBp is a more potent anticholinesterase compound than Bp. Since IC50 values for the brain AChE were similar for both OPs, the target enzyme sensitivity was not a major factor in their differential toxicity. In vitro reactivation of serum ChE was significantly higher in the case of EBp than that of Bp. AChE in the brain regions showed differential inhibition in vivo. The brain stem AChE inhibition was least by Bp, whereas it was highest in the case of EBp. Both the OPs produced high AChE inhibition in the hippocampus. Differential inhibition of AChE in the brain regions and its consequent effects may be important factors in the differential neurotoxicity of OPs.

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Section: Discussionmentioning

confidence: 97%

Neurotoxicity and Pattern of Acetylcholinesterase Inhibition in the Brain Regions of Rat by Bromophos and Ethylbromophos

Santhoshkumar

1996

Fundamental and Applied Toxicology

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“…The presence of phenothiazines might have potentiated the OP toxicity. However, this effect was shown in humans only in a single case report (Arterberry et al, 1962) and results from research on experimental animals are conflicting (Fernández et al, 1975;Michaleck and Stavinoha, 1978). Cardiac arrest was probably coincidental.…”

Section: Minimizing Further Exposurementioning

confidence: 99%

Clinical Toxicology of Anticholinesterase Agents in Humans

Lotti

2010

Hayes' Handbook of Pesticide Toxicology

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Interactions Between Anticholinesterase Agents and Neuroleptics in Terms of Cholinesterase Inhibition in Brain and Other Tissues of Rats

Michałek

Nemesio

Meneguz

et al. 1983

Archives of Toxicology

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Treatment of rats with chlorpromazine (CPZ, 15 mg/kg L p. 60 min before sacrifice) did not modify cholinesterase (ChE) activity, but considerably enhanced the inhibition of total ChE induced by physostigmine (PhS, 0.5 mg/kg Lp. 40, min fJ.ftyr C~~) in brain, skeletal muscle, myocardium, lung, liver, and kidney. Additional experiments also showed a prolongation of PhS inhibition by CPZ in brain. The enhanced inhibition of total ChE due to CPZ depended in most peripheral organs on the effect on pseudoChE (as measured by a spectrophotometric method), except in the case of skeletal muscle in which potentiation of PhS effect was observed on true acetylcholinesterase (AcChE). The results indicate that the potentiation by CPZ of PhS inhibition occurs in all organs tested and is relatively non specific. CPZ was found to potentiate slightly the effects of Mevinphos but did not interact with Carbaryl, Diazinon or Azinphos. Furthermore, haloperidol did not potentiate the effects of physostigmine.

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Effect of chlorpromazine pre-treatment on the inhibition of total cholinesterases and butyryl-cholinesterase in brain of rats poisoned by physostigmine or dichlorvos

Cited by 12 publications

References 15 publications

Neurotoxicity and Pattern of Acetylcholinesterase Inhibition in the Brain Regions of Rat by Bromophos and Ethylbromophos

Neurotoxicity and Pattern of Acetylcholinesterase Inhibition in the Brain Regions of Rat by Bromophos and Ethylbromophos

Clinical Toxicology of Anticholinesterase Agents in Humans

Interactions Between Anticholinesterase Agents and Neuroleptics in Terms of Cholinesterase Inhibition in Brain and Other Tissues of Rats

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