Effects of inhaled cholinesterase inhibitors on bronchial tonus and on plasma and erythrocyte acetylcholine estarase activity in rats

Pauluhn, Jürgen; Machemer, L.; Kimmerle, Georg

doi:10.1016/0300-483x(87)90126-0

Cited by 21 publications

(11 citation statements)

References 14 publications

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“…In support of this, in preliminary experiments (n=4; data not shown) we observed that in in vivo conditions Pth, at a dose high enough to cause more than 70% inhibition of plasma AChE activity and signs of neurotoxicity, did not produce modifications of the iRL in rabbits. This lack of functional response to Pth in animal species other than the guinea pig has been already observed by Pauluhn et al (1987), who reported that aerosolized Pth did not change the basal R L in rats.…”

Section: Mechanisms Of Acute Pulmonary Toxicity To Pthmentioning

confidence: 53%

Identification of mechanisms involved in the acute airway toxicity induced by parathion

Segura

Chávez

Montaño

et al. 1999

Naunyn-Schmiedeberg's Arch Pharmacol

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Organophosphates are still widely used worldwide and cause thousands of intoxications every year. In this work we investigated the mechanisms of parathion (Pth) airway toxicity, using biochemical and functional approaches. A plethysmographic technique for unrestrained guinea pigs was used to analyze Pth-induced modifications of airway mechanics and responsiveness to acetylcholine (ACh: 0.1-3.2 mg/ml, 2-min inhalation each dose). The isolated perfused rabbit lung preparation was used to study the acute effects of Pth on airway responsiveness to ACh (10(-8)-10(-3) M), histamine (10(-8)-10(-3) M) and substance P (10(-10)-10(-6) M), pulmonary acetylcholinesterase inhibition and cytochrome P450 (P450) activity, and their modifications with previous administration of Pth (1 mg/kg s.c. daily, 7 days). We found that: (1) In guinea pigs Pth (3.2-17 mg/kg i.p.) produced a dose-dependent increase in a lung resistance index (iRL), which was greatly reverted (approximately 50%) by salbutamol (2 mg/ml, 2-min inhalation, or 10 microg/kg i.p.). This salbutamol effect was transient (5-10 min), suggesting that this bronchodilator triggered additional obstructive mechanisms. (2) Pth increased the water content in lung parenchyma samples, but not in trachea or bronchi, and augmented the respiratory secretions measured through monosaccharide content in bronchoalveolar lavage. (3) The increase in iRL was greater in female animals, probably due to a higher P450 basal activity, and completely blocked by pharmacological inhibition of P450 with piperonyl butoxide (500 mg/kg i.p.). (4) In male guinea pigs a subclinical dose of Pth (10 mg/kg i.p.) induced airway hyperresponsiveness to ACh. In isolated perfused rabbit lung Pth (10(-6) M) produced airway hyperresponsiveness to ACh and histamine, the latter prevented by atropine (10(-5) M). (5) Repetitive exposure to subclinical doses (1 mg/kg s.c.) of Pth during 1 week caused approximately 80% inhibition of P450 activity in rabbits, which was not enough, however, to prevent the functional manifestation of Pth toxicity in the airways.

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Section: Mechanisms Of Acute Pulmonary Toxicity To Pthmentioning

confidence: 53%

Identification of mechanisms involved in the acute airway toxicity induced by parathion

Segura

Chávez

Montaño

et al. 1999

Naunyn-Schmiedeberg's Arch Pharmacol

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“…[18] The inhibition of AChE, for example, by nerve gases leads to perturbations in nerve conduction process and the rapid paralysis of vital functions of the living system. [19] Different methods to sense the activity of AChE and to follow its inhibition were developed.…”

Section: Resultsmentioning

confidence: 99%

An Os^II–Bisbipyridine–4‐Picolinic Acid Complex Mediates the Biocatalytic Growth of Au Nanoparticles: Optical Detection of Glucose and Acetylcholine Esterase Inhibition

Xiao

Pavlov

Shlyahovsky

et al. 2005

Chemistry A European J

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The complex Os(II)-bisbipyridine-4-picolinic acid, [Os(bpy)(2)PyCO(2)H](2+) (1), mediates the biocatalyzed growth of Au nanoparticles, Au NPs, and enables the spectroscopic assay of biocatalyzed transformations and enzyme inhibition by following the Au NP plasmon absorbance. In one system, [Os(bpy)(2)PyCO(2)H](2+) mediates the biocatalyzed oxidation of glucose and the growth of Au NPs in the presence of glucose oxidase, GOx, AuCl(4) (-), citrate and Au NP seeds. The mechanism of the Au NPs growth involves the oxidation of the [Os(bpy)(2)PyCO(2)H](2+) complex by AuCl(4) (-) to form [Os(bpy)(2)PyCO(2)H](3+) and Au(I). The [Os(bpy)(2)PyCO(2)H](3+) complex mediates the GOx biocatalyzed oxidation of glucose and the regeneration of the mediator 1. Citrate reduces Au(I) and enlarges the Au seeds by the catalytic deposition of gold on the Au NP seeds. In the second system, the enzyme acetylcholine esterase, AChE, is assayed by the catalytic growth of the Au NPs. The hydrolysis of acetylcholine (2) by AChE to choline is followed by the [Os(bpy)(2)PyCO(2)H](3+) mediated oxidation of choline to betaine and the concomitant growth of the Au NPs. The mediated growth of the Au NPs is inhibited by 1,5-bis(4-allyldimethylammonium-phenyl)pentane-3-one dibromide (3). A competitive inhibition process was demonstrated (K(M)=0.13 mM, K(I)=2.6 microM) by following the growth of the Au NPs.

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“…The inhibition of AChE by nerve gases leads to the perturbation of the nerve conduction system and to the rapid paralysis of vital functions of the living system. [23] The biocatalyzed hydrolysis of acetylthiocholine (7) (an analog of acetylcholine) to thiocholine (8), and the subsequent catalytic reduction of AuCl 4 -and the enlargement of the Au NP seeds, were used to follow the AChE activity (Fig. 4A).…”

Section: Enzyme-stimulated Synthesis Of Metal Nanoparticlesmentioning

confidence: 99%

Growing Metal Nanoparticles by Enzymes

2006

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Enzymes act as catalysts for the growth of metallic nanoparticles (NPs). The enzyme‐mediated growth of metallic NPs provides a general means to follow biocatalyzed transformations, and to develop optical sensors for different substrates such as glucose, L‐DOPA, alcohols, lactate or nerve gas analogs. Enzymes modified with Au NPs act as biocatalysts for the fabrication of metallic nanowires. The dip‐pen nanolithography of NP‐functionalized enzymes on Si surfaces yields biocatalytic templates that enable the orthogonal evolution of nanowires consisting of different metals.

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Effects of inhaled cholinesterase inhibitors on bronchial tonus and on plasma and erythrocyte acetylcholine estarase activity in rats

Cited by 21 publications

References 14 publications

Identification of mechanisms involved in the acute airway toxicity induced by parathion

Identification of mechanisms involved in the acute airway toxicity induced by parathion

An Os^II–Bisbipyridine–4‐Picolinic Acid Complex Mediates the Biocatalytic Growth of Au Nanoparticles: Optical Detection of Glucose and Acetylcholine Esterase Inhibition

Growing Metal Nanoparticles by Enzymes

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Effects of inhaled cholinesterase inhibitors on bronchial tonus and on plasma and erythrocyte acetylcholine estarase activity in rats

Cited by 21 publications

References 14 publications

Identification of mechanisms involved in the acute airway toxicity induced by parathion

Identification of mechanisms involved in the acute airway toxicity induced by parathion

An OsII–Bisbipyridine–4‐Picolinic Acid Complex Mediates the Biocatalytic Growth of Au Nanoparticles: Optical Detection of Glucose and Acetylcholine Esterase Inhibition

Growing Metal Nanoparticles by Enzymes

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An Os^II–Bisbipyridine–4‐Picolinic Acid Complex Mediates the Biocatalytic Growth of Au Nanoparticles: Optical Detection of Glucose and Acetylcholine Esterase Inhibition