The Antagonism of Curarizing Activity by Phenolic Substances*

Mogey, G. A.; Young, P. A.

doi:10.1111/j.1476-5381.1949.tb00562.x

Cited by 16 publications

(7 citation statements)

References 7 publications

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“…One could speculate that such an action is consistent with known effects of ethanol to increase Renshaw cell activity, a neuron activated by cholinergic collaterals from motor neurons. It is also consonant with the rather old observation that ethanol and other alcohols potentiate ACh actions and antagonize neuromuscular block produced by tubocurarine (NELEMANS, 1962;SACHDEV et aI., 1963), as do catechol and certain phenols (HOBBIGER, 1952;RUMMEL and SCHMITZ, 1954;MOGEY and YOUNG, 1949;BLABER and GALLAGHER, 1971).…”

Section: Evidence From the Skeletal Neuromuscular Junctionsupporting

confidence: 70%

The Pharmacology of Sedative/Hypnotics, Alcohol, and Anesthetics: Sites and Mechanisms of Action

Smith¹

1977

Drug Addiction I

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Section: Evidence From the Skeletal Neuromuscular Junctionsupporting

confidence: 70%

The Pharmacology of Sedative/Hypnotics, Alcohol, and Anesthetics: Sites and Mechanisms of Action

Smith¹

1977

Drug Addiction I

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“…25 Early studies suggested that HQ and related phenols increase the size of end-plate potentials in peripheral motor nerve terminals without altering acetylcholine sensitivity, 36 and that HQ does not possess anticholinesterase activity. 37 A CNS activation mechanism involving both presynaptic and postsynaptic actions has been proposed. 38 Acute exposure to HQ in humans by accidental or deliberate ingestion is also associated with CNS and other effects, although the attribution of specific signs and symptoms is frequently clouded by the presence of other components and by the difficulty in accurately establishing exposure levels.…”

Section: Acute Effects Of Hqmentioning

confidence: 99%

The Toxicology of Hydroquinone — Relevance to Occupational and Environmental Exposure

DeCaprio¹

1999

Critical Reviews in Toxicology

175

128

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Hydroquinone (HQ) is a high-volume commodity chemical used as a reducing agent, antioxidant, polymerization inhibitor, and chemical intermediate. It is also used in over-the-counter (OTC) drugs as an ingredient in skin lighteners and is a natural ingredient in many plant-derived products, including vegetables, fruits, grains, coffee, tea, beer, and wine. While there are few reports of adverse health effects associated with the production and use of HQ, a great deal of research has been conducted with HQ because it is a metabolite of benzene. Physicochemical differences between HQ and benzene play a significant role in altering the pharmacokinetics of directly administered when compared with benzene-derived HQ. HQ is only weakly positive in in vivo chromosomal assays when expected human exposure routes are used. Chromosomal effects are increased significantly when parenteral or in vitro assays are used. In cancer bioassays, HQ has reproducibly produced renal adenomas in male F344 rats. The mechanism of tumorigenesis is unclear but probably involves a species-, strain-, and sex-specific interaction between renal tubule toxicity and an interaction with the chronic progressive nephropathy that is characteristic of aged male rats. Mouse liver tumors (adenomas) and mononuclear cell leukemia (female F344 rat) have also been reported following HQ exposure, but their significance is uncertain. Various tumor initiation/promotion assays with HQ have shown generally negative results. Epidemiological studies with HQ have demonstrated lower death rates and reduced cancer rates in production workers when compared with both general and employed referent populations. Parenteral administration of HQ is associated with changes in several hematopoietic and immunologic endpoints. This toxicity is more severe when combined with parenteral administration of phenol. It is likely that oxidation of HQ within the bone marrow compartment to the semiquinone or p-benzoquinone (BQ), followed by covalent macromolecular binding, is critical to these effects. Bone marrow and hematologic effects are generally not characteristic of HQ exposures in animal studies employing routes of exposure other than parenteral. Myelotoxicity is also not associated with human exposure to HQ. These differences are likely due to significant route-dependent toxicokinetic factors. Fetotoxicity (growth retardation) accompanies repeated administration of HQ at maternally toxic dose levels in animal studies. HQ exposure has not been associated with other reproductive and developmental effects using current USEPA test guidelines. The skin pigment lightening properties of HQ appear to be due to inhibition of melanocyte tyrosinase. Adverse effects associated with OTC use of HQ in FDA-regulated products have been limited to a small number of cases of exogenous ochronosis, although higher incidences of this syndrome have been reported with inappropriate use of unregulated OTC products containing higher HQ concentrations. The most serious human health effect related to HQ is p...

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“…Although catechol itself has been shown to possess no anticholinesterase activity (Mogey & Young, 1949) and does not sensitize skeletal muscle acetylcholine receptors to acetylcholine (Blaber & Gallagher, 1971) it does increase the amount of acetylcholine released per nerve impulse at the neuromuscular junction (Otsuka & Nonomura, 1963;Blaber & Gallagher, 1971;Gallagher & Blaber, 1973) and it is possible that a similar presynaptic effect on acetylcholine release is responsible for its central action. This would fit in well with the results for the anticholinesterases and the cholinoceptor blockers and may indicate an action at both muscarinic and nicotinic synapses.…”

Section: Y-aminobutyric Acidmentioning

confidence: 99%

“…Thirdly, the action of catechol at the neuromuscular junction where it increases the amount of acetylcholine liberated per nerve impulse (Mogey & Young, 1949;Blaber & Gallagher, 1971) suggests a possible central cholinergic mechanism for its convulsant activity. Preliminary experiments in which physostigmine was found to potentiate and atropine to block partially the convulsions (Angel, 1969) led some support to this view.…”

Section: Introductionmentioning

confidence: 99%

A Pharmacological Study of the Spontaneous Convulsive Activity Induced by 1,2‐dihydroxybenzene (Catechol) in the Anaesthetized Mouse

Angel

Clarke

Dewhurst

1977

British J Pharmacology

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I The convulsive activity induced by catechol has been examined in anaesthetized mice either by determining the CD50 for the convulsions in drug-treated and control animals, or by studying the effects of various drugs on the total whole body activity. 2 The results indicate that catecholamines play no part in the mechanism of action of catechol. Drugs which alter cerebral catecholamine levels had no effect on the convulsions, nor did the a-and,6-adrenoceptor blocking drugs. 3 5-Hydroxytryptamine (5-HT) could possibly be important, though results with drugs which either change brain 5-HT levels, or block 5-HT receptors were inconsistent. 4 y-Aminobutyric acid also appears not to be involved in the mechanism of action of catechol. SThe results strongly suggest that catechol primarily activates a central cholinergic system, in that muscarinic and nicotinic receptor blocking drugs inhibit, and anticholinesterases potentiate the convulsions.

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The Antagonism of Curarizing Activity by Phenolic Substances*

Cited by 16 publications

References 7 publications

The Pharmacology of Sedative/Hypnotics, Alcohol, and Anesthetics: Sites and Mechanisms of Action

The Pharmacology of Sedative/Hypnotics, Alcohol, and Anesthetics: Sites and Mechanisms of Action

The Toxicology of Hydroquinone — Relevance to Occupational and Environmental Exposure

A Pharmacological Study of the Spontaneous Convulsive Activity Induced by 1,2‐dihydroxybenzene (Catechol) in the Anaesthetized Mouse

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