The influence of anaesthetic agents on the formation of methaemoglobin induced by aniline in cats

McLean, Sheila A.M.; Robinson, J.A.; Starmer, G. A.; Thomas, Jack

doi:10.1111/j.2042-7158.1967.tb09547.x

Cited by 10 publications

(2 citation statements)

References 6 publications

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“…Undoubtedly, this is a reflection of the fact that the cytochrome P-450 is a family of enzymes rather than a single protein and that inhibitors of this system show a high selectivity in their inhibitory effects on the different isozymes (Knodell et a1 1991). Thus 4aminopropriophenone-induced methaemoglobinaemia in the mouse (Smith et al 1967) and aniline-induced methaemoglobinaemia in the cat (McLean et al 1967) and mouse (Ali 1987) are not affected by SKF525A. However, this agent is able to inhibit the methaemoglobin-forming activity of 3,4-dichloroaniline in the mouse (Singleton & Murphy 1973) and the N-oxidation of 4-chloroaniline (Uehleke 1972) and dapsone (Cucinell et a1 1972) in the rat.…”

Section: Discussionmentioning

confidence: 99%

A Dapsone-induced Blood Dyscrasia in the Mouse: Evidence for the Role of an Active Metabolite

Ahmadi¹,

Khalaf²,

Smith³

et al. 1996

Journal of Pharmacy and Pharmacology

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In the female mouse, dapsone (50-500 mg kg-1, p.o.) caused a dose-related methaemoglobinaemia which peaked at 0.5-1 h with recovery to baseline values occurring by 4 h. Cimetidine (100 mg kg-1, p.o.), a known inhibitor of several hepatic P450 isozymes administered 1 h before dapsone, prevented the methaemoglobinaemia. In-vitro, dapsone required activation by mouse hepatic microsomes to cause methaemoglobin formation in mouse erythrocytes and cytotoxicity to human mononuclear leucocytes. In both instances, the toxic effects were markedly reduced by cimetidine. Daily dosing of mice with dapsone (50 mg kg-1, p.o.) for 3 weeks induced a blood dyscrasia, characterized by a fall of platelet and white blood cell counts, which was inhibited by cimetidine (100 mg kg-1, p.o. daily). It is concluded that an active metabolite of dapsone arising from a P450-dependent pathway is involved in the genesis not only of the methaemoglobinaemia but also the blood dyscrasia arising from repeated administration of the drug in this species.

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Section: Discussionmentioning

confidence: 99%

A Dapsone-induced Blood Dyscrasia in the Mouse: Evidence for the Role of an Active Metabolite

Ahmadi¹,

Khalaf²,

Smith³

et al. 1996

Journal of Pharmacy and Pharmacology

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“…Extensive experiments in diverse animal species fed with toxic oil or administered aniline derivatives have failed to reproduce the full spectrum of the disease (1,25,26). This may suggest a species-specific toxicity for humans; in this respect, species differences in aniline toxicity have been recognized for decades and attributed to metabolism differences (27)(28)(29)(30).…”

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confidence: 99%

Pharmacogenetic Profile of Xenobiotic Enzyme Metabolism in Survivors of the Spanish Toxic Oil Syndrome

Ladona¹,

Izquierdo-Martinez²,

Паз³

et al. 2001

Environmental Health Perspectives

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Among food-related toxic outbreaks that have occurred in the world, the Spanish toxic oil syndrome (TOS) emerges as a significant disaster because of the degree of severity and the huge population involved (1,2). In May 1981 the TOS appeared in Madrid and northwestern areas of Spain as a unique disease caused by the ingestion of adulterated rapeseed oil denatured with aniline (3-7). More than 20,000 people were affected; of these, over 11,000 required hospitalization and over 300 deaths were registered in the first 2 years (1,8). Although the majority of patients recovered after a long period, 30-40% continue to suffer mild symptoms or severe sequelae (9-12). TOS was characterized as a multisystemic disease with three consecutive phases. In the acute phase (1-2 months), patients presented fever, rash, eosinophilia, pulmonary edema, and myalgia. Many patients (59%) progressed to an intermediate phase with pulmonary hypertension, thromboembolism, persistent myalgia and eosinophilia, skin edema, alopecia, and sicca syndrome. The clinical signs of the chronic phase were principally pulmonary hypertension, scleroderma, peripheral neuropathy, and liver disease.

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Biomonitoring of aromatic amines II: hemoglobin binding of some monocyclic aromatic amines

Birner

Neumann

1988

Arch Toxicol

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Covalent binding of 13 monocyclic aromatic amines to hemoglobin was studied in female Wistar rats and hemoglobin binding indices were determined. The hemoglobin adducts were hydrolyzed under alkaline conditions. In all cases the parent amine could be identified by gas chromatography and with one exception represented the only cleavage product. The binding index varied considerably and was highest with p-chloroaniline (569) and lowest with 2,4,5-trimethylaniline (0.7). Five compounds were also studied in female B6C3F1 mice. Hemoglobin binding was lower than in rats, but to varying degrees. Hemoglobin binding correlated remarkably well with the maximum methemoglobin level achieved with the six examples studied. The results support the notion that the reaction of nitrosoarenes, as metabolites of arylamines, with hemoglobin represents a general pathway in vivo. The analysis of such hemoglobin adducts is recommended as a dosimeter in biological monitoring of humans in order to control exposure. It is too early, however, to assess the carcinogenic risk from hemoglobin binding data with these compounds.

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The influence of anaesthetic agents on the formation of methaemoglobin induced by aniline in cats

Cited by 10 publications

References 6 publications

A Dapsone-induced Blood Dyscrasia in the Mouse: Evidence for the Role of an Active Metabolite

A Dapsone-induced Blood Dyscrasia in the Mouse: Evidence for the Role of an Active Metabolite

Pharmacogenetic Profile of Xenobiotic Enzyme Metabolism in Survivors of the Spanish Toxic Oil Syndrome

Biomonitoring of aromatic amines II: hemoglobin binding of some monocyclic aromatic amines

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