Pulmonary Toxicity of Thioureas in the Rat

Administration of {alpha}-naphthylthiourea (ANTU) to rats causes damage to pulmonary endothelial cells and possibly mesothelial lining cells that together may account for the massive pleural effusion characteristic of thiourea toxicity. Using {sup 35}S-thiourea as a model compound, the extent of bin...

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Bibliographic Details
Published inEnvironmental health perspectives Vol. 85; p. 43
Main Authors Scott, Angus M., Powell, Gillian M., Upshall, David G., Curtis, C. Gerald
Format Journal Article
LanguageEnglish
Published United States 01.04.1990
Subjects
550201 - Biochemistry- Tracer Techniques
560300 - Chemicals Metabolism & Toxicology
ANIMAL TISSUES
ANIMALS
BASIC BIOLOGICAL SCIENCES
BETA DECAY RADIOISOTOPES
BETA-MINUS DECAY RADIOISOTOPES
BODY
CARBONIC ACID DERIVATIVES
DAYS LIVING RADIOISOTOPES
DIGESTIVE SYSTEM
DRUGS
EDEMA
ELECTRON MICROSCOPY
ENDOTHELIUM
EVEN-ODD NUCLEI
GLANDS
GLUTATHIONE
IN VITRO
IN VIVO
ISOTOPES
KIDNEYS
LABELLED COMPOUNDS
LIGHT NUCLEI
LIVER
LUNGS
MAMMALS
MICROSCOPY
MORPHOLOGICAL CHANGES
NUCLEI
ORGANIC COMPOUNDS
ORGANIC SULFUR COMPOUNDS
ORGANS
PATHOLOGICAL CHANGES
PEPTIDES
POLYPEPTIDES
PROTEINS
RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT
RADIOISOTOPES
RADIOPROTECTIVE SUBSTANCES
RATS
RESPIRATORY SYSTEM
RODENTS
SULFUR 35
SULFUR ISOTOPES
SYMPTOMS
THIOUREAS
TISSUES
TOXICITY
TRANSMISSION ELECTRON MICROSCOPY
ULTRASTRUCTURAL CHANGES
UPTAKE
VERTEBRATES
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Summary:Administration of {alpha}-naphthylthiourea (ANTU) to rats causes damage to pulmonary endothelial cells and possibly mesothelial lining cells that together may account for the massive pleural effusion characteristic of thiourea toxicity. Using {sup 35}S-thiourea as a model compound, the extent of binding of {sup 35}S to lung proteins correlated well with the extent of edema, suggesting that the extent of binding of thiourea metabolites is a measure of lung toxicity. ANTU and phenylthiourea (PTU) compete for {sup 35}S binding to lung slices, suggesting that these toxins may act in a similar way. Binding of {sup 35}S in lung slices from resistant rats is much less than in controls, and resistance cannot be explained by differences in either whole body metabolism or redistribution of thiourea in vivo. Lung glutathione levels (in vitro and in vivo) in normal and resistant rats following thiourea administration were essentially the same. However, at doses of thiourea that cause pleural effusion, there was an increase in total lung glutathione.
ISSN:0091-6765
1552-9924
DOI:10.2307/3430664