Diesel exhaust-induced airway hyperresponsiveness in c-Ha- ras transgenic mice

Recently the quantity of diesel exhaust (DE) emissions, which contain a variety of chemicals and can induce pulmonary carcinoma in animals, has been increasing in Japan. To assess the toxicity of DE, we evaluated airway hyperresponsiveness after exposure to DE in the rasH2 (CB6F1-TgH ras2) mouse, wh...

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Bibliographic Details
Published in:Toxicology (Amsterdam) 2001-06, Vol.163 (2), p.145-152
Main Authors: Birumachi, Jun-ichi, Suzuki, Akira K., Itoh, Kikuji, Hioki, Kyoji, Maruyama, Chika, Ohnishi, Yasuyuki
Format: Article
Language:English
Subjects:
Acetylcholine
Airway hyperresponsiveness
Airway Resistance - drug effects
Animals
Biological and medical sciences
Body Weight
Bronchoconstriction
c-Ha- ras gene
Chemical and industrial products toxicology. Toxic occupational diseases
diesel
Diesel exhaust
Gas, fumes
Gene Expression
Genes, ras
Male
Medical sciences
Mice
Mice, Transgenic
Respiratory Hypersensitivity - etiology
Respiratory Hypersensitivity - physiopathology
Time Factors
Toxicology
Tracheostomy
Transgenic mice
Vehicle Emissions - toxicity
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Summary:Recently the quantity of diesel exhaust (DE) emissions, which contain a variety of chemicals and can induce pulmonary carcinoma in animals, has been increasing in Japan. To assess the toxicity of DE, we evaluated airway hyperresponsiveness after exposure to DE in the rasH2 (CB6F1-TgH ras2) mouse, which carries c-Ha- ras genes and shows marked sensitivity to treatment with various genotoxic carcinogens such as methylnitrosourea and dimethylbenzanthracene. We exposed rasH2 mice ( n=18) and their nontransgenic littermates ( n=19) to room air or 3 mg/m 3 DE for 4 weeks, measured their respiratory resistance (Rrs) during inhalation of acetylcholine (ACh; 0.005, 0.01, 0.02, 0.04, 0.08, 0.16, 0.31, 0.63, 1.28, 2.5, 5, or 10 mg/ml) for 2 min, and calculated the provocative ACh concentration needed to cause a 50% increase (PC 150) in Rrs. At all doses of ACh, Rrs was significantly higher ( P
ISSN:0300-483X
1879-3185
DOI:10.1016/S0300-483X(01)00393-6