Journal Article

Chemoprevention of tobacco-smoke lung carcinogenesis in mice after cessation of smoke exposure

Hanspeter Witschi, Dale Uyeminami, Dexter Moran and Imelda Espiritu

in Carcinogenesis

Volume 21, issue 5, pages 977-982
Published in print May 2000 | ISSN: 0143-3334
Published online May 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.5.977
Chemoprevention of tobacco-smoke lung carcinogenesis in mice after cessation of smoke exposure

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Male strain A/J mice were exposed for 6 h per day, 5 days per week to a mixture of 89% cigarette sidestream smoke and 11% mainstream smoke. Total suspended particulate concentrations were 137 mg/m3. In experiment 1, animals were exposed for 5 months to tobacco smoke and given a 4 month recovery period in air. Lung tumor multiplicity was 2.4 and incidence 89%. Animals exposed to filtered air had 1.0 tumor per lung (65% incidence). In animals kept for 5 months in smoke, removed into air and then fed a diet containing a mixture of myoinositol and dexamethasone, tumor multiplicity was 1.0 and incidence was 62%. These values were significantly (P < 0.01) lower than in animals exposed to smoke and identical to values seen in controls. In animals fed a diet containing 250 mg/kg each of phenethyl isothiocyanate and benzyl isothiocyanate during the entire 9 months, lung tumor multiplicity was 2.1 and incidence 96%, not significantly different from animals exposed to smoke and fed control diet. In experiment 2, animals were exposed for 5 months to smoke, followed by a 4 month recovery period in air and were fed during the entire period a diet containing either d-limonene or 1,4-phenylenebis(methylene)selenoisocyanate (p-XSC). In animals exposed to tobacco smoke and fed control diet, lung tumor multiplicity was 2.8, whereas in the animals fed d-limonene it was 2.6 and in the animals fed p-XSC it was 2.4. The differences to the controls were statistically not significant. It was concluded that myoinositol–dexamethasone successfully prevents the development of tobacco smoke-induced lung tumors even if administered when the animals have `quit' smoking. On the other hand, agents otherwise shown to prevent lung tumor formation following administration of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone or benzo[a]pyrene were ineffective against tobacco smoke.

Keywords: BITC, benzyl isothiocyanate; NNK, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone; p-XSC, 1,4-phenylenebis(methylene)selenoisocyanate; PEITC, phenethyl isothiocyanate.

Journal Article.  5195 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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