作者: H Witschi
关键词: Respiratory disease 、 Medicine 、 Pathology 、 Toxicity 、 Carcinogen 、 Adenocarcinoma 、 Lung 、 Andrology 、 Tobacco smoke 、 Nicotine 、 Parenchyma
摘要: Male strain A/J mice were exposed for 6 h a day, 5 days week to environmental tobacco smoke (ETS) generated from Kentucky 1R4F reference cigarettes. Chamber concentrations 87 mg/m 3 of total suspended particulate matter (TSP), 246 p.p.m. CO and 16 nicotine. After months, 33% the ETS 11% control animals had one or several lung tumors; difference was statistically not significant. A second group months allowed recover another 4 in filtered air. When they killed, 85% tumors (average number per lung: 1.4 ± 0.2), whereas 38% all 0.5 0.2). The differences tumor incidence multiplicity More than 80% adenomas, rest adenocarcinomas. pretreated with carcinogen, lower after compared controls injected carcinogen kept However, an additional month recovery period air, multiplicities same plus as carcinogen-treated air-exposed controls. Histopathologic morphometric analysis tissue failed reveal any between animals. immediately exposure, immunohistochemistry revealed increased staining CYP1A1 airway epithelia parenchyma; following disappeared again. Analysis cell kinetics showed initial burst DNA synthesis epithelial cells airways smaller early positive response parenchyma. Feeding butylated hydroxytoluene during exposure did modulate development. It concluded that is pulmonary mice.