Cigarette smoke inhalation study for lung tumorigenicity in A/J mice

2010 ◽  
Vol 01 (01) ◽  
Author(s):  
R. B. Lichtner ◽  
B. Friedrichs ◽  
A. Buettner ◽  
F. Van Overveld ◽  
W. Stinn
Keyword(s):  
Cigarette Smoke ◽  
Smoke Inhalation ◽  
Inhalation Study

Comparative 13-week cigarette smoke inhalation study in Sprague–Dawley rats: Evaluation of cigarettes with two banded cigarette paper technologies

2007 ◽  
Vol 45 (6) ◽  
pp. 1076-1090 ◽  
Author(s):  
Eugenia H. Theophilus ◽  
W. Keith Shreve ◽  
Paul H. Ayres ◽  
Charles D. Garner ◽  
Deborah H. Pence ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Smoke Inhalation ◽  
Sprague Dawley ◽  
Inhalation Study ◽  
Sprague Dawley Rats ◽  
Cigarette Paper

scholarly journals Comprehensive systems biology analysis of a 7-month cigarette smoke inhalation study in C57BL/6 mice

2016 ◽  
Vol 3 (1) ◽  
Author(s):  
Sam Ansari ◽  
Karine Baumer ◽  
Stéphanie Boué ◽  
Sophie Dijon ◽  
Remi Dulize ◽  
...  
Keyword(s):  
Systems Biology ◽  
Cigarette Smoke ◽  
Smoke Inhalation ◽  
Inhalation Study

scholarly journals A 7-month inhalation toxicology study in C57BL/6 mice demonstrates reduced pulmonary inflammation and emphysematous changes following smoking cessation or switching to e-vapor products

2021 ◽  
Vol 5 ◽  
pp. 239784732199587
Author(s):  
Ashutosh Kumar ◽  
Ulrike Kogel ◽  
Marja Talikka ◽  
Celine Merg ◽  
Emmanuel Guedj ◽  
...  
Keyword(s):  
Smoking Cessation ◽  
Cigarette Smoke ◽  
Pulmonary Inflammation ◽  
Clinical Signs ◽  
Inhalation Study ◽  
Toxicology Study ◽  
Nasal Tissue ◽  
Product Switching ◽  
The Impact

Cigarette smoking causes serious diseases, including lung cancer, atherosclerotic coronary artery disease, peripheral vascular disease, chronic bronchitis, and emphysema. While cessation remains the most effective approach to minimize smoking-related disease, alternative non-combustible tobacco-derived nicotine-containing products may reduce disease risks among those unable or unwilling to quit. E-vapor aerosols typically contain significantly lower levels of smoke-related harmful and potentially harmful constituents; however, health risks of long-term inhalation exposures are unknown. We designed a 7-month inhalation study in C57BL/6 mice to evaluate long-term respiratory toxicity of e-vapor aerosols compared to cigarette smoke and to assess the impact of smoking cessation (Cessation group) or switching to an e-vapor product (Switching group) after 3 months of exposure to 3R4F cigarette smoke (CS). There were no significant changes in in-life observations (body weights, clinical signs) in e-vapor groups compared to the Sham Control. The 3R4F CS group showed reduced respiratory function during exposure and had lower body weight and showed transient signs of distress post-exposure. Following 7 months of exposure, e-vapor aerosols resulted in no or minimal increase in pulmonary inflammation, while exposure to 3R4F CS led to impairment of lung function and caused marked lung inflammation and emphysematous changes. Biological changes observed in the Switching group were similar to the Cessation group. 3R4F CS exposure dysregulated the lung and nasal tissue transcriptome, while these molecular effects were substantially lower in the e-vapor group. Results from this study demonstrate that in comparison with 3R4F CS, e-vapor aerosols induce substantially lower biological responses including pulmonary inflammation and emphysematous changes, and that complete switching from CS to e-vapor products significantly reduces biological changes associated with CS in C57BL/6 mice.

scholarly journals Cigarette smoke inhalation aggravates diabetic kidney injury in rats

2019 ◽  
Vol 8 (6) ◽  
pp. 964-971 ◽  
Author(s):  
Songling Jiang ◽  
Do Van Quan ◽  
Jae Hyuck Sung ◽  
Moo-Yeol Lee ◽  
Hunjoo Ha
Keyword(s):  
Kidney Disease ◽  
Cigarette Smoke ◽  
Density Lipoprotein ◽  
Kidney Injury ◽  
Diabetic Rats ◽  
Smoke Inhalation ◽  
Lipoprotein Cholesterol ◽  
Sprague Dawley ◽  
Experimental Conditions ◽  
Diabetic Kidney

Abstract Diabetic kidney disease (DKD) is the leading cause of end-stage kidney disease. Epidemiological studies have demonstrated that cigarette smoke or nicotine is a risk factor for the progression of chronic kidney injury. The present study analyzed the kidney toxicity of cigarette smoke in experimental rats with DKD. Experimental diabetes was induced in 7-week-old Sprague-Dawley rats by a single intraperitoneal injection of streptozotocin (60 mg kg−1). Four weeks after the induction of diabetes, rats were exposed to cigarette smoke (200 μg L−1), 4 h daily, and 5 days per week for 4 weeks. Cigarette smoke did not affect the levels of plasma glucose, hemoglobin A1c, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol or non-esterified fatty acids in both control and diabetic rats under the experimental conditions. Cigarette smoke, however, significantly increased diabetes-induced glomerular hypertrophy and urinary kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) excretion, suggesting exacerbation of diabetic kidney injury. Cigarette smoke promoted macrophage infiltration and fibrosis in the diabetic kidney. As expected, cigarette smoke increased oxidative stress in both control and diabetic rats. These data demonstrated that four weeks of exposure to cigarette smoke aggravated the progression of DKD in rats.

Effects of chronic cigarette smoke inhalation on the development of senile lung in senescence-accelerated mouse

1997 ◽  
Vol 197 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Shinji Teramoto ◽  
Yasuhide Uejima ◽  
Teruaki Oka ◽  
Kazuko Teramoto ◽  
Takeshi Matsuse ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Smoke Inhalation ◽  
Senescence Accelerated Mouse

Cigarette Smoke Inhalation Studies in Inbred Syrian Hamsters

1974 ◽  
pp. 320-330 ◽  
Author(s):  
Freddy Homburger ◽  
Peter Bernfeld ◽  
A. B. Russfield
Keyword(s):  
Cigarette Smoke ◽  
Smoke Inhalation ◽  
Syrian Hamsters

scholarly journals Oral Leukoplakia and Costochondral Hyperplasia Induced by Diethylnitrosamine in Hamsters Exposed to Cigarette Smoke with or without Dietary Vitamin C

1987 ◽  
Vol 24 (3) ◽  
pp. 257-264 ◽  
Author(s):  
T. Harada ◽  
A. Enomoto ◽  
T. Kitazawa ◽  
K. Maita ◽  
Y. Shirasu
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Vitamin C ◽  
Cigarette Smoke ◽  
Precancerous Lesions ◽  
Costal Cartilage ◽  
Oral Leukoplakia ◽  
Smoke Inhalation ◽  
Dietary Vitamin ◽  
Scanning Electron

Male Syrian golden hamsters receiving 12 weekly subcutaneous injections of diethylnitrosamine (DEN) were subjected to cigarette smoke inhalation and fed a diet with or without 1% vitamin C supplement for a period of 58 weeks. Another group was a sham-smoked control and was not fed vitamin C. Tissues of the oral cavity and costal cartilage were examined by light and/or scanning electron microscopy. Oral leukoplakia and costochondral hyperplasia occurred with high frequency in all groups treated with DEN. Leukoplakic lesions were found in the palate, tongue, and pharynx; the early change was focal erosion with mild epithelial hyperplasia and inflammatory cell infiltration. Advanced lesions had marked mucosal thickening due to acanthosis, parakeratosis, hyperkeratosis, and submucosal infiltration of lymphocytes and plasma cells. Precancerous lesions were noted in tongue and pharynx. Scanning electron microscopy of tongues revealed destruction of filiform papillae. The incidence of leukoplakic lesions was higher in smoke-exposed hamsters than in controls, but the incidence in vitamin C-supplemented hamsters was low when compared with the smoke-exposed hamsters without vitamin C. Costochondral hyperplasia was initiated by thickening of the perichondrium followed by proliferation of chondrocytes. Costochondral hyperplasia appeared earlier, and the incidence was higher in the vitamin C-supplemented hamsters. It could not be determined whether costochondral hyperplasia was the primary lesion induced by DEN or secondary change.

Acute effect of cigarette smoke on cytoplasmic motility of alveolar macrophages in dogs

1989 ◽  
Vol 66 (3) ◽  
pp. 1172-1178 ◽  
Author(s):  
M. Yamaya ◽  
K. Zayasu ◽  
K. Sekizawa ◽  
K. Yamauchi ◽  
S. Shimura ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Alveolar Macrophages ◽  
Lower Lobe ◽  
The Body ◽  
Sensory Nerves ◽  
Smoke Inhalation ◽  
Base Line ◽  
Particle Rotation ◽  
Lobe Bronchus

To study effects of cigarette smoke on the cytoplasmic motility (CM) of alveolar macrophages (AM), we measured remanent field strength (RFS) in dogs in vivo. Four days after instillation of ferrimagnetic particles (Fe3O4, 3 mg/kg) into the right lower lobe bronchus, RFS was measured at the body surface immediately after magnetization of the Fe3O4 particles by an externally applied magnetic field. RFS decreased with time due to particle rotation (relaxation), which is thought to be inversely related to CM of AM (J. Appl. Physiol. 55: 1196–1202, 1983). The initial relaxation curve was fitted to an exponential function. The relaxation rate (lambda 0) increased during cigarette smoke inhalation and returned to base-line values within 15 min. With the inhalation of the smoke of up to five cigarettes, peak lambda 0 was increased; with a further increase in the number of cigarettes, the effect of cigarette smoke decreased or disappeared. Nicotine injection and acetylcholine inhalation increased respiratory resistance to a degree similar to that observed with cigarette smoke but did not change lambda 0. However, either substance P (SP) or capsaicin injection increased lambda 0 in a fashion similar to that noted with cigarette smoke inhalation. Repeated administration of SP produced a significant tachyphylaxis of the effect, and capsaicin did not increase lambda 0 after the cigarette smoke-induced tachyphylaxis of the effect. Colchicine inhibited the cigarette smoke-induced increase in lambda 0. These results suggest that cigarette smoke increases CM of AM, probably through the release of tachykinins including SP from sensory nerves in the lung.

Sign in / Sign up

Export Citation Format

Share Document