102 Effect of long-term cigarette smoke inhalation in the brains of IM mice infected with 87V scrapie agent

1996 ◽  
Vol 17 (4) ◽  
pp. S26
Author(s):  
D.W. Lee ◽  
H.O. Sohn ◽  
H.B. Lim ◽  
Y.G. Lee ◽  
E.K. Choi ◽  
...  
1974 ◽  
Vol 8 (2) ◽  
pp. 217-235 ◽  
Author(s):  
W. Dontenwill ◽  
H.-J. Chevalier ◽  
H.-P. Harke ◽  
U. Lafrenz ◽  
G. Reckzeh ◽  
...  

After long-term exposure to cigarette smoke, erythrocyte and haemoglobin levels were higher due to the high carbon monoxide concentration in the smoking chamber. Other values were not affected by the exposure.


2021 ◽  
Vol 5 ◽  
pp. 239784732199587
Author(s):  
Ashutosh Kumar ◽  
Ulrike Kogel ◽  
Marja Talikka ◽  
Celine Merg ◽  
Emmanuel Guedj ◽  
...  

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.


2019 ◽  
Vol 8 (6) ◽  
pp. 964-971 ◽  
Author(s):  
Songling Jiang ◽  
Do Van Quan ◽  
Jae Hyuck Sung ◽  
Moo-Yeol Lee ◽  
Hunjoo Ha

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.


1997 ◽  
Vol 197 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Shinji Teramoto ◽  
Yasuhide Uejima ◽  
Teruaki Oka ◽  
Kazuko Teramoto ◽  
Takeshi Matsuse ◽  
...  

2021 ◽  
Author(s):  
Jader Joel Machado Junqueira ◽  
Juliana Dias Lourenço ◽  
Kaique Rodrigues da Silva ◽  
Vanda Jorgetti ◽  
Rodolfo Vieira ◽  
...  

1974 ◽  
pp. 320-330 ◽  
Author(s):  
Freddy Homburger ◽  
Peter Bernfeld ◽  
A. B. Russfield

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

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