Chronic Effects of Long Term Cigarette Smoke Inhalation upon the Development of Oxygen Debt Capacity in Albino Mice

Author(s):  
Donald H. Puretz
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.


1996 ◽  
Vol 17 (4) ◽  
pp. S26
Author(s):  
D.W. Lee ◽  
H.O. Sohn ◽  
H.B. Lim ◽  
Y.G. Lee ◽  
E.K. Choi ◽  
...  

Impact ◽  
2020 ◽  
Vol 2020 (3) ◽  
pp. 63-65
Author(s):  
Tomomi Higashi

Talk to any allergy sufferer and they will tell you how awful it can be. Runny noses, itchy eyes, coughing and difficulties breathing. For many these symptoms rise only to the level of annoyance and can be avoided by steering clear of the source of their allergy. What many people don't realise though is that allergies can become a far more serious issue for a large segment of the population. Shortness of breath and difficulty breathing due to allergies bring many people to emergency rooms and these are just the acute symptoms. Along with the potential for an allergic attack during a windy or dusty day, researchers and medical professionals are beginning to recognise that there are chronic, long term effects associated with allergies. In order to mitigate both the acute and chronic effects of allergies a better understanding of how genetic factors combine with environmental conditions to produce the ranges of symptoms and effects of allergy suffers is needed. Professor Tomomi Higashi, from the Department of Hygiene at Kanazawa University in Japan, is an expert in this field and is currently working to improve treatment and prevention of allergic disease.


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.


2015 ◽  
Vol 34 (4) ◽  
pp. 325-335 ◽  
Author(s):  
Masanao Yokohira ◽  
Nozomi Hashimoto ◽  
Toshitaka Nakagawa ◽  
Yuko Nakano ◽  
Keiko Yamakawa ◽  
...  

The present study was conducted to examine the chronic effects of potassium octatitanate fibers (trade name TISMO; chemical formula K2O·6TiO2) on the mouse lung and thoracic cavity. This method of infusion was employed to examine the direct effects of the fibers to the pleura. In the present study, 52- and 65-week experiments were employed to examine the long-term chronic effects after infusion of fiber-shaped TISMO into the thoracic cavities of A/J mice. Following this infusion, TISMO fibers were observed in the alveoli, indicating penetration through the visceral pleura. The additional histopathological detection of TISMO fibers in the liver, spleen, kidneys, ovary, heart, bone marrow, and brain of TISMO-infused mice indicated migration of the fibers out from the thoracic cavity. Atypical mesothelial cells with severe pleural proliferation were observed, but malignant mesotheliomas were not detected. This study demonstrated that intrathoracic infusion of TISMO fiber did not cause malignant mesothelioma but did cause severe chronic inflammation and proliferation of pleural mesothelial cells.


1992 ◽  
Vol 133 (2) ◽  
pp. R9-R11
Author(s):  
A.M. Wood ◽  
S.P. Bidey ◽  
J. Soden ◽  
W.R. Robertson

ABSTRACT We have studied the chronic effects of TSH (100μU/ml) and insulin (10μg/ml) on intracellular pH (pHi) in FRTL-5 cells using the pH sensitive probe 2′7-bis (2-carboxyethyl-5′-6′) carboxyfluorescein. FRTL-5 cells were cultured on Petri dishes either in the presence of 4H, ie. Coons F-12 containing cortisol (10nM), transferrin (0.5μg/ml), glycyl-histidyl lysine acetate (10ng/ml) and somatostatin (10μg/ml), or with 4H+insulin (5H), 4H+TSH, or 4H+TSH+insulin (6H). pHi was measured in small groups of cells by microspectrofluorimetry both in the presence and absence of bicarbonate ions after cells had been deprived of serum for at least a day. In


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

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