scholarly journals Effects of tobacco smoke inhalation on the morphology and cell proliferation rate in Wistar rats submandibular glands

2021 ◽  
Vol 10 (8) ◽  
pp. e28510817327
Author(s):  
Lorraine Stephanie Hiss ◽  
Anna Cecília Dias Maciel Carneiro ◽  
Rodrigo César Rosa ◽  
Adilha Misson Rua Micheletti ◽  
José Batista Volpon ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Wistar Rats ◽  
Cellular Proliferation ◽  
Proliferation Rate ◽  
Smoke Inhalation ◽  
Homogeneity Test ◽  
Serum Cotinine ◽  
Submandibular Glands ◽  
T1 And T2

Cigarette smoke compromises the salivary glands, altering saliva. Cotinine is the most effective biomarker to assess tobacco consumption, and passive smokers are characterized by serum cotinine levels above 2.1 ng/mL. This study aimed to evaluate the effect of exposure to cigarette smoke on rats submandibular glands. The morphology, the proliferative cells of intercalated ducts (immunohistochemistry for KI-67) and its correlation with serum cotinine levels were analyzed. Wistar rats were grouped: control (C); inhalation of smoke for 30 days (T1) and 60 days (T2). Data were analyzed with the Levene variance homogeneity test, Spearman's test, ANOVA and Tukey's post-test, with significance p<0.05. Morphology showed a preserved parenchyma in C, and altered secretory cells in T1 and T2. There was a significant reduction in the number of proliferative cells [ANOVA, F = 4.726; d.f. = 2, 26; p<0.05]: C vsT1 (p<0.05) and C vs T2 (p<0.05). T1 and T2 serum cotinine levels were significantly higher (p<0.05) than C. There was a significant negative correlation [ρ = -0.418, n=27, p<0.05] between serum cotinine levels and the rate of cellular proliferation. These results suggest that of tobacco smoke inhalation has a decreased of the cellular proliferation rate and altered morphology in submandibular glands de ratos Wistar.

Inhalation toxicity studies on cigarette smoke III. Tobacco smoke inhalation dosimetry study on rats

Toxicology ◽  
1976 ◽  
Vol 6 (2) ◽  
pp. 207-217 ◽  
Author(s):  
R. Binns ◽  
J.L. Beven ◽  
Lynda V. Wilton ◽  
W.G.D. Lugton
Keyword(s):  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Smoke Inhalation ◽  
Inhalation Toxicity ◽  
Toxicity Studies

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.

An experimental study of the influences of tobacco smoke on fertility and reproduction

1999 ◽  
Vol 18 (4) ◽  
pp. 272-278 ◽  
Author(s):  
Ewa Florek ◽  
Andrzej Marszalek
Keyword(s):  
Experimental Study ◽  
Carbon Monoxide ◽  
Tobacco Smoke ◽  
Female Rats ◽  
Dose Effect ◽  
Smoke Inhalation ◽  
Initial Number ◽  
Cigarette Brand ◽  
Duration Of Pregnancy ◽  
Parent Generation

1 The aim of this study was to evaluate the toxicological influence of tobacco smoke on fertility and reproduction of Wistar female rats. The influence of tobacco smoke from the Polish ‘Popularne’ cigarette brand was studied. The experiment was conducted on three generations of animals, each generation having two litters. The initial number of animals of the parent generation FO was 192 (128 females and 64 males). Animals were passively exposed to tobacco smoke in three different concentrations based on the content of carbon monoxide (500, 1000 and 1500 mg of CO per cubic meter of air). Animals were exposed to tobacco smoke for 6 h a day, 5 days a week, during 11 weeks. 2 The analysis of indices of mating and fertility revealed the decrease in those indices with animals exposed to tobacco smoke. We also observed an increased number of mothers breading among animals exposed to tobacco smoke. In animals exposed to tobacco smoke, the dose-effect or dose-response dependencies for mating, fertility and delivery indices were found. There was no influence of tobacco smoke on the duration of pregnancy. 3 Tobacco smoke inhalation caused increased levels of carboxyhaemoglobin. 4 Tobacco smoke did not change the duration of pregnancy in rats.

Contractile Performance of Rat Myocardium after Chronic Tobacco Smoke Inhalation

1982 ◽  
Vol 37 (2) ◽  
pp. 93-97 ◽  
Author(s):  
Wesley W. Brooks ◽  
Oscar H. L. Bing ◽  
Gary L. Huber ◽  
Walter H. Abelmann
Keyword(s):  
Tobacco Smoke ◽  
Smoke Inhalation ◽  
Rat Myocardium ◽  
Contractile Performance

Comparison of Oxidative Effects of Electronic Cigarette and Tobacco Smoke Exposure Performed Experimentally

2021 ◽  
pp. 1-7
Author(s):  
Oktay Aslaner
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Electronic Cigarette ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Exposure Group ◽  
Oxidative Effects

<b><i>Objective:</i></b> Cigarette smoking is a life-threatening habit that has rapidly spread in every socioeconomic part of the public worldwide. There exist mechanisms of nicotine delivery available to use in the hope of halting cigarette smoking, and the electronic cigarette (EC) is one of the common methods used for tobacco smoking replacement. This study aimed to investigate experimentally the oxidative effects of tobacco smoke and EC smoke which contain nicotine. <b><i>Method:</i></b> We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (<i>N</i> = 8); the electronic cigarette group (<i>N</i> = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (<i>N</i> = 8), exposure to traditional cigarette smoke for 2 h per day. After the first and second week of exposure, blood samples were obtained, and serum oxidative stress index (OSI), paraoxonase 1 (PON1) activity, and prolidase levels were evaluated. <b><i>Results:</i></b> Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (<i>p</i> &#x3c; 0.001) when compared with the control group, and partial decrements were observed in the second week. By contrast, elevated PON1 levels were observed in the second week after EC or tobacco smoke exposure. The highest OSI levels were observed in the tobacco smoke group (<i>p</i> &#x3c; 0.001). The lowest values of PON1 levels were detected in the first week of the electronic cigarette smoke group, and this decremental value was statistically different than normal, the second week of the electronic cigarette smoke group, the first week of the traditional cigarette smoke exposure group, and the second week of the traditional cigarette smoke exposure group values (<i>p</i> &#x3c; 0.000). <b><i>Conclusion:</i></b> Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.

scholarly journals The Composition of Cigarette Smoke. An Historical Perspective of Several Polycyclic Aromatic Hydrocarbons

2009 ◽  
Vol 23 (6) ◽  
pp. 384-410 ◽  
Author(s):  
A Rodgman ◽  
LC Cook
Keyword(s):  
Polycyclic Aromatic Hydrocarbons ◽  
Melting Point ◽  
Cigarette Smoke ◽  
Aromatic Hydrocarbons ◽  
Tobacco Smoke ◽  
Individual Component ◽  
Complex Mixtures ◽  
Polycyclic Aromatic ◽  
The Individual ◽  
Cigarette Mainstream Smoke

AbstractBecause of the significant advancements in fractionation, analytical, and characterization technologies since the early 1960s, hundreds of components of complex mixtures have been accurately characterized without the necessity of actually isolating the individual component. This has been particularly true in the case of the complex mixtures tobacco and tobacco smoke. Herein, an historical account of a mid-1950 situation concerning polycyclic aromatic hydrocarbons (PAHs) in cigarette smoke is presented. While the number of PAHs identified in tobacco smoke has escalated from the initial PAH, azulene, identified in 1947 to almost 100 PAHs identified by late 1963 to more than 500 PAHs identified by the late 1970s, the number of PAHs isolated individually and characterized by several of the so-called classical chemical means (melting point, mixture melting point, derivative preparation and properties) in the mid-1950s and since is relatively few, 14 in all. They were among 44 PAHs identified in cigarette mainstream smoke and included the following PAHs ranging from bicyclic to pentacyclic: Acenaphthylene, 1,2-dihydroacenaphthylene, anthracene, benz[a]anthracene, benzo[a]pyrene, chrysene, dibenz[a, h]anthracene, fluoranthene, 9H-fluorene, naphthalene, 1-methylnaphthalene, 2-methylnaphthalene, phenanthrene, and pyrene. One of them, benzo[a]pyrene, was similarly characterized in another study in 1959 by Hoffmann.

scholarly journals GAMBARAN HISTOPATOLOGI PARU TIKUS WISTAR SETELAH DIBERI PAPARAN ASAP ROKOK

2018 ◽  
Vol 2 (2) ◽  
Author(s):  
Novera Herdiani ◽  
Endah Budi Permana Putri
Keyword(s):  
Oxidative Stress ◽  
Alveolar Macrophage ◽  
Cigarette Smoke ◽  
Wistar Rats ◽  
Positive Control ◽  
Negative Control ◽  
Control Treatment ◽  
Rat Lung ◽  
Dragon Fruit ◽  
Lung Histopathology

Abstract: Cigarette smoke is the main cause of lung obstruction. One of the obstructions in real that iscaused by cigarette smoke is oxidative stress. Oxidative stress trigger inflammation response occur andlung obstruction. Cigarette smoke able to cause lung histopathology changes like lungs obstruction onalveolus wall. Red dragon fruit extract tackle free radical then able to against the oxidative stress. Theobjective of this study to examines the image of rat lung histopathology under exposed cigarette smoke.Twenty four Wistar rats divided four groups: negative control, positive control, red dragon fruit extracttreatment of 7,2 g/200 g WB, and red dragon fruit extract10,8 g/200 g WB. Negative control only givenstandard feed. Positive control given standar feed and exposed 21 cigarette per day. Treatment groupgiven feed during 21 days. In the 22nd day rats be sacrificed, the lung taken out for observation andimage of rat lung histopathology changes by making lung organ histopathology preparationhematoxicillin Eosion (HE) staining and observed under magnification light microscope 400x. The endresult of the study indicate the finding of changes in lung histopathology such as obstruction level overthe lung tissue higher, alveolar macrophage covered alveoli after being exposed cigarette smoke. Groupwhich does not exposed cigarette smoke, lung alveolus macrophage in normal condition, there are noobstruction or alveolus macrophage occurred, its alveolar macrophage does no covering alveoli.Treatment group administered fruit dragon extract dose 10,8 g/200 g WB and dose 7,2 g/200 g WB seemalmost the same with negative control treatment. Conclusion of the research is cigarette smoke exposecan influence the number of alveolar macrophage on wistar rats. Suggestion very required furtherresearch on oxdative stress parameter.

Sign in / Sign up

Export Citation Format

Share Document