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Effect of Cigarette Smoke on Spermatogenesis in Rats  [cached]
Hassan Ahmadnia,Mohsen Ghanbari,Mahmoud Reza Moradi,Mohammad Khaje-Dalouee
Urology Journal , 2007,
Abstract: Introduction: The aim of this study was to evaluate the process of spermatogenesis in rats exposed to the cigarette smoke. Materials and Methods: Thirty adult male rats were divided into 2 groups of cases and controls. An apparatus made especially for this study was used to produce smoke from a commonly used cigarette and expose the rats to the smoke. The rats in the case group were exposed to the cigarette smoke for 10 weeks (90 minutes every day for 6 days in each week). The rats in the control group were meanwhile in the fresh room air. Results: Development of the sperms was mildly reduced in 14 (93.3%) and 4 (26.7%) rats in the case and control groups, respectively (P < .001). The mean average diameter of the seminiferous tubules was reported to be 0.421 ± 0.097 mm and 0.493 ± 0.026 mm in the case and control groups, respectively (P = .04). The mean numbers of Sertoli cells were 9.2 ± 1.2 and 13.3 ± 1.8 in the case and control groups, respectively (P < .001). A concurrent reduction in the number of germ cells and Leydig cells with the decrease in the number of Sertoli cells was seen in the rats of the case group. Conclusion: Cigarette smoke has a rather obvious effect on spermatogenesis in rats which may be due to toxic substances in the cigarette or the histologic reactions due to hypoxemia induced by smoke. Although further documentation, especially in humans is required, the potential impact of smoking on fertility in men should be considered in public health education.
Egr-1 Regulates Autophagy in Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease  [PDF]
Zhi-Hua Chen, Hong Pyo Kim, Frank C. Sciurba, Seon-Jin Lee, Carol Feghali-Bostwick, Donna B. Stolz, Rajiv Dhir, Rodney J. Landreneau, Mathew J. Schuchert, Samuel A. Yousem, Kiichi Nakahira, Joseph M. Pilewski, Janet S. Lee, Yingze Zhang, Stefan W. Ryter, Augustine M. K. Choi
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0003316
Abstract: Background Chronic obstructive pulmonary disease (COPD) is a progressive lung disease characterized by abnormal cellular responses to cigarette smoke, resulting in tissue destruction and airflow limitation. Autophagy is a degradative process involving lysosomal turnover of cellular components, though its role in human diseases remains unclear. Methodology and Principal Findings Increased autophagy was observed in lung tissue from COPD patients, as indicated by electron microscopic analysis, as well as by increased activation of autophagic proteins (microtubule-associated protein-1 light chain-3B, LC3B, Atg4, Atg5/12, Atg7). Cigarette smoke extract (CSE) is an established model for studying the effects of cigarette smoke exposure in vitro. In human pulmonary epithelial cells, exposure to CSE or histone deacetylase (HDAC) inhibitor rapidly induced autophagy. CSE decreased HDAC activity, resulting in increased binding of early growth response-1 (Egr-1) and E2F factors to the autophagy gene LC3B promoter, and increased LC3B expression. Knockdown of E2F-4 or Egr-1 inhibited CSE-induced LC3B expression. Knockdown of Egr-1 also inhibited the expression of Atg4B, a critical factor for LC3B conversion. Inhibition of autophagy by LC3B-knockdown protected epithelial cells from CSE-induced apoptosis. Egr-1?/? mice, which displayed basal airspace enlargement, resisted cigarette-smoke induced autophagy, apoptosis, and emphysema. Conclusions We demonstrate a critical role for Egr-1 in promoting autophagy and apoptosis in response to cigarette smoke exposure in vitro and in vivo. The induction of autophagy at early stages of COPD progression suggests novel therapeutic targets for the treatment of cigarette smoke induced lung injury.
Lethal impacts of cigarette smoke in cultured tobacco cells
Masaru Yukihiro, Takuya Hiramatsu, Tomonori Kawano
Tobacco Induced Diseases , 2011, DOI: 10.1186/1617-9625-9-8
Abstract: By employing the tobacco cells as model materials for cigarette smoke toxicity assay, the impacts of the combustion by-products such as nitrogen oxides could be highlighted as the toxic impacts of the plant-derived endogenous chemicals could be excluded in the plant cells.Cigarette smoke-induced cell death was assessed in tobacco cell suspension cultures in the presence and absence of pharmacological inhibitors.Cigarette smoke was effective in induction of cell death. The smoke-induced cell death could be partially prevented by addition of nitric oxide (NO) scavenger, suggesting the role for NO as the cell death mediator. Addition of NO donor to tobacco cells also resulted in development of partial cell death further confirming the role of NO as cell death mediator. Members of reactive oxygen species and calcium ion were shown to be protecting the cells from the toxic action of smoke-derived NO.In the United States, the toxic impacts of various chemicals to various organisms have been documented in the Ecotoxicology Database (ECOTOX) of the US EPA. The cigarette smoke is known to be toxic and thus harmful to human health [1], both at cellular [2] and genetic levels [3]. On the other hand, the impacts of cigarette smoke in various organisms including living plants have been poorly documented to date. In order to understand and generalize the toxic mechanism of cigarette smoke in living cells, comparison of the data between animal systems and other biological system such as microbial and plant systems is highly beneficial.Since the cigarette smoke is derived from combustion of tobacco leaves, the chemical components in the smoke must be the mixture of (i) chemical contents originally present in the tobacco leaves and (ii) the chemicals formed through combustion process (combustion by-products) [4]. Both former (such as nicotine, phenolics, etc.) and latter chemicals (such as hydrogen peroxide) are known to be harmful to human health [3]. However, it is natural to assu
Cigarette smoke exposure facilitates allergic sensitization in mice
Katrien B Moerloose, Lander J Robays, Tania Maes, Guy G Brusselle, Kurt G Tournoy, Guy F Joos
Respiratory Research , 2006, DOI: 10.1186/1465-9921-7-49
Abstract: The aim of this study was to determine if cigarette smoke exposure could facilitate primary allergic sensitization.BALB/c mice were exposed to aerosolized ovalbumin (OVA) combined with air or tobacco smoke (4 exposures/day) daily for three weeks. Serology, lung cytopathology, cytokine profiles in bronchoalveolar lavage fluid (BALF) and on mediastinal lymph node cultures as well as lung function tests were performed after the last exposure. The natural history and the immune memory of allergic sensitization were studied with in vivo recall experiments.Exposure to OVA induced a small increase in OVA-specific serum IgE as compared with exposure to PBS (P < 0.05), while no inflammatory reaction was observed in the airways. Exposure to cigarette smoke did not induce IgE, but was characterized by a small but significant neutrophilic inflammatory reaction. Combining OVA with cigarette smoke not only induced a significant increase in OVA-specific IgE but also a distinct eosinophil and goblet cell enriched airway inflammation albeit that airway hyperresponsiveness was not evidenced. FACS analysis showed in these mice increases in dendritic cells (DC) and CD4+ T-lymphocytes along with a marked increase in IL-5 measured in the supernatant of lymph node cell cultures. Immune memory experiments evidenced the transient nature of these phenomena.In this study we show that mainstream cigarette smoke temporary disrupts the normal lung homeostatic tolerance to innocuous inhaled allergens, thereby inducing primary allergic sensitization. This is characterized not only by the development of persistent IgE, but also by the emergence of an eosinophil rich pulmonary inflammatory reaction.Cigarette smoke can trigger acute symptoms in patients with asthma, and exposure to cigarette smoke is strongly correlated with asthma severity [1-3]. Animal models support these findings [4,5]. Recent evidence suggests that active smoking is a risk factor for the onset of adult asthma [6], but whether th
Smoking and reproduction: The oviduct as a target of cigarette smoke
Prue Talbot, Karen Riveles
Reproductive Biology and Endocrinology , 2005, DOI: 10.1186/1477-7827-3-52
Abstract: Exposure to cigarette smoke may be either active or passive, and the type of smoke inhaled in each case has a different origin. Mainstream smoke is the smoke that an active smoker inhales with each puff, while sidestream smoke, the main component of environmental tobacco smoke, burns off the end of a lit cigarette and is the smoke inhaled by passive smokers. While the association between inhalation of mainstream smoke and cardiovascular disease and cancer has been established for many years, the impact of smoking on reproduction is recognized, but less well characterized and less well known [1]. Epidemiological studies have repeatedly shown that women of child bearing age who actively inhale mainstream smoke have higher rates of infertility, spontaneous abortion, ectopic pregnancy, tubal infertility, increased time to conception, and intrauterine growth retardation than nonsmokers [2-15]. Increases in infertility and ectopic pregnancy in smokers could be due to impairment of oviductal functioning. In patients with primary tubal infertility, 39% were smokers when they started trying to conceive in contrast to only 16% in the non-smoking group (OR = 2.7) [10]. Heavy smoking (> 5 pack-years) increased the odds ratio to 4.2, and similar dose related effects have been repeatedly observed [11,16].The realization that sidestream smoke exposure adversely affects human health is even more recent [17]. In 1992, the Environmental Protection Agency published a monograph summarizing evidence that exposure to environmental tobacco smoke can produce adverse effects on cardiovascular and lung health and encouraged broader investigation in this area [17]. Subsequently, a number of studies have addressed the effect of passive smoking on various aspects of human health including reproduction and have concluded that adverse reproductive outcomes, such as delayed time to conception and reduced birth weight, do occur as a consequence of exposure to environmental tobacco smoke during preg
Cigarette Smoke Extract Stimulates Rat Pulmonary Artery Smooth Muscle Cell Proliferation via PKC-PDGFB Signaling
Ai-ping Xing,Yong-cheng Du,Xiao-yun Hu,Jian-ying Xu,Huan-ping Zhang,Yi Li,Xin Nie
Journal of Biomedicine and Biotechnology , 2012, DOI: 10.1155/2012/534384
Abstract: Accumulating evidence suggests a direct role for cigarette smoke in pulmonary vascular remodeling, which contributes to the development of pulmonary hypertension. However, the molecular mechanisms underlying this process remain poorly understood. Platelet-derived growth factor (PDGF) is a potential mitogen and chemoattractant implicated in several biological processes, including cell survival, proliferation, and migration. In this study, we investigated the effect of cigarette smoke extract (CSE) on cell proliferation of rat pulmonary artery smooth muscle cells (rPASMCs). We found that stimulation of rPASMCs with CSE significantly increased cell proliferation and promoted cell cycle progression from G1 phase to the S and G2 phases. CSE treatment also significantly upregulated the mRNA and protein levels of PDGFB and PDGFRβ. Our study also revealed that Rottlerin, an inhibitor of PKCδ signaling, prevented CSE-induced cell proliferation, attenuated the increase of S and G2 phase populations induced by CSE treatment, and downregulated PDGFB and PDGFRβ mRNA and protein levels in rPASMCs exposed to CSE. Collectively, our data demonstrated that CSE-induced cell proliferation of rPASMCs involved upregulation of the PKCδ-PDGFB pathway.
Behavior of cardiac variables in animals exposed to cigarette smoke
Paiva, Sergio Alberto Rupp de;Zornoff, Leonardo Antonio Mamede;Okoshi, Marina Politi;Okoshi, Katashi;Cicogna, Antonio Carlos;Campana, Alvaro Oscar;
Arquivos Brasileiros de Cardiologia , 2003, DOI: 10.1590/S0066-782X2003001100002
Abstract: objective: to assess the behavior of cardiac variables in animals exposed to cigarette smoke. methods: two groups of wistar rats were studied as follows: control group (c), comprising 28 animals; and smoking group (s), comprising 23 animals exposed to cigarette smoke for 30 days. left ventricular cardiac function was assessed in vivo with transthoracic echocardiography, and myocardial performance was analyzed in vitro in preparations of isolated left ventricular papillary muscle. the cardiac muscle was assessed in isometric contractions with an extracellular calcium concentration of 2.5 mmol/l. results: no statistical difference was observed in the values of the body variables of the rats and in the mechanical data obtained from the papillary muscle between the control and smoking groups. the values of left ventricular systolic diameter were significantly greater in the smoking animals than in the control animals (c= 3.39 ± 0.4 mm and s= 3.71 ± 0.51 mm, p=0.02). a significant reduction was observed in systolic shortening fraction (c= 56.7 ± 4.2% and s= 53.5 ± 5.3%, p=0.02) and in ejection fraction (c= 0.92 ± 0.02 and s= 0.89 ± 0.04, p=0.01). conclusion: the rats exposed to cigarette smoke had a reduction in left ventricular systolic function, although their myocardial function was preserved.
Behavior of cardiac variables in animals exposed to cigarette smoke  [cached]
Paiva Sergio Alberto Rupp de,Zornoff Leonardo Antonio Mamede,Okoshi Marina Politi,Okoshi Katashi
Arquivos Brasileiros de Cardiologia , 2003,
Abstract: OBJECTIVE: To assess the behavior of cardiac variables in animals exposed to cigarette smoke. METHODS: Two groups of Wistar rats were studied as follows: control group (C), comprising 28 animals; and smoking group (S), comprising 23 animals exposed to cigarette smoke for 30 days. Left ventricular cardiac function was assessed in vivo with transthoracic echocardiography, and myocardial performance was analyzed in vitro in preparations of isolated left ventricular papillary muscle. The cardiac muscle was assessed in isometric contractions with an extracellular calcium concentration of 2.5 mmol/L. RESULTS: No statistical difference was observed in the values of the body variables of the rats and in the mechanical data obtained from the papillary muscle between the control and smoking groups. The values of left ventricular systolic diameter were significantly greater in the smoking animals than in the control animals (C= 3.39 ± 0.4 mm and S= 3.71 ± 0.51 mm, P=0.02). A significant reduction was observed in systolic shortening fraction (C= 56.7 ± 4.2% and S= 53.5 ± 5.3%, P=0.02) and in ejection fraction (C= 0.92 ± 0.02 and S= 0.89 ± 0.04, P=0.01). CONCLUSION: The rats exposed to cigarette smoke had a reduction in left ventricular systolic function, although their myocardial function was preserved.
Microbiological components in mainstream and sidestream cigarette smoke  [cached]
Larsson Lennart,Pehrson Christina,Dechen Tenzin,Crane-Godreau Mardi
Tobacco Induced Diseases , 2012, DOI: 10.1186/1617-9625-10-13
Abstract: Background Research has shown that tobacco smoke contains substances of microbiological origin such as ergosterol (a fungal membrane lipid) and lipopolysaccharide (LPS) (in the outer membrane of Gram-negative bacteria). The aim of the present study was to compare the amounts of ergosterol and LPS in the tobacco and mainstream (MS) and sidestream (SS) smoke of some popular US cigarettes. Methods We measured LPS 3-hydroxy fatty acids and fungal biomass biomarker ergosterol in the tobacco and smoke from cigarettes of 11 popular brands purchased in the US. University of Kentucky reference cigarettes were also included for comparison. Results The cigarette tobacco of the different brands contained 6.88-16.17 (mean 10.64) pmol LPS and 8.27-21.00 (mean 14.05) ng ergosterol/mg. There was a direct correlation between the amounts of ergosterol and LPS in cigarette tobacco and in MS smoke collected using continuous suction; the MS smoke contained 3.65-8.23% (ergosterol) and 10.02-20.13% (LPS) of the amounts in the tobacco. Corresponding percentages were 0.30-0.82% (ergosterol) and 0.42-1.10% (LPS) for SS smoke collected without any ongoing suction, and 2.18% and 2.56% for MS smoke collected from eight two-second puffs. Conclusions Tobacco smoke is a bioaerosol likely to contain a wide range of potentially harmful bacterial and fungal components.
The effects of exposure to cigarette smoke on the pharmacokinetics and pharmacodynamics of zonisamide in rats.
Araki H,Kawasaki M,Matsuka N,Nakatsuma A
Acta Medica Okayama , 1999,
Abstract: The effects of exposure to cigarette smoke on the pharmacokinetics and pharmacodynamics of zonisamide, an antiepileptic drug, were investigated in rats. Absorption of oral zonisamide was significantly inhibited by exposure to cigarette smoke. The Cmax, T1/2 and the area under the plasma concentration-time curve 0-24 values in the cigarette smoke exposure group were significantly lower than those in the control group. Although tonic extension (TE) induced by maximal electroshock was completely blocked by the administration of zonisamide in the control group, 50% of rats showed TE in the cigarette smoke exposure group. Exposure to cigarette smoke influences both the pharmacokinetics and antiepileptic effects of zonisamide. The effects of smoking on epileptic patients using zonisamide warrants further attention.
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