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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
Biological Effects of Cigarette Smoke in Cultured Human Retinal Pigment Epithelial Cells  [PDF]
Alice L. Yu, Kerstin Birke, Johannes Burger, Ulrich Welge-Lussen
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0048501
Abstract: The goal of the present study was to determine whether treatment with cigarette smoke extract (CSE) induces cell loss, cellular senescence, and extracellular matrix (ECM) synthesis in primary human retinal pigment epithelial (RPE) cells. Primary cultured human RPE cells were exposed to 2, 4, 8, and 12% of CSE concentration for 24 hours. Cell loss was detected by cell viability assay. Lipid peroxidation was assessed by loss of cis-parinaric acid (PNA) fluorescence. Senescence-associated ?-galactosidase (SA-?-Gal) activity was detected by histochemical staining. Expression of apolipoprotein J (Apo J), connective tissue growth factor (CTGF), fibronectin, and laminin were examined by real-time PCR, western blot, or ELISA experiments. The results showed that exposure of cells to 12% of CSE concentration induced cell death, while treatment of cells with 2, 4, and 8% CSE increased lipid peroxidation. Exposure to 8% of CSE markedly increased the number of SA-?-Gal positive cells to up to 82%, and the mRNA expression of Apo J, CTGF, and fibronectin by approximately 3–4 fold. Treatment with 8% of CSE also increased the protein expression of Apo J and CTGF and the secretion of fibronectin and laminin. Thus, treatment with CSE can induce cell loss, senescent changes, and ECM synthesis in primary human RPE cells. It may be speculated that cigarette smoke could be involved in cellular events in RPE cells as seen in age-related macular degeneration.
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.
Reduction of aldehydes and hydrogen cyanide yields in mainstream cigarette smoke using an amine functionalised ion exchange resin
Peter J Branton, Kevin G McAdam, Dinah B Winter, Chuan Liu, Martin G Duke, Christopher J Proctor
Chemistry Central Journal , 2011, DOI: 10.1186/1752-153x-5-15
Abstract: Resin surface chemistry was characterized using vapour sorption, XPS, TOF-SIMS and 15N NMR. Diaion?CR20 was found to have structural characteristics indicating weak physisorption properties, but sufficient surface functionalities to selectively remove aldehydes and HCN from cigarette smoke. Using 60 mg of Diaion?CR20 in a cigarette cavity filter gave reductions in smoke formaldehyde greater than 50% (estimated to be equivalent to >80% of the formaldehyde present in the smoke vapour phase) independent of a range of flow rates. Substantial removal of HCN (>80%) and acetaldehyde (>60%) was also observed. The performance of Diaion?CR20 was found to be consistent over a test period of 6 months. The overall adsorption for the majority of smoke compounds measured appeared to follow a pseudo-first order approximation to second order kinetics.This study has shown that Diaion?CR20 is a highly selective and efficient adsorbent for formaldehyde, acetaldehyde and HCN in cigarette smoke. The reductions for these compounds were greater than those achieved using an active carbon. The results also demonstrate that chemisorption can be an effective mechanism for the removal of certain vapour phase toxicants from cigarette smoke.Cigarette smoke is an aerosol stream containing an extremely complex mixture of chemicals [1]. Amongst the more than 5000 identified constituents of smoke, approximately 150 of these have been documented as toxicants [2,3]. Tobacco smoke toxicants cover a range of chemical groups and functionalities (for example nitrosamines, polynuclear aromatic hydrocarbons and carbonyls) [4-6], as well as a range of volatilities, from permanent gases to compounds with very low vapour pressures at ambient temperatures. In 2001 the Institute of Medicine [7] reported that, since smoking related diseases were dose-related, and because epidemiologic studies show reduction in the risk of smoking related diseases following cessation, it might be possible to reduce smoking related
Real-time assessment of cigarette smoke particle deposition in vitro
Jason Adamson, Sophie Hughes, David Azzopardi, John McAughey, Marianna D Ga?a
Chemistry Central Journal , 2012, DOI: 10.1186/1752-153x-6-98
Abstract: The QCM chamber was able to detect mass differences between the different products within the nanogram range. 3R4F reference cigarette smoke deposition ranged from 25.75 ±2.30?μg/cm2 (1:5) to 0.22 ±0.03?μg/cm2 (1:400). 1?mg cigarette smoke deposition was less and ranged from 1.42 ±0.26?μg/cm2 (1:5), to 0.13 ±0.02?μg/cm2 (1:100). Spectrofluorometric analysis demonstrated statistically significant correlation of particulate deposition with the QCM (p?<?0.05), and regression R2 value were 97.4?%. The fitted equation for the linear model which describes the relationship is: QCM?=??0.6796?+?0.9744 chemical spectrofluorescence.We suggest the QCM is a reliable, effective and simple tool that can be used to quantify smoke particulate deposition in real-time, in vitro and can be used to quantify other aerosols delivered to our chamber for assessment.Cigarette smoke is a complex and dynamic aerosol consisting of at least 5,600 chemicals and toxicants found across two phases, the particulate (tar) and vapour phase [1]. Recently, there has been a rapid increase in the development of systems for in vitro biological and toxicological assessment of whole smoke [2-11]. However, despite these advancements there have not been consistent approaches in reporting accurately the dose of whole smoke delivered to in vitro cultures.Understanding dosimetry is essential when attempting to mimic or extrapolate human smoking behavior and in vivo doses to in vitro models. Whole smoke dose is dependent on the machine used to generate, dilute and deliver smoke and is variously described as a percentage of smoke, a fraction of smoke, ratios of smoke to air, puff number, total exposure of micrograms per insert, or as a flow rate of mixing air and vacuum applied to a smoke dilutor [2,3,5,6,9-11]. This is a relatively new and challenging field but is an increasingly important point of discussion within the industry. On a broader note, the need to quantify absolute chemical or particle deposition in in
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.
Changes in Water Sorption and Solubility of Dental Adhesive Systems after Cigarette Smoke  [PDF]
Lívia Andrade Vitória,Thaiane Rodrigues Aguiar,Poliana Ramos Braga Santos,Andrea Nóbrega Cavalcanti,Paula Mathias
ISRN Dentistry , 2013, DOI: 10.1155/2013/605847
Abstract: Aim. To evaluate the effect of cigarette smoke on water sorption and solubility of four adhesive systems. Materials and Methods. Sixteen disks of each adhesive system were prepared (Adper Scotchbond Multipurpose Adhesive (SA); Adper Scotchbond Multipurpose Adhesive System (Adhesive + Primer) (SAP); Adper Single Bond Plus (SB); Adper Easy One (EO)). Specimens were desiccated until a constant mass was obtained and divided into two groups . One-half of the specimens were immersed in deionized water, while the other half were also immersed, but with daily exposure to tobacco smoke. After 21 days, disks were measured again and stored in desiccators until constant mass was achieved. Data were calculated according to ISO specifications and statistically analyzed. Results. The tobacco smoke only significantly affected the water sorption and solubility of EO. There were significant differences in both analyses among materials tested. The SB exhibited the highest water sorption, followed by EO, which demonstrated significantly higher solubility values than SB. The SA and SAP showed low water sorption and solubility, and there were no significant differences between the two. Conclusion. Regardless of smoke exposure, both simplified adhesive systems presented an inferior performance that could be related to the complex mixture of components in such versions. 1. Introduction Many studies have shown that cigarette smoking is associated with deleterious health effects such as heart disease [1], chronic obstructive pulmonary disease, cancer [2], fertility problems [3], and periodontal disease [4]. In cosmetic restorative dentistry, some of the substances coming from tobacco can be absorbed by resin composite, dentin, and enamel surface [5] and lead to tooth/composite discoloration [6–10]. Moreover, bond strength reduction has been described due to the fact that cigarette particles may prevent effective contact between dentin and resin composite [11]. The mainstream smoke emitted from the mouth end is complex and composed by many physical and chemical processes [12]. In general, smoke formation is mostly produced by combustion and pyrolysis reactions and can be classified in two distinct phases. The first is called the vapour phase, consisting mainly of nitrogen, oxygen, carbon monoxide, carbon dioxide, acetaldehyde, methane, hydrogen cyanide, nitric acid, and acetone. The second category is the particulate phase. It consists of nicotine, water, and tobacco-specific nitrosamines ranging from 0.1 to 1.0?μm in diameter [12–17]. Beside many research reports on the staining
In vitro and clinical studies examining the expression of osteopontin in cigarette smoke-exposed endothelial cells and cigarette smokers  [cached]
Bishop Emma,Theophilus Eugenia H,Fearon Ian M
BMC Cardiovascular Disorders , 2012, DOI: 10.1186/1471-2261-12-75
Abstract: Background Cigarette smoking is a leading cause of mortality and morbidity and is associated with cardiovascular disease via contributory processes such as endothelial dysfunction, inflammation and thrombosis. Cigarette smoke both contains and stimulates the production of cellular oxidants and it may also promote vascular inflammation. Osteopontin is a non-collagenous matrix protein first identified in bone and there is increasing evidence for its role in inflammation and cardiovascular disease via its action as a soluble cytokine. Methods In this study we have examined the mechanisms underlying the expression of osteopontin in human vascular endothelial cells in vitro following exposure to cigarette smoke particulate matter (PM), using PCR, electrochemiluminescence, immunostaining and Western blotting. We further determined if serum osteopontin levels changed in humans who quit smoking. Results Non-cytotoxic concentrations of PM increased osteopontin levels in cultured human endothelial cells and this effect was reduced in the presence of ascorbate, suggesting a role for oxidants in the response to PM. However, oxidant production played no role in the PM-evoked induction MMP-3, an enzyme which cleaves osteopontin. In smokers who quit smoking for 5 days, serum osteopontin levels were significantly lowered compared to those measured prior to smoking cessation. Conclusions In vitro cigarette smoke extract exposure induced osteopontin expression in human endothelial cells in an oxidative stress-dependent manner, which may involve MMP-3 cleavage. In humans, serum osteopontin was decreased with short-term smoking cessation. Endothelial-derived osteopontin may contribute to inflammation in smokers, and may also contribute to atherosclerosis and cardiovascular disease-related processes.
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
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