Evaluation of hospitalized patients in terms of their knowledge related to smoking

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Oxidative stress status and lipid profiles of diabetic pregnant rats exposed to cigarette smoke

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Cigarette smoke affects apoptosis in rat tongue mucosa: Role of bcl-2 gene family

While it has been clearly demonstrated that smoking is the most significant exogenous factor involved in oral carcinogenesis, little is known about the global molecular and cellular changes that occur prior to the appearance of clinically detectable symptoms. Thus, the aim of this study was to investigate the expressivity of bcl-2, bax and PCNA in the rat tongue mucosa exposed to cigarette smoke by means of immunohistochemistry. A total of twelve male Wistar rats were distributed into 2 groups: negative control and experimental group exposed to cigarette smoke during 75 days. After experimental period, no histopathological changes in the tongue mucosa were detected in the negative control and the experimental group. on the other hand, an overexpression of bcl-2 was detected (p < 0.01) throughout all layers of the epithelium, whereas bax did not show significant differences (p > 0.05). Also, the labeling index for bcl-2 and bax showed an increase 75 days after cigarette exposure (p < 0.01). PCNA-labeling index did not show remarkable changes between groups. Taken together, our results show that bcl-2 is overexpressed in the rat tongue keratinocytes after cigarette smoke exposure.

Genotoxicity of cigarette smoking in maternal and newborn lymphocytes

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effects of cigarette smoke on the Meckel's cartilage of rat fetus : Morphologic, morphometric and stereologic study

The purpose of this study was to investigate the effects of cigarette smoke on the development of the embryo mandible (Meckel's) cartilage in rat fetuses. When inhaled by female Wistar rats between the 9th and the 12th day of pregnancy, cigarette smoke (5 cigarettes a day) caused intrauterine growth retardation, providing smaller fetuses and placentas. In fetuses from the experimental group, the histopathologic examination revealed a poorly developed Meckel' s cartilage with smaller chondroblasts showing a scanty cytoplasm with spherical and paler central nuclei, as well as more abundant cartilage matrix. Morphometric analysis revealed that Meckel's cartilage lacunae were smaller in the fetuses from the experimental group, although not showing any remarkable alteration in shape. The results suggested that inhalation of cigarette smoke by pregnant rats during the organogenic period induced growth retardation and delayed cellular differentiation in rat fetal Meckel's cartilage.

Efectos de la administración de betabloqueante en la remodelación ventricular inducida por el tabaquismo en ratas

Background: The role of the adrenergic system on ventricular remodeling induced by cigarette smoking is unknown. Objective: To investigate the influence of propranolol on ventricular remodeling induced by exposure to tobacco smoke. Methods: Rats were divided into three groups: 1) C, n=10 - control group; 2) F, n=10 - animals exposed to tobacco smoke; 3) BB, n=10 - animals receiving propranolol and exposed to tobacco smoke (40 mg/kg/day). After 2 months, the animals underwent echocardiographic and morphometric analyses. One-way ANOVA (mean ± standard deviation) or the Kruskal-Wallis test (median and interquartile interval) was used. Results: Group BB showed a lower heart rate than group F (C = 358 ± 74 bpm, F = 374 ± 53 bpm, BB = 297± 30; P = 0.02). Group F showed greater end-diastolic diameters (C = 18.6 ± 3.4 mm/kg, F = 22.8 ± 1.8 mm/kg, BB = 21.7 ± 1.8 mm/kg; P = 0.003) and left ventricular (LV) end-systolic diameters (C = 8.6 ± 2.1 mm/kg, F = 11.3 ± 1.3 mm/kg, BB = 9.9 ± 1.2 mm/kg; P = 0.004), adjusted for body weight (BW) and a tendency towards a lower ejection fraction (C = 0.90 ± 0.03, F = 0.87 ± 0.03, BB =0.90 ± 0.02; P = 0.07) than group C. Group BB showed a tendency towards a lower LV/BW ratio than group F (C = 1.94 (1.87 - 1.97), F = 2.03 (1.9-2.1) mg/g, BB = 1.89 (1.86-1.94); P = 0.09). Conclusion: Administration of propranolol attenuated some of the variables of ventricular remodeling induced by the exposure to tobacco smoke in rats.

Cardiovascular remodeling induced by passive smoking

Coronary heart disease (CHD) is the most common cause of death in many developed countries. The major risk factors for CHD are smoking, high blood pressure, diabetes, high cholesterol levels, and lack of physical activity. Importantly, passive smoke also increases the risk for CHD. The mechanisms involved in the effects of passive smoke in CHD are complex and include endothelial dysfunction, lipoprotein modification, increased inflammation and platelet activation. Recently, several studies have shown that exposure to tobacco smoke can result in cardiac remodeling and compromised cardiac function. Potential mechanisms for these alterations are neurohumoral activation, oxidative stress, and MAPK activation. Although the vascular effects of cigarette smoke exposure are well known, the effects of tobacco smoking on the heart have received less attention. Therefore, this review will focus on the recent findings as to the effects of passive smoking in acute and chronic phases of vascular and cardiac remodeling. © 2009 Bentham Science Publishers Ltd.

Efeito da exposição à fumaça de cigarro durante a prenhez e a lactação de ratas e sua prole sobre parâmetros séricos e morfométricos

PURPOSE: to investigate the effect of cigarette smoke exposure on body and tissue weight gain, serum parameters and milk yield during pregnancy and lactation in rats, and the impact on offspring from birth toil young adulthood. METHODS: 40 Wistar pregnant rats were randomly divided into: CG - not exposed to cigarette smoke and sacrificed at the end of pregnancy; CL - not exposed to cigarette smoke and sacrificed at the end of lactation; FG - exposed to cigarette smoke and sacrificed at the end of pregnancy; FL - exposed to cigarette smoke and sacrificed at the end of lactation. The offspring were separated by gender and divided according to their mothers' groups. Tissue weight, body weight and serum parameters were evaluated in rats and offspring. Milk yield per pup was calculated. RESULTS: body weight was decreased in FL during lactation (CL=267.0±7.2; FL=235.5±7.2 g*, *p<0.05). Adipose tissue was not detected in the CL and FL groups, and was reduced in FG compared to CG (CG=3.3±0.3; FG=2.4±0.3 g*, *p<0.05). Rats exposed to cigarette smoke had higher blood glucose levels (CG=113±17, CL=86±16, FG=177±21*, FL=178±23 mg/dL*, *p<0.05 CG versus FG e CL versus FL), CL and FL groups presented lower HDL-cholesterol with no change in total cholesterol. Finally, rats exposed to cigarette smoke had lower milk yield compared to unexposed rats (CL=6.7±0.4, FL=5.4±0.3 g*, *p<0.05). In offspring from the FG and FL groups, there was a decrease of body weight from birth to young adulthood, with no changes in gastrocnemius, liver or heart weights in any group, and adipose tissue was no detected in female offspring. There was an increase in blood glucose in offspring of both sexes from rats exposed to cigarette smoke (males: Pcg=107±10.5, Pcl=115±8.6, Pfg=148±16.8*, Pfl=172±11.2**; females: Pcg=109±27.2, Pcl=104±9.7, Pfg=134±20.0*, Pfl=126±13.3**; p<0.05 *Pcg versus Pfg and **Pcl versus Pfl). CONCLUSIONS: exposure to cigarette smoke provokes impairment of morphometric and serum parameters during pregnancy and lactation both in mothers and offspring, which is maintained during young adulthood.

Possible mechanism by which zinc protects the testicular function of rats exposed to cigarette smoke

Background: The aim of this study was to evaluate the changes in testicular function of rats due to cigarette smoke exposure and the possible mechanism by which zinc protects against these alterations. Methods: MaleWistar rats (60 days old) were randomly divided into 3 groups: control (G1, n = 10); exposed to cigarette smoke (G2, n = 10; 20 cigarettes/day/9 weeks) and exposed to cigarette smoke and supplemented with zinc (G3, n = 8; 20 cigarettes/day/9 weeks; 20 mg/kg zinc chloride daily for 9 weeks, by gavage). After the treatment period, the animals were euthanized, and materials were collected for analyses. Results: G2 rats showed a reduction in body mass; impaired sperm concentration, motility, morphology and vitality; and increased malonaldehyde and thiol group levels and superoxide dismutase activity as compared to G1. Zinc prevented the reduction of sperm concentration and the excessive increase of lipid peroxidation and induced an increase in plasma testosterone levels, wet weight of testis and thiol group concentration. Conclusions: Exposure to cigarette smoke led to harmful effects on testicular function at least partially due to the exacerbation of oxidative stress. Supplementary zinc had an important modulator/protector effect on certain parameters. The mechanism of zinc protection can be through an increase of SH concentration. Thus, zinc supplementation may be a promising addition to conventional treatments for male infertility related to smoking. Copyright © 2012 by Institute of Pharmacology Polish Academy of Sciences.

Smoking is associated with remodeling of gap junction in the rat heart: Smoker's paradox explanation?

Background: In a previous study utilizing the rat model, exposure to tobacco smoke for 5 weeks increased survival after AMI, despite similar age and infarct size between the smokers and nonsmokers, and absence of reperfusion. Objective: Thus, this study aimed to analyze the effects of exposure to tobacco smoke on intensity, distribution or phosphorylation of connexin 43 in the rat heart. Methods: Wistar rats weighing 100 g were randomly allocated into 2 groups: 1) Control (n = 25); 2) Exposed to tobacco smoke (ETS), n = 23. After 5 weeks, left ventricular morphometric analysis, immunohisthochemistry and western blotting for connexin 43 (Cx43) were performed. Results: Collagen volume fraction, cross-sectional areas, and ventricular weight were not statistically different between control and ETS. ETS showed lower stain intensity of Cx43 at intercalated disks (Control: 2.32 ± 0.19; ETS: 1.73 ± 0.18; p = 0.04). The distribution of CX43 at intercalated disks did not differ between the groups (Control: 3.73 ± 0.12; ETS: 3.20 ± 0.17; p = 0.18). ETS rats showed higher levels of dephosphorylated form of Cx43 (Control: 0.45 ± 0.11; ETS: 0.90 ± 0.11; p = 0.03). On the other hand, total Cx43 did not differ between control and ETS groups (Control: 0.75 ± 0.19; ETS: 0.93 ± 0.27; p = 0.58). Conclusion: Exposure to tobacco smoke resulted in cardiac gap junction remodeling, characterized by alterations in the quantity and phosphorylation of the Cx43, in rats hearts. This finding could explain the smoker's paradox observed in some studies.

Influência da suplementação de vitamina D na dieta sobre remodelação cardíaca em ratos expostos à fumaça do cigarro

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Efeitos da exposiçao à fumaça de cigarro e a ingestão crônica de etanol sobre a mucosas da língua e da faringe: estudo histopatológico em ratos

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Função testicular de raos expostos à fumaça do cigarro e possível papel protetor do zinco: análises seminais, morfológicas e moleculares

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Influência da taurina na remodelação cardíaca induzida pela exposição à fumaça do cigarro

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Influência do tempo de exposição à fumaça de cigarro na remodelação ventricular em ratos

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)