590 resultados para cigarette cravings


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The effect of caffeine consumption on mortality was evaluated in a historical cohort study of 10064 hypertensive individuals participating in the Hypertension Detection and Follow-Up Program (HDFP) from 1973 to 1979. The study cohort was stratified into caffeine consumption groups (none, low, medium and high) based on their total level of caffeine intake from beverages (coffee and tea) and certain medications at the One-year follow-up home visit. Stratification was also made by sex, race, type of care and age. The total relative risks (RRs) when computed across strata for each caffeine consumer group (low, medium and high) were not significantly different when compared to the noncaffeine consumer group for all-cause or cause-specific mortality rates. The point estimates and 95 per cent confidence intervals for relative risks of all-cause mortality when compared to nonconsumers were as follows: Low = 0.82 (0.65-1.03), Medium: = 0.82 (0.62-1.82) and High = 0.90 (0.63-1.28). For all sex, race combinations there was an increase in the per cent of current smokers within each caffeine consumer group as the level of caffeine consumption increased. Cigarette smoking was an important confounder correlated with caffeine consumption and associated with mortality in this cohort. When confounding by cigarette smoking was adjusted for in the analysis, no association was found between the level of caffeine consumption and all-cause or cause-specific mortality. ^

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Excessively high, accelerating lung cancer rates among women in Harris County, Texas, prompted this case-comparison study. Objectives were to compare patterns of employment, indirect exposures, and sociodemographic variables of lung cancer cases with comparison subjects (compeers) after standardizing for possible confounders, such as age and cigarette smoking. Lung cancer cases were microscopically confirmed, white, Harris County residents. Compeers, chosen from Medicare records and Texas Department of Public Safety records, were matched on gender, race, age, resident and vital status. Personal interviews were conducted with study subjects or next-of-kin. Industries and occupations were categorized as high risk, based on previous studies.^ Almost all cases (95.0%) and 60.0% of compeers smoked cigarettes. The odds ratio for lung cancer and smoking is 13.9. Stopping smoking between ages 30-50 years carries a lower risk than stopping at age 58 or more years. Women's employment in a high risk industry or occupation results in consistently elevated, smoking-adjusted odds ratios. Frequency and duration of employment demonstrate a moderate dose-response effect. A temporal association exists with employment in a high risk occupation during 1940-1949.^ No increased risk appeared with passive smoking. Husband's employment in a construction industry or a structural occupation significantly increased the smoking-adjusted odds ratios among cases and compeers (O.R. = 2.9, 2.2). Smoking-adjusted odds ratios increased significantly when women had resided with persons employed in cement (O.R. = 3.2) or insulation (O.R. = 5.5) manufacturing, or a high rise construction industry (O.R. = 2.4). A family history of lung cancer resulted in a two-fold increase in smoking-adjusted odds ratios. Vital status of compeers affected the odds ratios.^ Work-related exposures appear to increase the risk of lung cancer in women although cigarette smoking has the single highest odds ratio. Indirect exposure to certain employment also plays a significant role in lung cancer in women. Investigations of specific direct and indirect hazardous exposures in the workplace and home are needed. Cigarette smoking is as hazardous for women as for men. Smoking should be prevented and eliminated. ^

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Smoking is major cause of premature mortality and morbidity in the United States. The health consequences of tobacco usage are increasingly concentrated in minority and lower socioeconomic groups. One of the most effective means of deterring tobacco consumption and generating revenue to fund prevention activities is the levying of excise taxes. In 2007 the state of Texas increased the excise tax on cigarettes by $1.00 per pack. This study sought to determine if there was a significant effect on smoking prevalence in the state by examining Behavioral Risk Factor Surveillance System (BRFSS) data for two years leading up to the tax increase-2005 and 2006- and two years post tax increase -2007 and 2008. Results were compared against a chi square distribution and three multiple logistic regression models were created to adjust for race/ethnicity, age, education and income. Results from this study show that there was not a significant decrease in smoking prevalence for most of the groups stratified by age, income and ethnicity. There was not a significant decrease in the younger adults aged 18-34 by income, ethnicity, or education. Smoking prevalence increased for some groups, e.g., Hispanic females. In the regression models, the tax effect was not significant. While overall prevalence decreased by 9%, there were not significant reductions among non-White or Hispanic survey participants. Taxed sales dropped by approximately 17% according to the Texas Comptroller. Without BRFSS data measuring daily cigarette consumption among current smokers, now not assessed, it is impossible to determine whether the discrepancy in reported prevalence and taxes sales is attributable to consumption of fewer cigarettes among smokers or tax avoidance.^

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Little is known about the etiology of colorectal adenomatous polyps, although they are generally considered to be precursor lesions to colorectal carcinoma. To investigate the associations of colorectal adenomatous polyps with dietary intake of calcium, total fat and fiber, a case comparison study was conducted among 98 persons who had first occurrences of adenomatous polyps and 408 persons who did not have colorectal polyps.^ The study population comprised Black, White and Hispanic males and females ages 35 to 80 inclusive, who underwent a sigmoidoscopy or total colonoscopy at collaborating clinics in the Texas Medical Center at Houston between September 1991 and November 1992, and met the eligibility criteria. Case participants were those who had a first-time diagnosis of adenomatous polyps. Comparison participants were individuals who underwent the same diagnostic procedure as the cases and met the same eligibility criteria but had no colorectal polyps. A food frequency questionnaire was administered by interview to obtain information about diet during the 28 days preceding the interview.^ Dietary intake of total fiber was inversely associated with risk of adenomatous polyps. An increment of 15 gm/day in energy-adjusted intake of fiber was associated with a relative odds of 0.39 with a 95% confidence interval of 0.20 to 0.79, after adjustment for age, sex, ethnicity, body mass index, cigarette smoking, family history of colorectal cancer and intake of nonsteroidal anti-inflammatory drugs. No association between dietary intake of total fat and risk of adenomatous polyps was observed. When total fat was analyzed as percent of energy, an increment of 15.3% in intake was associated with a relative odds of 0.98 with a 95% confidence interval of 0.53 to 1.80. However, few persons in the study group had intakes below 25% of energy from total fat. An inverse association was observed between energy-adjusted intake of dietary calcium and risk of adenomatous polyps, but this was not statistically significant; an increment of 638 mg/day was associated with a relative odds of 0.77 with a 95% confidence interval of 0.41 to 1.38. Intake of calcium did not appear to strongly modify the association between intake of fat and risk of adenomatous polyps, perhaps because the study group included few people with calcium intake below 400 mg/day.^ These results support the idea that dietary fiber decreases risk of adenomatous polyps. Further studies are needed on the association of dietary calcium and fat with risk of colorectal adenomatous polyps in populations where individuals vary widely in intake of these nutrients. ^

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Breast cancer is the most common cancer diagnosis and second leading cause of death in women. Risk factors associated with breast cancer include: increased age, alcohol consumption, cigarette smoking, white race, physical inactivity, benign breast conditions, reproductive and hormonal factors, dietary factors, and family history. Hereditary breast and ovarian cancer syndrome (HBOC) is caused by mutations in the BRCA1 and BRCA2 genes. Women carrying a mutation in these genes are at an increased risk to develop a second breast cancer. Contralateral breast cancer is the most common second primary cancer in patients treated for a first breast cancer. Other risk factors for developing contralateral breast cancer include a strong family history of breast cancer, age of onset of first primary breast cancer, and if the first primary was a lobular carcinoma, which has an increased risk of being bilateral. A retrospective chart review was performed on a select cohort of women in an IRB approved database at MD Anderson Cancer Center. The final cohort contained 572 women who tested negative for a BRCA1 or BRCA2 mutation, had their primary invasive breast cancer diagnosed under the age of 50, and had a BRCAPro risk assessment number over 10%. Of the 572 women, 97 women developed contralateral breast cancer. A number of predictors of contralateral breast cancer were looked at between the two groups. Using univariable Cox Proportional Hazard model, thirteen statistically interesting risk factors were found, defined as having a p-value under 0.2. Multivariable stepwise Cox Proportional Hazard model found four statistically significant variables out of the thirteen found in the univariable analysis. In our study population, the incidence of contralateral breast cancer was 17%. Four statistically significant variables were identified. Undergoing a prophylactic mastectomy was found to reduce the risk of developing contralateral breast cancer, while not having a prophylactic mastecomy, a young age at primary diagnosis, having a positive estrogen receptor status of the primary tumor, and having a family history of breast cancer increased a woman’s risk to develop contralateral breast cancer.

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Since heroin was introduced to East Africa during the 1980s, heroin use practices have changed rapidly in response to various internal and external pressures. The aim of this study was to identify and describe the population of heroin users and locations of heroin use in Dar es Salaam, Tanzania, in order to understand recent contexts of heroin use. The study took place between June 30 and August 19, 2011, in all three districts (Kinondoni, Ilala, and Temeke) of Dar es Salaam. We mapped sites using a Global Positioning System device, counted numbers of heroin users, and conducted informal interviews with heroin users. The mixed-methods analyses of the data included quantifying the basic demographic and aggregate information about the sites and heroin users, as well as qualitative analysis and coding of fieldnotes from observations and responses to interviews which was used to identify themes and characteristics of heroin users. ^ We identified a total of 150 sites and counted a total of 1046 male and 46 female non-injecting drug users and 78 male and 9 female injecting drug users (IDUs) of heroin. We found that social organization existed at some of the sites, with 31% (n=47) of sites reporting having a leader and 44% (n=66) of sites reporting mutual aid between users frequenting the site. We had difficulty locating IDUs and female drug users, and the majority of users we encountered were heroin smokers of kokteli, a mixture of heroin, cannabis, and/or tobacco which is smoked like a cigarette. ^ This research highlighted heroin smokers’ desire for access to drug treatment services. The current methadone-based medication assisted treatment (MAT) program is funded and operates as an HIV prevention program for IDUs to reduce HIV infection in this population and slow or stop the spread of a second wave of HIV infection in the general population. However, smokers perceived MAT to be primarily a drug use prevention or cessation program and felt unjustly neglected from the intervention, leading to a tense relationship with IDUs. From a public health standpoint, future interventions should include heroin smokers to prevent HIV transmission. ^

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Data from the Chicago Western Electric Study were used to investigate whether central fat distribution, as estimated by the ratio of subscapular-to-triceps skinfold, was associated with 25-year risk of death from coronary heart disease in a cohort of 1,945 middle-aged employed men. Subscapular-triceps skinfold ratio was found positively and significantly associated with risk of coronary death after adjustment for age and body mass index. The age-adjusted proportional hazards regression coefficient was 0.2078 with 95% confidence interval of 0.0087 to 0.4069. A difference of 1.1 in the subscapular-triceps skinfold ratio (the difference between the mean of the fifth quintile and of the first and second quintiles combined) was associated with a relative risk of 1.31 with 95% confidence interval of 1.06 to 1.62. The coefficient was decreased to 0.1961 (95% confidence interval of ($-$0.0028 to 0.3950) after adjustment for diastolic blood pressure, serum cholesterol and cigarette smoking as well as age and body mass index. At least some of the effect of central fat on coronary risk is probably mediated by blood pressure and serum lipids, but whether all of the effect can be accounted for blood pressure and serum lipids is uncertain.^ This study supports the concept that central fat distribution is a risk factor for 25-year risk of coronary death in middle-aged men. ^

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This cross-sectional study examines the association between health and academic achievement among Hispanic eighth-grade students in the Houston Independent School District. As part of the district's 3 year Safe Schools/Healthy Students Initiative to enhance comprehensive educational programs, a brief anonymous questionnaire was administered in the classroom to 359 students in two schools during a one-month period in the early part of the 2001 school year. ^ The primary study questions are: Among this sample of Hispanic adolescents, is there a significant association between academic achievement and health status? and in this same population, is there a significant association between health risk behavior and health status? The specific aims of this research are: (1) to describe the association between academic achievement and health status; (2) to describe the association between health risk behaviors and health status; and (3) to describe the relative contribution of health risk behaviors and academic achievement to adolescent health status among this sample of Hispanic adolescents. ^ The survey instrument was a 32-item questionnaire that incorporated: several academic achievement questions measuring usual grades, school-related performance, attendance, student and perceived parental satisfaction with academic achievement, and educational aspirations; two health and quality of life scales measuring adolescent self-reported health; and specific measures of health risk behavior, e.g., frequency of tobacco cigarette smoking, alcohol and other drug use, aggression, and suicidal ideation and behavior that were incorporated from the national Youth Risk Behavior Survey. Questions pertaining to sexual behavior and pregnancy were omitted to comply with school district guidelines. ^ Analysis revealed that strong associations between academic achievement and health status and between health risk behaviors and health status were observed after controlling for the covariates. Eight factors were found to be significantly associated with poor health status: usual grades (low), academic performance (low), academic achievement beliefs (low), classroom and homework performance satisfaction (low), ever drinking alcohol (6 or more times), suicidality (ever thought about, planned for, or sought medical help after attempting suicide), gender (female), and age (15 years and older). (Abstract shortened by UMI.) ^

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Objetivo: Identificar abuso, dependencia, adicciones (tabaquismo, problemas con alcohol y alimentación) y automedicación en el personal de la salud de un Hospital de agudos.- Material y Métodos: Estudio protocolizado y observacional mediante. encuesta estructurada, autoadministrada y anónima. Se realizó el análisis en 4 grupos: Médicos (M) (MS: Staff y MF: en formación), NO M: enfermeros (E) y otros (O: administración, laboratorio, farmacia, servicios generales). Se realizó un estudio comparativo con una población encuestada en el año 2004. Resultados: Se incluyeron 373 personas: 195 M (73 MS y 122 MF), 83 E y 92 O; 225 mujeres (60,3%); edad promedio grupal: 36.1 años (DS± 9.98). El 77.5% con pareja estable, el 98.1% heterosexuales y 67,3% universitarios. El 67.3% se automedicaba, el 35.1% eran tabaquistas activos; el 28.4% presentaba problemas con el alcohol y el 36.2% con la alimentación. El tabaquismo fue más frecuente entre 40-50 años (42,5%) y en E: 56.6%; MS: 21,9%; MF: 27% y O: 36.9%(p<0.05). Se incrementó la intención de abandonar el cigarrillo comparado con el año 2004 (74.6 vs 56.3%)(p<0.05). Los problemas con el alcohol fueron frecuentes entre 20 y 30 años (47.2%), en personas con pareja inestable (73.6%), sin diferencias entre los grupos y en 51.8% coexistía con tabaquismo. Los problemas de alimentación ocurrieron significativamente en MF (46,9%) comparados con MS (22.5%) (p<0.05). Se detectó automedicación en el 68.3 del Grupo O y en 48.1% del Grupo M (p<0.05). Al comparar la automedicación en las encuestas del año 2004 y 2007, se comprobó una reducción en E (87.8 vs 52.4%) y en O (77.5 vs 48.1%)(p<0.05).- Conclusiones: Se detectó elevada prevalencia de tabaquismo, problemas con el alcohol, alimentación y automedicación en todo el personal hospitalario. El tabaquismo predominó en enfermeros, los trastornos alimentarios en médicos en formación y el alcoholismo en solteros con pareja inestable.

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Smokers have a significantly higher risk for developing coronary and cerebrovascular disease than nonsmokers. Advanced glycation end products (AGEs) are reactive, cross-linking moieties that form from the reaction of reducing sugars and the amino groups of proteins, lipids, and nucleic acids. AGEs circulate in high concentrations in the plasma of patients with diabetes or renal insufficiency and have been linked to the accelerated vasculopathy seen in patients with these diseases. Because the curing of tobacco takes place under conditions that could lead to the formation of glycation products, we examined whether tobacco and tobacco smoke could generate these reactive species that would increase AGE formation in vivo. Our findings show that reactive glycation products are present in aqueous extracts of tobacco and in tobacco smoke in a form that can rapidly react with proteins to form AGEs. This reaction can be inhibited by aminoguanidine, a known inhibitor of AGE formation. We have named these glycation products “glycotoxins.” Like other known reducing sugars and reactive glycation products, glycotoxins form smoke, react with protein, exhibit a specific fluorescence when cross-linked to proteins, and are mutagenic. Glycotoxins are transferred to the serum proteins of human smokers. AGE-apolipoprotein B and serum AGE levels in cigarette smokers were significantly higher than those in nonsmokers. These results suggest that increased glycotoxin exposure may contribute to the increased incidence of atherosclerosis and high prevalence of cancer in smokers.

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2-Nitropropane (2-NP), an important industrial solvent and a component of cigarette smoke, is mutagenic in bacteria and carcinogenic in rats. 8-Amino-2′-deoxyguanosine (8-amino-dG) is one of the types of DNA damage found in liver, the target organ in 2-NP-treated rats. To investigate the thermodynamic properties of 8-amino-dG opposite each of the four DNA bases, we have synthesized an 11mer, d(CCATCG*CTACC), in which G* represents the modified base. By annealing a complementary DNA strand to this modified 11mer, four sets of duplexes were generated each containing one of the four DNA bases opposite the lesion. Circular dichroism studies indicated that 8-amino-dG did not alter the global helical properties of natural right-handed B-DNA. The thermal stability of each duplex was examined by UV melting measurements and compared with its unmodified counterpart. For the unmodified 11mer, the relative stability of the complementary DNA bases opposite G was in the order C > T > G > A, as determined from their –ΔG° values. The free energy change of each modified duplex was lower than its unmodified counterpart, except for the G*:G pair that exhibited a higher melting transition and a larger –ΔG° than the G:G duplex. Nevertheless, the stability of the modified 11mer duplex also followed the order C > T > G > A when placed opposite 8-amino-dG. To explore if 8-amino-dG opposite another 8-amino-dG has any advantage in base pairing, a G*:G* duplex was evaluated, which showed that the stability of this duplex was similar to the G*:G duplex. Mutagenesis of 8-amino-dG in this sequence context was studied in Escherichia coli, which showed that the lesion is weakly mutagenic (mutation frequency ∼10–3) but still can induce a variety of targeted and semi-targeted mutations.

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O tabagismo é um problema de saúde pública em todo o mundo. Entre as mulheres, devido ao aumento da prevalência comparada aos homens, o tabagismo feminino tem merecido atenção. Para o enfrentamento, é necessário entender o fenômeno e criar estratégias mais adequadas que incluam aspectos emocionais e sociais da dependência do tabagismo. Este estudo buscou descrever os esquemas cognitivos, sintomas de ansiedade e depressão de 112 mulheres que procuraram tratamento para cessação do tabagismo e sua relação com o insucesso do tratamento. A coleta de dados incluiu roteiro de entrevista estruturada e escalas validadas para a população brasileira que têm o objetivo de avaliar os esquemas cognitivos, sintomas de ansiedade e de depressão, e aspectos da dependência do cigarro. O conhecimento de fatores emocionais envolvidos no tabagismo e sua cessação podem ser úteis às ações de apoio à mudança comportamental do fumante. Objetivo: Descrever o perfil psicológico de mulheres que buscam cessação do tabagismo quanto aos esquemas cognitivos, sintomas de ansiedade e depressão antes e depois do tratamento com Terapia Cognitivo- Comportamental em grupo, e analisar fatores que contribuem para o desfecho de cessação. O desenho do estudo foi longitudinal e transversal. Para avaliar os esquemas cognitivos, o Questionário de Esquemas de Young em sua forma curta foi utilizado. Os grupos de terapia cognitivo-comportamental foram realizados concomitantes ao cuidado usual por médicos do estudo. Esses profissionais foram treinados no protocolo do estudo e o seguimento foi realizado por telefone por um membro do estudo independente e cego. Resultados: Os resultados forneceram evidências de que esquemas cognitivos tiveram relação significativa com os sintomas de depressão e ansiedade, com a adesão e os resultados do tratamento (cessação do tabagismo)

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Introdução: Demonstramos previamente que em modelo experimental de enfisema pulmonar induzido por instilação de elastase, o inibidor de serinoprotease rBmTI-A promoveu a melhora da destruição tecidual em camundongos. Considerando que o tabagismo é o principal fator de risco para o desenvolvimento da Doença Pulmonar Obstrutiva Crônica (DPOC) e que o modelo de exposição à fumaça de cigarro é considerado o que melhor mimetiza esta doença em humanos, este estudo teve por objetivo verificar a ação do inibidor para serinoproteases rBmTI-A sobre os processos fisiopatológicos envolvidos no desenvolvimento do enfisema pulmonar, em modelo de exposição ao tabaco. Métodos: Para a indução do enfisema pulmonar, os animais foram expostos à fumaça de cigarro (duas vezes ao dia/ 30 minutos/ 5 dias por semana/ durante 12 semanas), e os animais controle permaneceram expostos ao ar ambiente. Dois protocolos de tratamento com o inibidor rBmTI-A foram realizados. No primeiro, os animais receberam duas administrações do inibidor rBmTI-A ou de seu veículo (Solução Salina 0,9%) por via intranasal, sendo a primeira após 24h do término das exposições ao cigarro e outra, 7 dias após à primeira instilação do inibidor. No segundo protocolo, os animais receberam 3 administrações do inibidor rBmTI-A, durante o tempo de exposição (1ª dose: 24h antes do início da exposição à fumaça de cigarro; 2ª dose: um mês após o início da exposição; 3ª dose: dois meses após o início). Após o término dos protocolos de exposição e tratamento, os animais foram submetidos aos procedimentos para coleta dos dados de mecânica respiratória e avaliação do Intercepto Linear Médio (Lm). Para o segundo protocolo, realizamos também as medidas para quantificação de fibras de colágeno e elástica, da densidade de células positivas para MAC-2, MMP-12 e 9, TIMP-1, Gp91phox e TNFalfa; no parênquima através de imunohistoquímica, contagem de células polimorfonucleares além da expressão gênica de MMP-12 e 9 no pulmão através de RT-qPCR. Resultados e Discussão: O tratamento com o inibidor para serinoprotease rBmTI-A atenuou o desenvolvimento do enfisema pulmonar apenas no segundo protocolo, quando foi administrado durante a exposição à fumaça de cigarro. Embora os grupos Fumo-rBmTIA e Fumo-VE apresentem aumento de Lm comparados aos grupos controles, houve uma redução deste índice no grupo Fumo-rBmTIA comparado ao grupo Fumo-VE. O mesmo comportamento foi observado para as análises de proporção em volume de fibras de elástica e colágeno no parênquima. Além disto, observamos aumento de macrófagos, MMP-12, MMP-9 e TNFalfa; nos grupos expostos à fumaça de cigarro, mas o tratamento com o inibidor rBmTI-A diminuiu apenas a quantidade de células positivas para MMP-12. Na avaliação da expressão gênica para MMP-12 e 9, não observamos diferença entre os grupos experimentais e o mesmo comportamento foi observado para a quantidade de células polimorfonucleares no parênquima. Além disso, observamos aumento de GP91phox e TIMP-1 nos grupos tratados com rBmTIA. Conclusões: Tais resultados sugerem que o inibidor rBmTI-A não foi efetivo como tratamento da lesão após a doença instalada. Entretanto, atenuou o desenvolvimento da doença quando administrado durante a indução do enfisema, possivelmente através do aumento de GP91phox e TIMP-1, acompanhados pela diminuição de MMP-12.

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Apesar de diversos estudos in vitro e em populações indicarem um efeito protetor do β-caroteno em sistemas biológicos, estudos epidemiológicos como o \"The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study\" (ATBC) e o \"The Beta-Carotene and Retinol Efficacy Trial\" (CARET) mostraram um aumento na incidência de câncer pulmonar em indivíduos fumantes suplementados com β-caroteno. Essa ação contraditória tem sido chamada na literatura de \"Paradoxo do β-Caroteno\". Sabe-se que este carotenóide sob altas pressões de oxigênio ou na presença de peróxidos pode sofrer oxidação e levar a formação de compostos como aldeídos, epóxidos, etc, que são capazes de se adicionarem covalentemente ao DNA. Estudos, in vitro e in vivo têm demonstrado a possibilidade de os metabólitos do β-caroteno agirem como agentes pró-carcinogênicos. Estes agentes quando ativados quimicamente podem levar à formação de adutos de DNA. Já se sabe que alguns desses adutos encontramse em níveis aumentados em diversas situações de risco de câncer. Diversos grupos, incluindo o nosso, têm demonstrado a formação de lesões em DNA a partir de aldeídos e epóxidos exógenos ou gerados endogenamente. O presente trabalho mostra que a reação do β-caroteno e dois de seus produtos de oxidação, retinal e β-apo-8\'-carotenal, com 2\'-desoxiguanosina e DNA leva à formação de adutos. Dentre os adutos formados, foi caracterizado o aduto 1,N2eteno-2\'-desoxiguanosina (1 ,N2-εdGuo). Os níveis de outro aduto de DNA, a 8-oxo-7,8-dihidro-2\'-deoxiguanosina (8-oxodGuo), também foram monitoradas para estudo comparativo. A formação dos adutos também foi verificada em fibroblastos normais de pulmão humano (linhagem IMR-90) expostos ao β-caroteno e aos seus produtos de oxidação. Experimentos com ratos suplementados com β-caroteno e expostos à fumaça de cigarro em períodos de 7, 30 e 180 dias, mostraram níveis aumentados de 1,N2-εdGuo nos animais suplementados com o carotenóide comparado ao grupo veículo. Aumento no nível de 8-oxodGuo também foi verificado nos tratamentos de 7 e 180 dias. Um aumento significativo no nível do eteno aduto também foi verificado nos animais suplementados com β-caroteno e expostos à fumaça de cigarro, comparado ao grupo apenas exposto à fumaça após 7 e 180 dias de exposição. Nestes mesmos grupos, o aumento do 8-oxodGuo só foi observado no tratamento por 180 dias. Sabendo que estas lesões são comprovadamente mutagênicas, nossos estudos podem contribuir para o esclarecimento dos mecanismos envolvidos na formação de câncer em fumantes suplementados ou não com β-caroteno.

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Comunicación presentada en forma de póster en el "12th Mediterranean Congress of Chemical Engineering", Barcelona (Spain), November 15-18, 2011