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1.
David J Horne Monica Campo Justin R. Ortiz Eyal Oren Matthew Arentz Kristina Crothers Masahiro Narita 《PloS one》2012,7(11)
Background
Evidence of an association between cigarette smoking and latent tuberculosis infection (LTBI) is based on studies in special populations and/or from high prevalence settings. We sought to evaluate the association between LTBI and smoking in a low prevalence TB setting using population-based data from the National Health and Nutrition Examination Survey (NHANES).Methods
In 1999–2000, NHANES assessed LTBI (defined as a tuberculin skin test measurement ≥10 mm) in participants, and those ≥20 years of age were queried regarding their tobacco use and serum cotinine was measured. We evaluated the association of LTBI with self-reported smoking history and smoking intensity in multivariable logistic regression models that adjusted for known confounders (gender, age, birthplace, race/ethnicity, poverty, education, history of BCG vaccination, and history of household exposure to tuberculosis disease).Results
Estimated LTBI prevalence was 5.3% among those ≥20 years of age. The LTBI prevalence among never smokers, current smokers, and former smokers was 4.1%, 6.6%, and 6.2%, respectively. In a multivariable model, current smoking was associated with LTBI (OR 1.8; 95% CI, 1.1–2.9). The association between smoking and LTBI was strongest for Mexican-American and black individuals. In multivariate analysis stratified by race/ethnicity, cigarette packs per day among Mexican-American smokers and cotinine levels among black smokers, were significantly associated with LTBI.Conclusions
In the large, representative, population-based NHANES sample, smoking was independently associated with significantly increased risks of LTBI. In certain populations, a greater risk of LTBI corresponded with increased smoking exposure. 相似文献2.
Many studies have examined the association between the APE1 T1349G (Asp148Glu) gene polymorphisms and lung cancer risk in
various populations, but their results have been inconsistent. To assess this relationship more precisely, a meta-analysis
was performed. The PubMed, Embase, Web of Science, and CNKI database was searched for case–control studies published up to
June 2010. Data were extracted and pooled odds ratios (OR) with 95% confidence intervals (CI) were calculated. Ultimately,
ten studies, comprising 2,696 lung cancer cases and 3,948 controls were included. Overall, for the G allele carriers (TG + GG)
versus homozygote TT, the pooled OR was 1.037 (95% CI = 0.928–1.159 P = 0.001 for heterogeneity), for GG versus TT the pooled OR was 0.997 (95% CI = 0.861–1.154 P = 0.005 for heterogeneity). In the stratified analysis by ethnicity, significantly risks were not found among Asians or Caucasians.
However, in the subgroup analyses by smoking status, significantly risks were found among smokers not in non-smokers. This
meta-analysis suggested that the APE1 T1349G (Asp148Glu) polymorphism was not associated with lung cancer risk among Asians
or Caucasians. But, the APE1 G allele was an increased risk factor for developing lung cancer among smokers. 相似文献
3.
Mikhlid H. Almutairi Nouf S. Al-Numair Narasimha Reddy Parine Bader O. Almutairi Abdulwahed F. Alrefaei Mahmoud Rouabhia Abdelhabib Semlali 《Saudi Journal of Biological Sciences》2021,28(7):3972-3980
Methylenetetrahydrofolate reductase (MTHFR) polymorphism plays a fundamental role in susceptibility to various diseases, including cancers and autoimmune diseases. In the current study, we aimed to compare genotype and allele frequency variations of rs1801131, one of the most common variants found in the MTHFR gene, among Saudi smokers and non-smokers. We hypothesized that genetic variations of this gene are responsible for many diseases, particularly those caused by cigarette smoking (CS) such as pulmonary diseases, oral cancer and lung cancer. We performed a case-control study on a sample of 235 healthy smokers and 239 healthy non-smokers in Saudi Arabia. The rs1801131 SNP genotypes were determined using a genotyping assay and multiple in silico algorithmic software programs were used to identify the effects and structural functions of the rs1801131 (Glu429Ala) mutation. Using chi-squared tests, we found that, among smokers, TG and GG genotype carriers had 0.209-fold (OR = 0.209, P < 0.005) and 0.427-fold (OR = 0.427, P = 0.003) lower risks of CS-related disease compared to TT reference genotypes. In addition, this protective effect was observed in Saudi smokers independent of age, gender, types of smoking, duration, and average daily smoking consumption. Filling a research gap by exploring this topic in the Saudi population, the current findings indicate that genotype and allele distributions of MTHFR rs1801131 polymorphism present fundamental protective effects against the risk of CS-related disease. These findings should be verified in future studies with larger sample sizes, different ethnicities, and patients suffering from CS-related diseases, such as oral cancer and lung cancer. 相似文献
4.
Cigarette smoking is generally believed to be responsible for a substantial number of human health problems. However, the causal relationship between smoking, the induction of biological effects and the extent of health problems among smokers have not been fully documented. Using the recently developed lymphocyte micronucleus (MN) assay, we have evaluated the chromosome aberration frequencies in 67 cigarette smokers and 59 matched non-smoking control subjects. We found that the mean MN frequency (per 100 cells) in the smokers was slightly higher than that found in the non-smokers (0.71 +/- 0.23 and 0.58 +/- 0.05 respectively; p less than 0.08). Factors which contribute to the expression of chromosome aberrations were also investigated. A significant age-dependent increase in MN frequencies was observed in both groups (p less than 0.05). Linear regression analysis showed that the age-dependent effects among smokers (r = 0.54; p less than 0.02) was further enhanced by cigarette consumption (r = 0.62; p less than 0.005). Consumption of low potency 'one-a-day' type multivitamins had no effect on MN frequencies in either sex of non-smokers and in the 1 male smoker who took multivitamins but vitamin intake consistently reduced the MN frequencies among female smokers. Using a challenge assay, fidelity of DNA repair was evaluated. Lymphocytes from both smokers and non-smokers were irradiated with single doses of 0 or 100 cGy of X-rays or with double doses of 100 cGy of X-rays each separated by 15 or 60 min (100/15 or 100/60). Chromosome translocation frequencies were consistently higher after irradiation in lymphocytes from smokers than in those from non-smokers. Statistically significant differences were detected when the cells were irradiated with the double doses of 100 cGy X-rays each separated by 60 min (p less than 0.05). These data suggest that lymphocytes from smokers made more mistakes in the repair of DNA damage than cells from non-smokers. Our studies provide new insights into the genotoxic effects of cigarette smoke and new information which may be useful for understanding the mechanisms for induction of health problems from smoking. 相似文献
5.
Ahmed Faisal Sumit Anindya Das Zinat Sharmin Nazmul Ahsan Nobutaka Ohgami Masashi Kato Anwarul Azim Akhand 《PloS one》2015,10(3)
Lifestyle including smoking, noise exposure with MP3 player and drinking alcohol are considered as risk factors for affecting hearing synergistically. However, little is known about the association of cigarette smoking with hearing impairment among subjects who carry a lifestyle without using MP3 player and drinking alcohol. We showed here the influence of smoking on hearing among Bangladeshi subjects who maintain a lifestyle devoid of using MP3 player and drinking alcohol. A total of 184 subjects (smokers: 90; non-smokers: 94) were included considering their duration and frequency of smoking for conducting this study. The mean hearing thresholds of non-smoker subjects at 1, 4, 8 and 12 kHz frequencies were 5.63±2.10, 8.56±5.75, 21.06±11.06, 40.79±20.36 decibel (dB), respectively and that of the smokers were 7±3.8, 13.27±8.4, 30.66±12.50 and 56.88±21.58 dB, respectively. The hearing thresholds of the smokers at 4, 8 and 12 kHz frequencies were significantly (p<0.05) higher than those of the non-smokers, while no significant differences were observed at 1 kHz frequency. We also observed no significant difference in auditory thresholds among smoker subgroups based on smoking frequency. In contrast, subjects smoked for longer duration (>5 years) showed higher level of auditory threshold (62.16±19.87 dB) at 12 kHz frequency compared with that (41.52±19.21 dB) of the subjects smoked for 1-5 years and the difference in auditory thresholds was statistically significant (p<0.0002). In this study, the Brinkman Index (BI) of smokers was from 6 to 440 and the adjusted odds ratio showed a positive correlation between hearing loss and smoking when adjusted for age and body mass index (BMI). In addition, age, but not BMI, also played positive role on hearing impairment at all frequencies. Thus, these findings suggested that cigarette smoking affects hearing level at all the frequencies tested but most significantly at extra higher frequencies. 相似文献
6.
A study of the relation between smoking habits and lung cancer in male industrial workers over a period of three years has confirmed the earlier findings in doctors that the death-rate from lung cancer correlates closely with the number of cigarettes smoked. Of 54,460 men studied 68.7% were current cigarette smokers. The annual mortality rate from lung cancer was 0.33 per thousand in non-smokers and ex-smokers, and 1.2 per thousand for all cigarette smokers, and higher in heavy smokers.Heavy cigarette smokers who retained the cigarette in the mouth between puffs (“drooping” cigarette habit) had an annual mortality rate of 4.1 per thousand.The mortality from coronary thrombosis in smokers was nearly three times that in non-smokers. A mortality gradient with rising consumption of cigarettes was observed.Some correlation between smoking and cancer of other sites and from non-neoplastic lung disease was observed in older men, but no correlation was found with other cardiovascular diseases and cerebrovascular diseases. 相似文献
7.
Ranjini Valiathan Maria J. Miguez Bijal Patel Kristopher L. Arheart Deshratn Asthana 《PloS one》2014,9(5)
Background
The influence of tobacco smoking on the immune system of HIV infected individuals is largely unknown. We investigated the impact of tobacco smoking on immune activation, microbial translocation, immune exhaustion and T-cell function in HIV infected individuals.Method
HIV infected smokers and non-smokers (n = 25 each) with documented viral suppression on combination antiretroviral therapy and HIV uninfected smokers and non-smokers (n = 15 each) were enrolled. Markers of immune activation (CD38 and HLA-DR) and immune exhaustion (PD1, Tim3 and CTLA4) were analyzed in peripheral blood mononuclear cells (PBMCs) by flow cytometry. Plasma markers of microbial translocation (soluble-CD14 - sCD14 and lipopolysaccharide - LPS) were measured. Antigen specific functions of CD4+ and CD8+ T-cells were measured, by flow cytometry, in PBMCs after 6 hours stimulation with Cytomegalovirus, Epstein-Barr virus and Influenza Virus (CEF) peptide pool.Results
Compared to non-smokers, smokers of HIV infected and uninfected groups showed significantly higher CD4+ and CD8+ T-cell activation with increased frequencies of CD38+HLA-DR+ cells with a higher magnitude in HIV infected smokers. Expressions of immune exhaustion markers (PD1, Tim3 and CTLA4) either alone or in combinations were significantly higher in smokers, especially on CD4+ T-cells. Compared to HIV uninfected non-smokers, microbial translocation (sCD14 and LPS) was higher in smokers of both groups and directly correlated with CD4+ and CD8+ T-cell activation. Antigen specific T-cell function showed significantly lower cytokine response of CD4+ and CD8+ T-cells to CEF peptide-pool stimulation in smokers of both HIV infected and uninfected groups.Conclusions
Our results suggest that smoking and HIV infection independently influence T-cell immune activation and function and together they present the worst immune profile. Since smoking is widespread among HIV infected individuals, studies are warranted to further evaluate the cumulative effect of smoking on impairment of the immune system and accelerated disease progression. 相似文献8.
Xuhong Hou Jieyuzhen Qiu Peizhu Chen Jun Lu Xiaojing Ma Juming Lu Jianping Weng Linong Ji Zhongyan Shan Jie Liu Haoming Tian Qiuhe Ji Dalong Zhu Jiapu Ge Lixiang Lin Li Chen Xiaohui Guo Zhigang Zhao Qiang Li Zhiguang Zhou Wenying Yang Weiping Jia China National Diabetes Metabolic Disorders Study Group 《PloS one》2016,11(3)
Different studies have produced conflicting results regarding the association between smoking and diabetes mellitus, and detailed analysis of this issue in Chinese males based on nationwide samples is lacking. We explored the association between cigarette smoking and newly-diagnosed diabetes mellitus (NDM) in Chinese males using a population-based case-control analysis; 16,286 male participants without previously diagnosed diabetes were included. Prediabetes and NDM were diagnosed using the oral glucose tolerance test. The cohort included 6,913 non-smokers (42.4%), 1,479 ex-smokers (9.1%) and 7,894 current smokers (48.5%). Age-adjusted glucose concentrations (mmol/L) were significantly lower at fasting and 120 min in current smokers than non-smokers (5.25 vs. 5.30, 6.46 vs. 6.55, respectively, both P < 0.01). After adjustment for demographic and behavioral variables (age, region, alcohol consumption status, physical activity, education, and family history of diabetes), logistic regression revealed significant negative associations between smoking and NDM in males of a normal weight (BMI < 25 kg/m2: adjusted odds ratio [AOR] = 0.75, P = 0.007; waist circumference < 90 cm: AOR = 0.71, P = 0.001) and males living in southern China (AOR = 0.75, P = 0.009), but not in males who were overweight/obese, males with central obesity, or males living in northern China. Compared to non-smokers, current smokers were less likely to be centrally obese or have elevated BP (AOR: 0.82 and 0.74, both P < 0.05), and heavy smokers (≥ 20 pack-years) were less likely to have elevated TG (AOR = 0.84, P = 0.012) among males of a normal weight. There were no significant associations between quitting smoking and metabolic disorders either among males of a normal weight or males who were overweight/obese. In conclusion, smokers have a lower likelihood of NDM than non-smokers among Chinese males with a lower BMI/smaller waist. 相似文献
9.
《Free radical research》2013,47(10):1230-1237
AbstractThe significance of 5-lipoxygenase and myeloperoxidase activities has not been extensively studied among young male smokers. Leukotriene B4, 20-hydroxy-leukotriene B4, 20-carboxy-leukotriene B4 and 3-chlorotyrosine were measured in plasma and urinary samples of young male smokers at 8 hours following cigarette abstinence and an hour after cigarette smoking. Leukotriene B4 and 3-chlorotyrosine were determined in neutrophils isolated from these individuals. The levels of these markers were compared with those of age-matched controls. In vitro studies were performed to evaluate the production of leukotriene B4 and 3-chlorotyrosine from human neutrophils following exposure to nicotine and cotinine. Thirty male smokers (mean age, 27.4 years) and 28 male non-smokers (mean age, 28.7 years) were studied. Plasma levels of leukotriene B4, 20-carboxy-leukotriene B4 and 3-chlorotyrosine were higher in smokers than in non-smokers; leukotriene B4 and 20-carboxy-leukotriene B4 levels increased further an hour after cigarette smoking. Peripheral neutrophils isolated from smokers showed greater expressions of myeloperoxidase and 5-lipoxygenase activities compared with non-smokers, while plasma leukotriene B4 and 3-chlorotyrosine were correlated significantly with high-sensitivity C-reactive protein and plasma nicotine concentrations. Exposure of human neutrophils to nicotine and cotinine resulted in a higher production of leukotriene B4 and 3-chlorotyrosine. To conclude, leukotriene B4 and 3-chlorotyrosine levels are increased in young male cigarette smokers. These results suggest that cigarette smoking aggravates neutrophil-mediated inflammation by modulating the activities of myeloperoxidase and 5-lipoxygenase pathways. 相似文献
10.
J. Rimington 《BMJ (Clinical research ed.)》1973,1(5856):776-778
Male volunteers for mass radiography examination, aged 40 or more, were questioned about their sputum production, smoking habits, and, when applicable, their method of smoking cigarettes.Of 5,438 cigarette smokers 460 (8·4%) smoked their cigarettes without removing the cigarette from the mouth between puffs (“drooping” cigarette smokers) whereas the rest smoked in the normal manner.Persons who admitted to producing sputum from their chests on most days of the year or on most days for at least three months of the year for a minimum of two years were classified as chronic bronchitics in the absence of other causative disease.The rate of chronic bronchitis among the “drooping” cigarette smokers (41·5%) was considerably greater than that among those smoking cigarettes in the normal manner (33·6%). The same pattern was maintained when age and cigarette consumption were standardized, though “drooping” cigarette smokers had a slight bias towards plain as distinct from filter cigarettes and towards a lower social class this was not sufficient to account for the excess of chronic bronchitis among those using this method of smoking. 相似文献
11.
Jae Won Hong Cheol Ryong Ku Jung Hyun Noh Kyung Soo Ko Byoung Doo Rhee Dong-Jun Kim 《PloS one》2015,10(5)
BackgroundSeveral Western studies have revealed that among non-diabetics, glycosylated hemoglobin A1c (HbA1c) levels are higher in smokers than non-smokers. While studies conducted in Western populations consistently support this association, a recent meta-analysis reported that studies carried out in non-Western populations, including studies of Chinese, Egyptian, and Japanese-Americans, did not detect any significant differences in HbA1c levels between smokers and non-smokers.ObjectivesWe assessed the association between smoking habits and HbA1c levels in the general Korean adult population using data from the Korean National Health and Nutrition Examination Survey (KNHANES) performed in 2011–2012.MethodsA total of 10,241 participants (weighted n=33,946,561 including 16,769,320 men and 17,177,241 women) without diabetes were divided into four categories according to their smoking habits: never smokers (unweighted n/ weighted n= 6,349/19,105,564), ex-smokers (unweighted n/ weighted n= 1,912/6,207,144), current light smokers (<15 cigarettes per day, unweighted n/ weighted n=1,205/5,130,073), and current heavy smokers (≥15 cigarettes per day, unweighted n/ weighted n=775/3,503,781).ResultsIn age- and gender-adjusted comparisons, the HbA1c levels of each group were 5.52 ± 0.01% in non-smokers, 5.49 ± 0.01% in ex-smokers, 5.53 ± 0.01% in light smokers, and 5.61 ± 0.02% in heavy smokers. HbA1c levels were significantly higher in light smokers than in ex-smokers (p = 0.033), and in heavy smokers compared with light smokers (p < 0.001). The significant differences remained after adjusting for age, gender, fasting plasma glucose, heavy alcohol drinking, hematocrit, college graduation, and waist circumference. Linear regression analyses for HbA1c using the above-mentioned variables as covariates revealed that a significant association between current smoking and HbA1c (coefficient 0.021, 95% CI 0.003–0.039, p = 0.019).ConclusionsCurrent smoking was independently associated with higher HbA1c levels in a cigarette exposure-dependent manner in a representative population of Korean non-diabetic adults. In this study, we have observed an association between smoking status and HbA1c levels in non-diabetics drawn from a non-Western population, consistent with previous findings in Western populations. 相似文献
12.
Huachun Weng Zuquan Weng Yuquan Lu Kunio Nakayama Kanehisa Morimoto 《Mutation Research - Genetic Toxicology and Environmental Mutagenesis》2009,679(1-2):59-64
The aim of this study was to investigate the effects of smoking, polymorphisms of XRCC1 codons 194 and 399, and age on levels of basal DNA damage (as measured by an alkaline comet assay) on mononuclear cells in 122 healthy Japanese workers. In the whole group of 122 individuals, the tail moment (TM) values of current smokers (P < 0.001) or former smokers (P = 0.03) were significantly higher than those of nonsmokers. Individuals bearing the XRCC1 399Gln variant allele showed significant increases in TM values in all subjects or in referent subgroups stratified by age or smoking status except in the current smokers group; in contrast, the TM values of individuals bearing the XRCC1 194Trp variant allele were significantly lower than those of individuals bearing wild-type Arg/Arg genotypes. Furthermore, older subjects (≥47 years old) had significantly higher TM values than younger subjects (<47 years old) in all subjects (P = 0.008). Multiple regression analysis indicated that smoking habits, polymorphisms of XRCC1 codons 194 and 399, and age were important variables affecting individuals basal DNA damage. 相似文献
13.
Loke WM Lam KM Chong WL Chew SE Quek AM Lim ECh Seet RC 《Free radical research》2012,46(10):1230-1237
Abstract The significance of 5-lipoxygenase and myeloperoxidase activities has not been extensively studied among young male smokers. Leukotriene B(4), 20-hydroxy-leukotriene B(4), 20-carboxy-leukotriene B(4) and 3-chlorotyrosine were measured in plasma and urinary samples of young male smokers at 8 hours following cigarette abstinence and an hour after cigarette smoking. Leukotriene B(4) and 3-chlorotyrosine were determined in neutrophils isolated from these individuals. The levels of these markers were compared with those of age-matched controls. In vitro studies were performed to evaluate the production of leukotriene B(4) and 3-chlorotyrosine from human neutrophils following exposure to nicotine and cotinine. Thirty male smokers (mean age, 27.4 years) and 28 male non-smokers (mean age, 28.7 years) were studied. Plasma levels of leukotriene B(4), 20-carboxy-leukotriene B(4) and 3-chlorotyrosine were higher in smokers than in non-smokers; leukotriene B(4) and 20-carboxy-leukotriene B(4) levels increased further an hour after cigarette smoking. Peripheral neutrophils isolated from smokers showed greater expressions of myeloperoxidase and 5-lipoxygenase activities compared with non-smokers, while plasma leukotriene B(4) and 3-chlorotyrosine were correlated significantly with high-sensitivity C-reactive protein and plasma nicotine concentrations. Exposure of human neutrophils to nicotine and cotinine resulted in a higher production of leukotriene B(4) and 3-chlorotyrosine. To conclude, leukotriene B(4) and 3-chlorotyrosine levels are increased in young male cigarette smokers. These results suggest that cigarette smoking aggravates neutrophil-mediated inflammation by modulating the activities of myeloperoxidase and 5-lipoxygenase pathways. 相似文献
14.
Water-pipe (WP) smoking has significantly increased in the last decade worldwide. Compelling evidence suggests that the toxicants in WP smoke are similar to that of cigarette smoke. The WP smoking in a single session could have acute harmful health effects even worse than cigarette smoking. However, there is no evidence as such on long term WP smoking and its impact on chronic health conditions particularly cardiovascular and metabolic conditions. Therefore, we conducted this study to investigate the relationship between WP smoking and metabolic syndrome (MetS). This was a cross-sectional study carried out in Punjab province of Pakistan using the baseline data of a population-based study - Urban Rural Chronic Diseases Study (URCDS). Information was collected by trained nurses regarding the socio-demographic profile, lifestyle factors including WP smoking, current and past illnesses. A blood sample was obtained for measurement of complete blood count, lipid profile and fasting glucose level. MetS was ascertained by using the International Diabetic Federation's criteria. We carried out multiple logistic regressions to investigate the association between WP smoking and MetS. Final sample included 2,032 individuals - of those 325 (16.0%) were current WP smokers. Age adjusted-prevalence of MetS was significantly higher among current WP smokers (33.1%) compared with non-smokers (14.8%). Water-pipe smokers were three times more likely to have MetS (OR 3.21, 95% CI 2.38-4.33) compared with non-smokers after adjustment for age, sex and social class. WP smokers were significantly more likely to have hypertriglyceridemia (OR 1.63, 95% CI 1.25-2.10), hyperglycaemia (OR 1.82, 95% CI 1.37-2.41), Hypertension (OR 1.95, 95% CI 1.51-2.51) and abdominal obesity (OR 1.93, 95% CI 1.52-2.45). However, there were no significant differences in HDL level between WP smokers and non-smokers. This study suggests that WP smoking has a significant positive (harmful) relationship with MetS and its components. 相似文献
15.
It is well known that cigarette smoking and physical activity have significant impacts on cardiovascular disease (CVD) mortality and morbidity. Meanwhile, it is of interest to understand whether physical activity protects against CVD for smokers in a similar manner as it does for non-smokers. The present study examined how leisure-time physical activity (LTPA) is associated with the prevalence of CVD in relation to smoking status among adult Nevadans, using data from the 2010 Nevada Behavioral Risk Factor Surveillance System. Of the 3,913 survey respondents, 8.5% self-reported that they had ever been diagnosed with CVD. People with a history of CVD were significantly less likely to engage in LTPA than those with no history of CVD (p < 0.05). After adjusting for common sociodemographic variables, it was revealed that people with CVD were twice more likely to not engage in LTPA than their counterparts independent of smoking status. Without taking LTPA into account, the odds of having CVD for current and former smokers was 1.87–2.25 times higher than the odds for non-smokers. Interestingly, however, if LTPA was accounted for, there was no significant difference in the odds of having CVD between current and non-smokers. These results indicate that LTPA is inversely associated with the prevalence of CVD independent of smoking status, and that regular physical activity may protect against CVD for smokers as well as for non-smokers. Physical activity, along with smoking cessation, should be promoted to better prevent and control CVD among smokers. 相似文献
16.
The purpose of this investigation was to determine and compare the activities of arginase and rhodanese in the blood plasma of cigarette smokers and non-smokers.The activity of arginase in the blood plasma of smokers was higher than arginase activity in the non-smokers (NS), however,in the smokers with diseases (SWD), the increase was significant. The comparison between the activity of rhodanese in the SWD, smokers without diseases (SWOD) and NS blood plasma revealed a decrease in the activity of rhodanese in NS and no significant difference in the three groups with P=0.8677. This paper reported the enhancing effect of cigarette smoking could have on the disease state of smokers due to high arginase activity. Keywords; Rhodanese, Arginase, Cigarette smoking, Plasma. 相似文献
17.
Mary N. Mohankumar S. Janani B. Karthikeya Prabhu P. R. Vivek Kumar R. K. Jeevanram 《Mutation Research - Genetic Toxicology and Environmental Mutagenesis》2002,520(1-2):179-187
DNA damage was assessed in smoker lymphocytes by subjecting them to the single cell gel electrophoresis (SCGE) assay. In addition to the appearance of comet tails, smoker cells exhibited enlarged nuclei when analysed by the comet assay. On comparing basal DNA damage among smokers and a non-smoking control group, smoker lymphocytes showed higher basal DNA damage (smokers, 36.25±8.45 μm; non-smokers, 21.6±2.06 μm). A significant difference in DNA migration lengths was observed between the two groups at 10 min after UV exposure (smokers, 65.5±20.34 μm; non-smokers, 79.2±11.59 μm), but no significant differences were seen at 30 min after UV exposure (smokers, 21.13±10.73 μm; non-smokers, (27.2±4.13 μm). The study thus implies that cigarette smoking perhaps interferes with the incision steps of the nucleotide excision repair (NER) process. There appeared be no correlation between the frequency of smoking and DNA damage or the capacity of the cells to repair UV-induced DNA damage that suggests inherited host factors may be responsible for the inter-individual differences in DNA repair capacities. The study also suggests monitoring NER following UV insult using the SCGE assay is a sensitive and simple method to assess DNA damage and integrity of DNA repair in human cells exposed to chemical mutagens. 相似文献
18.
Saadat M 《Molecular biology reports》2009,36(6):1353-1356
Objectives It is reported that parental exposure to toxicants can influence offspring sex ratio at birth. Studies have reported that
several chemicals found in cigarette smoke are substrates of glutathione S-transferase T1 (GSTT1, a member of GSTθ). To determine
the effect of cigarette smoke on serum levels of testosterone and gonadotrophins of smokers and possible association of these
hormones levels with GSTT1 polymorphism, the present study was done. Methods Our study was conducted on 181 (40 smokers, 141 non-smokers) male subjects. Genomic DNA was extracted from peripheral blood.
The GSTT1 genotyping was performed using PCR-based method. All measurements for testosterone, follicle stimulating hormone (FSH), and
luteinizing hormone (LH) were done in one laboratory. Results In smoker subjects the mean ± sd of serum testosterone, FSH, and LH were 4.64 ± 1.63 ng/ml, 2.72 ± 1.17 IU/l, and 3.03 ± 1.04 IU/l,
respectively. In non-smoker subjects the mean ± sd of serum testosterone, FSH, and LH were 4.49 ± 1.24 ng/ml, 2.89 ± 1.26 IU/l,
and 3.07 ± 1.28 IU/l, respectively. There was no significant difference between smokers and non-smokers for serum testosterone
(t = 0.622, df = 179, P = 0.535), FSH (t = −0.757, df = 179, P = 0.450), and LH (t = −0.179, df = 179, P = 0.858). Also there was no significant difference between smokers and non-smokers in either GSTT1 null or positive genotypes for levels of testosterone, FSH, and LH. Conclusion Based on present data, it might be concluded that serum levels of testosterone and gonadotrophins were not significantly
different between smoker and non-smoker males in both null and present GSTT1 genotypes. 相似文献
19.
Sofia Pavanello Alessandra Pulliero Bruno Onofrio Saia Erminio Clonfero 《Mutation Research - Genetic Toxicology and Environmental Mutagenesis》2006,611(1-2):54-63
We evaluated determinants of anti-benzo[a]pyrenediolepoxide-(B[a]PDE)–DNA adduct formation (adduct induced by the ultimate carcinogenic metabolite of B[a]P) in lymphomonocytes of subjects environmentally exposed to low doses of polycyclic aromatic hydrocarbons (PAHs) (B[a]P). Our study population consisted of 585 Caucasian subjects, all municipal workers living in North-East Italy and recruited during their periodic check-ups after informed consent. PAH (B[a]P) exposure was assessed by questionnaire. Anti-B[a]PDE–DNA levels were measured by HPLC fluorescence analysis.We found that cigarette smoking (smokers (22%) versus non-smokers, p < 0.0001), dietary intake of PAH-rich meals (≥52 (38%) versus <52 times/year, p < 0.0001), and outdoor exposure (≥4 (19%) versus <4 h/day; p = 0.0115) significantly influenced adduct levels. Indoor exposure significantly increased the frequency of positive subjects (≥0.5 adducts/108 nucleotides; χ2 for linear trend, p = 0.051). In linear multiple regression analysis the major determinants of increased DNA adduct levels (ln values) were smoking (t = 6.362, p < 0.0001) and diet (t = 4.035, p < 0.0001). In this statistical analysis, indoor and outdoor exposure like other factors of PAH exposure had no influence. In non-smokers, the influence of diet (p < 0.0001) and high indoor exposure (p = 0.016) on anti-B[a]PDE–DNA adduct formation became more evident, but not that of outdoor exposure, as was confirmed by linear multiple regression analysis (diet, t = 3.997, p < 0.0001 and high indoor exposure, t = 2.522, p = 0.012).This study indicates that anti-B[a]PDE–DNA adducts can be detected in the general population and are modulated by PAH (B[a]P) exposure not only with smoking – information already known from studies with limited number of subjects – but also with dietary habits and high indoor exposure. In non-smokers, these two factors are the principal determinants of DNA adduct formation. The information provided here seems to be important, since DNA adduct formation in surrogate tissue is an index of genotoxic exposure also in target organs (e.g., lung) and their increase may also be predictive of higher risk for PAH-related cancers. 相似文献
20.
Sierra-Torres MS Arboleda-Moreno YY Hoyos LS Sierra-Torres CH 《Mutation research》2004,562(1-2):67-75
Worldwide, the annual morbimortality caused by cigarette smoking is a major public health concern. In Colombia, up to 33% of the adult population has smoked at some point in life, raising important national issues on the disease burden from tobacco. The aim of this study was to establish whether cigarette smoking increases the frequency of chromosome aberrations (CA) in peripheral blood lymphocytes of smokers (n = 52) compared with non-smokers (n = 52) in Popayán, Colombia. After signing a consent form, volunteers provided a blood sample (20 ml) to establish cell cultures at 52 h. For CA analysis, 100 complete metaphase cells from each subject were evaluated. The CA frequency was significantly higher in smokers (8.38 +/- 0.61) than in non-smokers (3.13 +/- 0.29), showing the highest number of CA (14.83 +/- 1.01) among heavy smokers (>20 pack-years). Interestingly, light smokers (< or =10 pack-years) also showed a significant increase in CA when compared to non-smokers (6.62 +/- 0.53 versus 3.13 +/- 0.29, P < 0.01, respectively). In addition, a significant positive correlation was found between the frequency of CA and the intensity of smoking in pack-years (R2 = 0.60). Our study indicates that the genotoxic effects in lymphocytes from smokers are most likely caused by cigarette smoke constituents, providing scientific evidence to encourage national campaigns to prevent tobacco consumption. 相似文献