N-nitrosamines are strong carcinogens for humans. This paper gives an overview of the nitrosmaines in cigarette smoke including the formation, the harmfulness, the analytical methods of the nitrosmaines and the adsorp...N-nitrosamines are strong carcinogens for humans. This paper gives an overview of the nitrosmaines in cigarette smoke including the formation, the harmfulness, the analytical methods of the nitrosmaines and the adsorptions and degradations of N –nitrosamines.展开更多
Background: Asthma is a chronic multifactorial disease with high prevalence. Among asthma risk factors, the effect of tobacco smoke exposure on bronchial asthma is still debated. Aim: The aim of this study was to dete...Background: Asthma is a chronic multifactorial disease with high prevalence. Among asthma risk factors, the effect of tobacco smoke exposure on bronchial asthma is still debated. Aim: The aim of this study was to determine the association between environmental and direct tobacco smoke (cigarette and hookah) exposure and incidence and control of bronchial asthma. Materials & Methods: This descriptive study was conducted on 109 patients with asthma referring to Imam Khomeini Hospital in Ardabil city. Asthma Control Questionnaire was used for evaluating of asthma control. Patients’ asthma control was individually evaluated and compared with together with particular attention to history of tobacco smoke exposure. Chi square and Tav-Kendal were used to analyze the data in SPSS15 software. Results: The history of tobacco smoke exposure was found in 31.2% of the 109 patients. Patients with uncontrolled asthma with 60.6% constituted the largest volume of all samples. There was no significant correlation between tobacco smoke exposure and asthma occurrence (P > 0.05), also there was not found significant correlation between tobacco smoke exposure and asthma control (Error coefficient > 0.10). Conclusion: According to the results, history of tobacco (cigarette and hookah) smoke exposure (environmental and direct) has no effect on the asthma occurs and control status.展开更多
DNA hypermethylation of tumor suppressor genes has been frequently observed in cancer patients, and therefore, may provide a valuable biomarker for cancer prevention and treatment. DNA hypermethylation may also provid...DNA hypermethylation of tumor suppressor genes has been frequently observed in cancer patients, and therefore, may provide a valuable biomarker for cancer prevention and treatment. DNA hypermethylation may also provide an important mechanism in cancer progression. Lung cancer is strongly associated with exposure to environmental carcinogens, especially tobacco smoke. DNA damage generated by tobacco smoke is believed to play an important role in lung cancer development. XPC is a DNA damage recognition protein required for DNA repair and other DNA damage responses and attenuated XPC protein levels have been detected in many lung cancer patients. We studied the role of XPC protein deficiency in tobacco smoke-caused DNA hypermethylation of important tumor suppressor genes. Using both normal human fibroblasts (NF) and XPC-deficient hu man fibroblasts (XPC), our DNA methylation studies demonstrated that the XPC deficiency caused elevated levels of DNA hypermethylation in both Brca1 and Mlh1 tumor suppressor genes following exposure to tobacco smoke condensate (TSC). The results of our ChIP studies revealed that the XPC deficiency led to an increased binding of DNA methyltransferase 3A (DNMT3A) at the promoter region CpG island-containing sequences of these genes under the TSC treatment;however, this increase was partially diminished with prior treatment with caffeine. The results of our immuno-precipitation (IP) studies demonstrated a protein-protein interaction of the ATR with DNMT3A. Our western blots revealed that the XPC deficiency caused an increase in TSC-induced ATR phosphorylation at serine 428, an indicator of ATR activation. All these results suggest that XPC deficiency causes an accelerated DNA hypermethylation in important tumor suppressor genes under tobacco smoke exposure and activation of the ATR signaling pathway is involved in this DNA hypermethylation process.展开更多
Environmental tobacco smoke(ETS)is a wellknown reason of many adverse health consequences in pregnant women.Exposure of ETS during pregnancy may increase the risk of some fetal diseases in pregnant women and/or birth ...Environmental tobacco smoke(ETS)is a wellknown reason of many adverse health consequences in pregnant women.Exposure of ETS during pregnancy may increase the risk of some fetal diseases in pregnant women and/or birth defects in neonates.Many countries have implemented laws to control smoking and free of second hand smoke in all enclosed workplaces.In China,antismoking law was enforced in March 2010.We aimed to assess the exposure of pregnant women to cotinine after anti-smoking law was implemented in China.The urine samples were collected from 2,100 volunteers from Zhejiang Province,China and urinary concentration of cotinine was measured using gas chromatography and mass spectrometry.Cotinine was detected in 87%of the pregnant women.The GM and 95th percentile concentration inpregnant women were 4.28 and 44.00 lg/L,respectively.Similarly,the GM and 95th concentration of cotinine were significantly higher in smoking group than in non-smoking group(P\0.0001).Our results indicate that pregnant women in China are at the high risk of exposure ETS.Further attempts are required to make strategies to find out the sources of ETS exposure and prevent smoking at public places especially during pregnancy.展开更多
To study the genotoxicity effect of environmental tobacco side-stream smokes (ETSS) on oxidative DNA damage and its molecular mechanism. Methods DNA adduct 8-hydroxydeoxyguanosine (8-OHdG) was used ...To study the genotoxicity effect of environmental tobacco side-stream smokes (ETSS) on oxidative DNA damage and its molecular mechanism. Methods DNA adduct 8-hydroxydeoxyguanosine (8-OHdG) was used as a biomarker of oxidative DNA damage. The level of 8-OHdG in DNA exposed to ETSS was detected by high performance liquid chromatography with electrochemical detection. Organic and inorganic components in ETSS were analyzed by gas chromatography-mass spectrum and atomic absorption spectrum respectively. Results Particle matters (PMs) and volatile organic compounds (VOCs) in ETSS could directly induce oxidative DNA damage and formation of 8-OHdG. There were 123 and 84 kinds of organic components in PMs and VOCs respectively, and 7 kinds of inorganic components in ETSS. Some components, especially quinones and polyphenols in ETSS, could produce free radicals in vitro by auto-oxidation without any biological activity systems, and with the catalytic reaction of metals, the DNA adduct 8-OHdG was produced. Conclusion ETSS have biological oxidative effect on DNA in vitro and in vivo, and expressed direct genotoxicity. 8-OHdG is a valuable biomarker of oxidative DNA damage.展开更多
Tobacco smoking is a prevalent and detrimental habit practiced worldwide,increasing the risk of various diseases,including chronic obstructive pulmonary disease(COPD),cardiovascular disease,liver disease,and cancer.Al...Tobacco smoking is a prevalent and detrimental habit practiced worldwide,increasing the risk of various diseases,including chronic obstructive pulmonary disease(COPD),cardiovascular disease,liver disease,and cancer.Although previous research has explored the detrimental health effects of tobacco smoking,recent studies suggest that gut microbiota dysbiosis may play a critical role in these outcomes.Numerous tobacco smoke components,such as nicotine,are found in the gastrointestinal tract and interact with gut microbiota,leading to lasting impacts on host health and diseases.This review delves into the ways tobacco smoking and its various constituents influence gut microbiota composition and functionality.We also summarize recent advancements in understanding how tobacco smoking-induced gut microbiota dysbiosis affects host health.Furthermore,this review introduces a novel perspective on how changes in gut microbiota following smoking cessation may contribute to withdrawal syndrome and the degree of health improvements in smokers.展开更多
Each year there will be an estimated 2.1 million new lung cancer cases and 1.8 million lung cancer deaths worldwide.Tobacco smoke is the No.1 risk factors of lung cancer,accounting for>85%lung cancer deaths.Air pol...Each year there will be an estimated 2.1 million new lung cancer cases and 1.8 million lung cancer deaths worldwide.Tobacco smoke is the No.1 risk factors of lung cancer,accounting for>85%lung cancer deaths.Air pollution,or haze,comprises ambient air pollution and household air pollution,which are reported to cause 252,000 and 304,000 lung cancer deaths each year,respectively.Tobacco smoke and haze(hereafter,smohaze)contain fine particles originated from insufficient combustion of biomass or coal,have quite similar carcinogens,and cause similar diseases.Smohaze exert hazardous effects on exposed populations,including induction of a large amount of mutations in the genome,alternative splicing of mRNAs,abnormalities in epigenomics,initiation of tumor-promoting chronic inflammation,and facilitating immune escape of transformed cells.Tackling smohaze and development of multi-targets-based preventive and therapeutic approaches targeting smohaze-induced carcinogenesis are the key to conquer lung cancer in the future.展开更多
文摘N-nitrosamines are strong carcinogens for humans. This paper gives an overview of the nitrosmaines in cigarette smoke including the formation, the harmfulness, the analytical methods of the nitrosmaines and the adsorptions and degradations of N –nitrosamines.
文摘Background: Asthma is a chronic multifactorial disease with high prevalence. Among asthma risk factors, the effect of tobacco smoke exposure on bronchial asthma is still debated. Aim: The aim of this study was to determine the association between environmental and direct tobacco smoke (cigarette and hookah) exposure and incidence and control of bronchial asthma. Materials & Methods: This descriptive study was conducted on 109 patients with asthma referring to Imam Khomeini Hospital in Ardabil city. Asthma Control Questionnaire was used for evaluating of asthma control. Patients’ asthma control was individually evaluated and compared with together with particular attention to history of tobacco smoke exposure. Chi square and Tav-Kendal were used to analyze the data in SPSS15 software. Results: The history of tobacco smoke exposure was found in 31.2% of the 109 patients. Patients with uncontrolled asthma with 60.6% constituted the largest volume of all samples. There was no significant correlation between tobacco smoke exposure and asthma occurrence (P > 0.05), also there was not found significant correlation between tobacco smoke exposure and asthma control (Error coefficient > 0.10). Conclusion: According to the results, history of tobacco (cigarette and hookah) smoke exposure (environmental and direct) has no effect on the asthma occurs and control status.
文摘DNA hypermethylation of tumor suppressor genes has been frequently observed in cancer patients, and therefore, may provide a valuable biomarker for cancer prevention and treatment. DNA hypermethylation may also provide an important mechanism in cancer progression. Lung cancer is strongly associated with exposure to environmental carcinogens, especially tobacco smoke. DNA damage generated by tobacco smoke is believed to play an important role in lung cancer development. XPC is a DNA damage recognition protein required for DNA repair and other DNA damage responses and attenuated XPC protein levels have been detected in many lung cancer patients. We studied the role of XPC protein deficiency in tobacco smoke-caused DNA hypermethylation of important tumor suppressor genes. Using both normal human fibroblasts (NF) and XPC-deficient hu man fibroblasts (XPC), our DNA methylation studies demonstrated that the XPC deficiency caused elevated levels of DNA hypermethylation in both Brca1 and Mlh1 tumor suppressor genes following exposure to tobacco smoke condensate (TSC). The results of our ChIP studies revealed that the XPC deficiency led to an increased binding of DNA methyltransferase 3A (DNMT3A) at the promoter region CpG island-containing sequences of these genes under the TSC treatment;however, this increase was partially diminished with prior treatment with caffeine. The results of our immuno-precipitation (IP) studies demonstrated a protein-protein interaction of the ATR with DNMT3A. Our western blots revealed that the XPC deficiency caused an increase in TSC-induced ATR phosphorylation at serine 428, an indicator of ATR activation. All these results suggest that XPC deficiency causes an accelerated DNA hypermethylation in important tumor suppressor genes under tobacco smoke exposure and activation of the ATR signaling pathway is involved in this DNA hypermethylation process.
基金supported by Major Science and Technology Projects and Special Priority Themes of Zhejiang Province of China(2010C13030)
文摘Environmental tobacco smoke(ETS)is a wellknown reason of many adverse health consequences in pregnant women.Exposure of ETS during pregnancy may increase the risk of some fetal diseases in pregnant women and/or birth defects in neonates.Many countries have implemented laws to control smoking and free of second hand smoke in all enclosed workplaces.In China,antismoking law was enforced in March 2010.We aimed to assess the exposure of pregnant women to cotinine after anti-smoking law was implemented in China.The urine samples were collected from 2,100 volunteers from Zhejiang Province,China and urinary concentration of cotinine was measured using gas chromatography and mass spectrometry.Cotinine was detected in 87%of the pregnant women.The GM and 95th percentile concentration inpregnant women were 4.28 and 44.00 lg/L,respectively.Similarly,the GM and 95th concentration of cotinine were significantly higher in smoking group than in non-smoking group(P\0.0001).Our results indicate that pregnant women in China are at the high risk of exposure ETS.Further attempts are required to make strategies to find out the sources of ETS exposure and prevent smoking at public places especially during pregnancy.
基金The research was supported and financed by brainstorm project and public good fund from the Ministry of Science and TechnologyChina (2001BA704B01& 2001DIA10001).
文摘To study the genotoxicity effect of environmental tobacco side-stream smokes (ETSS) on oxidative DNA damage and its molecular mechanism. Methods DNA adduct 8-hydroxydeoxyguanosine (8-OHdG) was used as a biomarker of oxidative DNA damage. The level of 8-OHdG in DNA exposed to ETSS was detected by high performance liquid chromatography with electrochemical detection. Organic and inorganic components in ETSS were analyzed by gas chromatography-mass spectrum and atomic absorption spectrum respectively. Results Particle matters (PMs) and volatile organic compounds (VOCs) in ETSS could directly induce oxidative DNA damage and formation of 8-OHdG. There were 123 and 84 kinds of organic components in PMs and VOCs respectively, and 7 kinds of inorganic components in ETSS. Some components, especially quinones and polyphenols in ETSS, could produce free radicals in vitro by auto-oxidation without any biological activity systems, and with the catalytic reaction of metals, the DNA adduct 8-OHdG was produced. Conclusion ETSS have biological oxidative effect on DNA in vitro and in vivo, and expressed direct genotoxicity. 8-OHdG is a valuable biomarker of oxidative DNA damage.
基金supported by the National Natural Science Foundation of China (31925021, 82130022)the National Key Research and Development Program of China (2018YFA0800700, 2022YFA0806403)。
文摘Tobacco smoking is a prevalent and detrimental habit practiced worldwide,increasing the risk of various diseases,including chronic obstructive pulmonary disease(COPD),cardiovascular disease,liver disease,and cancer.Although previous research has explored the detrimental health effects of tobacco smoking,recent studies suggest that gut microbiota dysbiosis may play a critical role in these outcomes.Numerous tobacco smoke components,such as nicotine,are found in the gastrointestinal tract and interact with gut microbiota,leading to lasting impacts on host health and diseases.This review delves into the ways tobacco smoking and its various constituents influence gut microbiota composition and functionality.We also summarize recent advancements in understanding how tobacco smoking-induced gut microbiota dysbiosis affects host health.Furthermore,this review introduces a novel perspective on how changes in gut microbiota following smoking cessation may contribute to withdrawal syndrome and the degree of health improvements in smokers.
基金supported by the National Key Research and Development Program of China (Grant No. 2016YFC0905501)the National Natural Science Funds for Distinguished Young Scholar (Grant No. 81425025)+3 种基金the Key Project of the National Natural Science Foundation of China (Grant No. 81830093)the CAMS Innovation Fund for Medical Sciences (Grant No. CIFMS 2019-I2M-1-003)the National Natural Science Foundation of China (Grant No. 81672765)
文摘Each year there will be an estimated 2.1 million new lung cancer cases and 1.8 million lung cancer deaths worldwide.Tobacco smoke is the No.1 risk factors of lung cancer,accounting for>85%lung cancer deaths.Air pollution,or haze,comprises ambient air pollution and household air pollution,which are reported to cause 252,000 and 304,000 lung cancer deaths each year,respectively.Tobacco smoke and haze(hereafter,smohaze)contain fine particles originated from insufficient combustion of biomass or coal,have quite similar carcinogens,and cause similar diseases.Smohaze exert hazardous effects on exposed populations,including induction of a large amount of mutations in the genome,alternative splicing of mRNAs,abnormalities in epigenomics,initiation of tumor-promoting chronic inflammation,and facilitating immune escape of transformed cells.Tackling smohaze and development of multi-targets-based preventive and therapeutic approaches targeting smohaze-induced carcinogenesis are the key to conquer lung cancer in the future.