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At least 19 recordsLinked to original sources
PubMed1994

Modulation of the mutagenic activity of cigarette smoke, cigarette smoke condensate and benzo[a]pyrene in vitro and in vivo.

A series of naturally occurring compounds were tested for the ability to modulate the mutagenicity induced by cigarette smoke (CS), cigarette smoke condensate (CSC) and benzo[a]pyrene (BP) in the Salmonella/microsome mutagenicity assay and the micronucleus test in mouse bone marrow. Sodium selenite, retinol acetate and alpha-tocopherol significantly decreased the mutagenic activity of CS in Salmonella typhimurium TA98. Ascorbic acid, reduced glutathione (GSH), cysteine, caffeine, theophylline, cobalt chloride, folic acid, adenine, adenosine, guanosine, cytidine and cytosine were conversely devoid of any significant effect. Sodium selenite slightly decreased the mutagenic activity of CSC in the same bacterial strain, while caffeine was ineffective and ascorbic acid potentiated its mutagenicity. Ascorbic acid inhibited the mutagenic activity of BP in S. typhimurium TA98, but not in TA100. Retinol acetate diminished the number of BP-induced his+ revertants in TA98 but only at the highest concentrations used, whereas alpha-tocopherol, GSH, cysteine, sodium selenite and caffeine had no effect. Selenite and GSH, which were ineffective when applied individually, inhibited in a dose-dependent manner the BP-induced mutagenesis in S. typhimurium TA98 when simultaneously added to the top agar. All other combinations tested, including selenite plus either GSH, cysteine or caffeine towards CS or CSC, or selenite plus cysteine, or selenite plus retinol acetate and alpha-tocopherol towards BP, failed to produce interactive effects. Sodium selenite and caffeine, given either alone or in combination in drinking water, did not influence the clastogenesis induced in mouse bone marrow by a single treatment with CS or BP. Ascorbic acid was also ineffective towards CS clastogenicity but significantly decreased the number of micronucleated polychromatic erythrocytes induced by BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

The effect of exposure to nicotine, carbon monoxide, cigarette smoke or cigarette smoke condensate on the mutagenicity of rat urine.

Cigarette smokers have been reported to void urine which is more mutagenic than that voided by non-smokers, but the specific urinary mutagen(s) have not been identified. Since mechanistic studies are best performed in animal models, the objective of this study was to determine if a model to study the role of cigarette smoke and its components in urinary mutagenicity could be developed in rats. XAD-2 resin was used to concentrate the urine and the microsuspension modification of the Ames test used to quantify mutagenicity. Nicotine administered by intraperitoneal injection at 0.8 mg/kg (the maximum tolerated dose) or inhalation of carbon monoxide for 14 days at the maximum tolerated dose (1800 ppm, resulting in 68% carboxyhemoglobin) did not increase urinary mutagenicity. Cigarette smoke condensate (CSC) prepared by electrostatic precipitation of mainstream smoke increased urinary mutagenicity at doses of 100 and 200 mg/kg when administered acutely by either i.p. injection or gavage, verifying that the assay system was capable of detecting cigarette smoke-related mutagens in the urine. However, cigarette smoke administered by the appropriate route of exposure, nose-only inhalation, for 1, 7, 14 or 90 days (1 h per day) did not increase urinary mutagenicity. The smoke concentration administered was at or near the maximum tolerated dose as evidenced by carboxyhemoglobin concentrations of approximately 50%, and of 10% or more weight loss in exposed animals. Thus, although cigarette smoke condensate is mutagenic in vitro and mutagenic urine was observed when rats were given high doses of CSC by inappropriate routes of administration, acute or subchronic inhalation exposure to the maximum tolerated dose of whole cigarette smoke did not increase urinary mutagenicity in rats. These results indicate that the rat may be an inappropriate model to study urinary mutagenicity following the inhalation of tobacco smoke.

Administration, Inhalation↗
PubMed1979

Organ specificity of induction of activating and inactivating enzymes by cigarette smoke and cigarette smoke condensate.

Inhalation of cigarette smoke specifically induces the rat lung and kidney aryl hydrocarbon hydroxylase (AHH) in less than 4 h. The epoxide hydratase (EH) and the glutathione S-transferase are not significantly modified by a similar treatment in any of the rat tissues. Compared to the kidney AHH, the lung hydroxylase is 3--4 times more sensitive to small concentrations of cigarette smoke and seems to have a longer biological half-life. In both tissues, the induced AHH presents the same in vitro sensitivity to various inhibitors as a polycyclic hydrocarbon induced AHH. In primary fetal rat liver cell culture, the cigarette smoke condensate fractions (CSCF) induce both the AHH and EH activity. Nevertheless, the AHH activity responds faster and to lower concentrations of CSCF than the EH activity. The liver cell culture constitutes a unique tool for a comparative study of the AHH and EH induction mechanism. Low concentration (10 muM) of benz(a)anthracene induces only the AHH activity while trans-stilbene oxide enhances selectively the EH activity. Appropriate concentrations of CSCF or of phenobarbital (PB) determine a parallel induction of both enzymes. The results are discussed on the basis of (a) the existence of specific mechanisms of AHH regulation in the lung and in the kidney and (b) the existence of coordinated or independent biochemical control of the AHH and EH activity.

Animals↗
PubMed1989

Benzo[a]pyrene-DNA-adducts and monooxygenase activities in mice treated with benzo[a]pyrene, cigarette smoke or cigarette smoke condensate.

Synchronous fluorescence spectrophotometry (SFS), developed to study benzo[a]pyrene-7,8-diol-9,10-epoxide(BPDE)-DNA, was used to measure the in vivo formation of DNA-adducts in genetically responsive C57BL/6 (B6) and non-responsive DBA/2 (D2) mice. Treatment with cigarette smoke by inhalation for 3-16 days, or i.p. injection of cigarette smoke condensate or neutral fraction did not lead to detectable levels of BPDE-DNA-adducts in either lungs or liver, although aryl hydrocarbon hydroxylase (AHH) activity, an indicator of benzo[a]pyrene (BP) metabolism, was clearly induced in lungs of B6 mouse. A dose-dependent amount of BPDE-DNA-adducts in lung and somewhat less in liver was found after i.p. injection with BP (20-80 mg/kg). Mice treated with vehicle or 4 mg/kg of BP were negative for adducts by SFS. In B6 mice AHH was induced both in lungs and livers while there was no AHH induction in D2 mice although the levels of BPDE-DNA-adducts were somewhat higher than in B6 mice. Thus, no clear correlation seems to exist between AHH activity and the formation of BPDE-DNA-adducts. Also, according to our results SFS can be used to quantitate adduct-formation in in vivo animal studies.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1985

N-acetylcysteine protection against the toxicity of cigarette smoke and cigarette smoke condensates in various tissues and cells in vitro.

The protective effect of N-acetylcysteine on the toxicity of tobacco smoke condensates was investigated using different cellular in vitro systems. Cigarette smoke condensates, and the non-volatile and semi-volatile fractions separated from the condensate were used. All three smoke condensate fractions were toxic to isolated rat hepatocytes and lung cells and caused a loss of cell membrane integrity. A rapid depletion of cellular reduced glutathione (GSH) preceded the toxicity. The loss of GSH was due to conjugation of reactive compounds in the condensate fractions and not to oxidation since no increase in oxidized glutathione (GSSG) could be observed. N-acetylcysteine at a concentration of 1 mM protected both from the GSH loss and cell toxicity caused by the condensate fractions. The effect of the tobacco smoke condensate on the colony forming efficiency (CFE) of cultured human bronchial cells was also investigated. Already at concentrations of 50 micrograms/ml the survival decreased to 40% of control and at 100 micrograms/ml almost no cells formed colonies. N-acetylcysteine substantially increased survival when added at 10 mM concentration.

Acetylcysteine↗
PubMed1998

Oxidative damage in tissues of rats exposed to cigarette smoke.

Cigarette smoke is known to contain high concentrations of free radicals and oxidants. To examine the oxidative effect of cigarette smoking, we subjected rats to inhalation of cigarette smoke, and measured cellular free glutathione, the degree of protein S-thiolation, and 8-oxo-2'-deoxyguanosine (oxo8dG) in DNA. Inhalation of the cigarette smoke for 30 days, three times a day, resulted in a significant decrease of the total free glutathione contents in tissues, especially in the lung. Elevated levels of oxidized glutathione and protein S-thiolation were observed in the lung but not in other tissues. Increased contents of oxo8dG in DNA were found in all tissues analyzed. When rats were treated with buthionine sulfoximine (BSO, 80 mg/kg/day) to deplete glutathione, the oxidative effect of cigarette smoking was greatly potentiated. The effect of glutathione depletion was most evident in the lung. Cigarette smoking for only 7 days resulted in extreme depletion of the glutathione both in the lungs and in the liver of BSO-treated rats. Furthermore, oxo8dG in DNA increased markedly, especially in lung. The results verified that the lung is a primary target of cigarette smoke-induced oxidative damage, and cigarette smoke exerts its oxidative effects on the rest of the entire organs eventually. Our results indicate that glutathione plays crucial roles in protecting proteins and DNA from oxidation caused by cigarette smoking.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1985

Buprenorphine effects on cigarette smoking.

Cigarette smoking increased during administration of buprenorphine, an opioid mixed agonist-antagonist, in comparison to drug-free baseline in seven heroin addicts maintained on buprenorphine for 24 days (P less than 0.01-0.001). Ascending buprenorphine doses (0.5 - 8.0 mg/day) were associated with significant increases in cigarette smoking at doses of 2.0 mg/day sc and above. Cigarette smoking during 10 days of buprenorphine maintenance at 8 mg/day was significantly higher than during the buprenorphine induction phase (P less than 0.01). Six subjects given placebo buprenorphine over 14 days showed no change in cigarette smoking. The placebo group self-administered heroin for 10 days, and cigarette smoking increased significantly during heroin use (P less than 0.001). The rate of cigarette smoking defined by intercigarette intervals was highest during the 10 days of high-dose buprenorphine maintenance or placebo plus heroin self-administration. Both groups requested significantly more cigarettes at intervals of 0-10, 11-20, and 21-30 min than during the drug-free baseline. These data confirmed previous findings that opioid agonist administration is associated with increased cigarette smoking and suggest that buprenorphine has primarily agonist effects on cigarette smoking.

Adult↗
PubMed1972

Inhibition of pancreatic secretion in man by cigarette smoking.

Cigarette smoking has been linked to an elevated incidence of duodenal ulcer disease in smokers, although the mechanism is unclear. In 23 young normal subjects single or double secretin tests were performed during non-smoking and smoking periods. Cigarette smoking inhibited the secretion of pancreatic juice and bicarbonate in light smokers (< one pack/day for < three years). Heavy smokers (> one pack/day for > three years) exhibited depressed pancreatic secretory rates during non-smoking periods. Inhibition of pancreatic alkaline secretion by cigarette smoking could be the link between the habit and duodenal ulcer disease.

Adult↗
PubMed2000

Reduction of EGF is associated with the delay of ulcer healing by cigarette smoking.

Cigarette smoking is associated with peptic ulcer diseases. Smokers have lower levels of salivary epidermal growth factor (EGF) than nonsmokers. We investigated whether reduction of EGF is involved in the delay of gastric ulcer healing by cigarette smoking. Rats with acetic acid-induced ulcers were exposed to cigarette smoke (0, 2, or 4% vol/vol) 1 day after ulcer induction. EGF level was elevated 1 day after ulcer induction in salivary glands and serum, and 4 days after ulcer induction in the gastric mucosa. However, cigarette smoke depressed these beneficial effects and EGF mRNA expression in salivary glands and gastric mucosa. Cigarette smoke delayed gastric ulcer healing and reduced cell proliferation, angiogenesis, and mucus synthesis. Exogenous EGF (10 and 20 microg/kg i.v.) before smoke exposure reversed the adverse effects of cigarette smoke, whereas vascular endothelial growth factor level and nitric oxide synthase activity were unaffected. It is concluded that the detrimental effect of cigarette smoke on ulcer healing is a consequence of reduction of angiogenesis, cell proliferation, and mucus secretion through the depressive action on EGF biosynthesis and its mRNA expression in salivary glands and gastric mucosa.

Animals↗
PubMed2004

Nitric oxide formation in the oropharyngeal tract: possible influence of cigarette smoking.

Cigarette smoking reduces the level of nitric oxide (NO) in exhaled air by an unknown mechanism. The view that part of the effect of cigarette smoking on NO production should occur in the oropharyngeal tract is supported by several studies. We have therefore compared smokers and non-smokers regarding non-enzymatic formation of NO from nitrite in the oral cavity since this is a primary candidate target for cigarette smoke. We have also looked at NO synthase-dependent NO formation in the mucosa of the oropharyngeal tract as an alternative target for the inhibitory effect induced by cigarette smoke. Smokers exhaled 67% lower levels of NO than controls (p<0.01, n=15 each group). We could not detect any significant difference in salivary nitrite, nitrate or ascorbate between smokers and non-smokers. Mouthwash with the antibacterial agent chlorhexidine reduced salivary nitrite (-65%) and exhaled NO levels (-10%) similarly in the two groups. Immunohistochemical techniques revealed dense expression of inducible (but not endothelial or neuronal) NO synthase in the squamous epithelium of non-inflamed tonsillar and gingival tissue biopsies. In the same biopsies, significant Ca2+ -independent citrulline-forming activity was detected. We found no difference between smoking and non-smoking subjects regarding NO-synthase expression and in vitro activity. In another group of non-smoking subjects (n=10), spraying the oropharyngeal tract with the NO-synthase inhibitor NG-monomethyl-L-arginine (250 mg) significantly reduced exhaled NO levels for at least 30 min (-18%, p<0.01). Our data suggest that cigarette smoking does not affect non-enzymatic NO formation from nitrite in saliva. However, NO is also formed by inducible NO synthase in the squamous epithelium of the normal oropharyngeal tract. We suggest that cigarette smoking may down-regulate enzymatic NO formation in the oropharyngeal compartment as well as in the bronchial compartment.

Adult↗
PubMed1999

Cigarette smoking.

Cigarette smoking is the largest preventable risk factor for morbidity and mortality in developed countries. Dramatic changes in the prevalence of cigarette smoking in the second half of this century in the United States (i.e., a reduction among men and an increase among women) have reduced current smoking levels to approximately one quarter of the adult population and have reduced differences in smoking prevalence and smoking-attributable diseases between the sexes. Current smoking in the United States is positively associated with younger age, lower income, reduced educational achievement, and disadvantaged neighborhood environment. Daily smokers smoke cigarettes to maintain nicotine levels in the brain, primarily to avoid the negative effects of nicotine withdrawal, but also to modulate mood. Regular smokers exhibit higher and lower levels of stress and arousal, respectively, than nonsmokers, as well as higher impulsivity and neuroticism trait values. Nicotine dependence is the single most common psychiatric diagnosis in the United States, and substance abuse, major depression, and anxiety disorders are the most prevalent psychiatric comorbid conditions associated with nicotine dependence. Studies in twins have implicated genetic factors that explain most of the variability in vulnerability to smoking and in persistence of the smoking phenotype. Future research into the causes of smoking must take into account these associated demographics, social factors, comorbid psychiatric conditions, and genetic factors to understand this complex human behavior.

Adult↗
PubMed2000

Peroxynitrite-generating species: good candidate oxidants in aqueous extracts of cigarette smoke.

Cigarette smoking is a well-known risk factor for atherosclerosis, but the mechanism of the adverse biological effect of smoking remains to be established. Cigarette smoke contains high concentrations of free radicals and oxidants. We show here that cigarette smoke extracts (CSE), prepared by bubbling the gas phase of smoke into phosphate-buffered saline, could convert tyrosine to 3-nitrotyrosine. The tyrosine nitration terminated 6 h after incubating tyrosine with CSE at 37 degrees C. These results indicate that the active oxidants in CSE are peroxynitrite-generating species like 3-morpholinosydnonimine (SIN-1), suggesting that they modify plasma lipoproteins and contribute to the pathogenesis of atherosclerosis.

Arteriosclerosis↗
PubMed2002

Glutathione prevents inhibition of fibroblast-mediated collagen gel contraction by cigarette smoke.

Cigarette smoke, the major risk factor for the development of emphysema, contains over 4,700 chemical compounds, including free radicals and other oxidants (10(14)/puff). An imbalance between oxidants and antioxidants has been proposed in the pathogenesis of chronic obstructive pulmonary disease. Inhibition of repair processes has been suggested to be one pathway contributing to the development of emphysema. We hypothesized that cigarette smoke inhibition of repair might result from a shift of the oxidant/antioxidant balance in favor of oxidants. To evaluate this hypothesis, N-acetyl-L-cysteine (NAC), which serves as a substrate for glutathione (GSH) production, and buthionine sulfoximine (BSO), which inhibits GSH production, were incubated in the presence and absence of cigarette smoke extract (CSE) with fibroblasts in three-dimensional collagen gels. Neither agent alone altered gel contraction. CSE inhibition of gel contraction, however, was mitigated by NAC and potentiated by BSO. Parallel effects were observed on cigarette smoke inhibition of fibronectin production and mRNA expression as well as by changes in intracellular GSH content. Pretreatment of fibroblasts with NAC or BSO resulted in similar effects, suggesting that neither agent was acting directly on smoke but, rather, was altering cellular response to smoke. In conclusion, smoke inhibition of fibroblast repair, as reflected by collagen gel contraction and fibronectin production, may be modulated by intracellular GSH levels.

Acetylcysteine↗
PubMed1984

Abnormal phagolysosome fusion in pulmonary alveolar macrophages of rats exposed chronically to cigarette smoke.

Cigarette smoking is strongly associated with functional and morphologic changes in pulmonary alveolar macrophages (PAM). Phagocytic activity is a primary function of PAM, and although the ingestion of particles appears to be normal in the PAM of cigarette smokers, published data suggest that antimicrobial activity of these cells might be diminished. Because phagolysosome fusion (PLF) is an important aspect of the phagocytic process subsequent to the ingestion phase, PLF was evaluated in PAM lavaged from the lungs of male Fisher 344 rats that had been exposed for 8 wk to whole cigarette smoke, to the gas phase of cigarette smoke, or to air as a sham control. Using the acridine orange assay with viable yeast as the phagocytic challenge, we found no difference in the numbers of PAM from each group that had phagocytic activity after a 2-h challenge. However, PLF expressed as the number of orange-fluorescing phagosomes per total number of yeast-containing phagosomes was 35 +/- 1% (X +/- SE) for the group exposed to whole smoke, 53 +/- 2% for the gas phase group, and 65 +/- 1% for the control group. These differences are highly significant, with p less than 0.001 for the whole smoke versus control and p less than 0.01 for the gas phase versus control. Tight phagosomal membranes suggest normal PLF, whereas loose membranes suggest that PLF is inhibited. When the structure of yeast-containing phagosomes was examined and PLF was calculated with the number of phagosomes with tight membranes substituted for the number of orange-fluorescing phagosomes, PLF in smoke-exposed PAM was found to be significantly (p less than 0.01) different from that in sham-exposed control PAM.(ABSTRACT TRUNCATED AT 250 WORDS)

Acridine Orange↗
PubMed1991

[Assessment of cadmium and lead released from cigarette smoke].

Cigarette smoke, which contains many harmful compounds, affects not only the smoker's health but also indoor air quality. To evaluate indoor air contamination by cadmium (Cd) and lead (Pb), we measured Cd and Pb contained in the mainstream and sidestream smoke exhaled by experimental smoking of Japanese cigarettes and also determined urinary and blood Cd and Pb levels in smokers and non-smokers and air Cd and Pb levels in smoky environments. 1. One cigarette of each of 7 Japanese brands contained about 1 microgram each of Cd and Pb, of which about 50 ng each was released to the mainstream and 250 ng of Cd and 50 ng of Pb to the sidestream by smoking. 2. The blood Cd level in the smokers was significantly higher than that in the non-smokers. The urinary Cd level in the smokers was slightly higher than that in the non-smokers. The blood Cd level was related to the number of cigarettes smoked daily. Blood and urinary Pb levels did not differ between the smokers and non-smokers, but the blood Pb level was also related to the number of cigarettes smoked daily. 3. The air Cd levels in smoky places such as the smoking car of the special express train, an office, and a pachinko parlor were markedly higher than that in outdoor air. The air Cd concentration was well correlated with the environmental tobacco smoke concentration. On the other hand, the air Pb level was slightly higher in the above smoky places than outdoors. The mean air Pb concentration was not correlated with the environmental tobacco smoke concentration but was higher at higher environmental tobacco smoke concentration in each place.

Adolescent↗
PubMed2002

[Juvenile cigarette smoking].

Cigarette smoking continues to be the main undesirable habit among children and adolescents. Its monitoring may provide valuable information about the effectiveness of health education programmes. The aim of the study was to assess the prevalence of cigarette smoking among the schoolchildren in the city of Poznań. The study was conducted in the school years 2000/2001 and 2001/2002 on the group of 1909 pupils. A lecture "Why I do not smoke" was delivered in every class prior to the distribution of questionnaire about cigarette smoking. 20% of children-more boys than girls-admitted they smoke. Percentage of smokers increases with age. A significant increase in the habit was observed among the 14-16 year olds. There continuous is still a need for health education among the young people in order to limit the unhealthy habits.

Adolescent↗
PubMed1997

Induction of endothelial cell injury by cigarette smoke.

Cigarette smoke contains different populations of free radicals which may be responsible for endothelial cell (EC) injury of smokers. The purpose of this study was to examine the effects of gas-phase cigarette smoke on EC endothelium-derived relaxing factor (EDRF)/NO-guanylate cyclase (GC)-cGMP pathway and on EC detachment-type injury after incubation with smoke. Furthermore, we examined whether different kind of antioxidants can prevent smoke-caused EC injury. We measured cGMP pathway using direct (sodium nitroprusside, SNP) and indirect (A23187, the calcium ionophore and bradykinin, BK) activators of GC. Directly and indirectly stimulated EC cGMP production dose-dependently decreased and EC detachment increased after incubation with smoke. Externally added thiols (glutathione, GSH; D-Penicillamine, DP; N-acetylcysteine, NAC) protected EC from damage of cGMP production and cell detachment. Other antioxidants (catalase, deferoxamine and superoxide dismutase) were ineffective. These results suggest that the thiol containing GC in EC is destroyed or inactivated or thiol like species responsible for activation of GC is incomplete in EC after incubation with smoke. It is also possible that externally added thiols bind an unknown component of smoke and this way, EC is protected. EC injury may contribute to vascular diseases associated with cigarette smoking.

Animals↗