• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.5
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• pp.1149-1154
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• 2006

Repeated administration of all addictive drugs, including nicotine, can produce sensitization of extracellular dopamine levels in the nucleus accumbens and behavioral sensitization in rat, as evidenced by an enhanced locomotor response and increased dopamine release in brain to a subsequent injection of the drug. In order to investigate the effect of Zizyphus jujuba extract on repeated nicotin-induced sensitization, rats were given repeated injection of saline or nicotine (0.4 mg/kg s.c., twice a day for 7 d), followed by one challenge injection on the 4th day after the last daily injection. Systemic challenge with nicotine (0.4 mg/kg s.c.) and a direct local challenge of 3 mM a larger increase in locomotor activity and extracellular dopamine release in the nucleus accumbens in nicotine-pretreated rats than in saline-pretreated rats, respectively. Zizyphus jujuba extract significantly decreases locomotor activitiy and dopamine release in the nucleus accumbens induced by a nicotine challenge. These results suggest that Zizyphus jujuba extract may attenuate nicotine-induced neurochemical and behavioral sensitization and may be effective in suppressing compulsive nicotine-seeking behavior.

• Journal of Periodontal and Implant Science
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• v.28 no.4
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• pp.703-721
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• 1998

In order to observe the effects of Nicotine and NNK on cultured human gingival fibroblast, several factors were examined including mutagenicity, the number of cells attached culture plate surface through MTT test, the abundance of collagen & collagenase in mRNA level and collagenolytic activity in extracellular matrix. The results were as follows; 1. Regardless of the co-existence of S9, Nicotine did not show the mutagenicity by itself and NNK by itself showd the same result; However, dose related mutagenicity was shown in NNK with S9. 2. The number of fibroblasts attached cultured plate surface was measured by MTT procedure. The number of cells in Non-smokers increased at all time periods as compared to those of smoker. 3. Non-smoker's fibroblast treated by NNK or Nicotine was dosedependently dosedependently decreased in the number of cells when compared to untreated control. In higher dose, Nicotine showed the cellular toxicity, but NNK did not. 4. No change in the abundance of mRNA for pro${\alpha}1$ and pro${\alpha}2$ was shown in Nicotine treated group but in gingival fibroblasts following treatment with NNK, the abundance of mRNA for pro${\alpha}1$, but not pro${\alpha}2$ collagen was decreased. 5. The abundance of mRNA for collagenase was decreased when NNK was treated but no change occurred in Nicotine treated group. 6. The effect of NNK and Nicotine in collagenolytic activity showed that, collagenase activity exclusively react to type I collagen, was increased in both group, but gelatinase exclusively react to type IV collagen was not influenced at all. Collagenase activity of smoker's fibroblast was also increased as much as Nicotine and NNK group. The findings suggest that both of Nicotine and NNK lead gingival fibroblast to decrease in the abundance of collagen. And it seems to be that Nicotine and NNK have independent pathway toward the gingival fibroblast.

• Molecular & Cellular Toxicology
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• v.4 no.2
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• pp.106-112
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• 2008

Parkinson's disease (PD) progresses severely by a gradual loss of dopaminergic neurons in the substantia nigra (SN). Epidemiological studies showed that the incidences of PD were reduced by smoking of which the major component, nicotine might be neuroprotective. But the function of nicotine, which might suppress the incidences of PD, is still unknown. Fortunately, recently it was reported that a glial reaction and inflammatory processes might participate in a selective loss of dopaminergic neurons in the SN. The levels of tumour necrosis factor (TNF)-${\alpha}$ synthesised by astrocytes and microglia are elevated in striatum and cerebrospinal fluid (CSF) in PD. TNF-${\alpha}$ kills the cultured dopaminergic neurons through the apoptosis mechanism. TNF-${\alpha}$ release from glial cells may mediate progression of nigral degeneration in PD. Nicotine pretreatment considerably decreases microglial activation with significant reduction of TNF-${\alpha}$ mRNA expression and TNF-${\alpha}$ release induced by lipopholysaccharide (LPS) stimulation. Thus, this study was intended to explore the role of nicotine pretreatment to inhibit the expressions of TNF-${\alpha}$ mRNA in human fetal astrocytes (HFA) stimulated with IL-$1{\beta}$. The results are as follows: HFA were pretreated with 0.1, 1, and $10{\mu}g/mL$ of nicotine and then stimulated with IL-$1{\beta}$ (100 pg/mL) for 2h. The inhibitory effect of nicotine on expressions of TNF-${\alpha}$ mRNA in HFA with pretreated $0.1{\mu}g/mL$ of nicotine was first noted at 8hr, and the inhibitory effect was maximal at 12 h. The inhibitory effect at $1{\mu}g/mL$ of nicotine was inhibited maximal at 24 h. Cytotoxic effects of nicotine were noted above $10{\mu}g/mL$ of nicotine. Moreover, Nicotine at 0.1, 1 and $10{\mu}g/mL$concentrations significantly inhibited IL-$1{\beta}$-induced TF-${\kappa}B$ activation. Collectively, these results indicate that in activated HFA, nicotine may inhibit the expression of TNF-${\alpha}$ mRNA through the pathway which suppresses the NF-${\kappa}B$ activation. This study suggests that nicotine might be neuroprotective to dopaminergic neurons in the SN and reduce the incidences of PD.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.11
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• pp.5483-5488
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• 2012

Background: Although nicotine dependence plays a role as a main barrier for smoking cessation, there is still a lack of solid evidence on the validity of biomarkers to determine nicotine dependence in clinical settings. This study aimed to investigate whether urinary cotinine levels could reflect the severity of nicotine dependence in active smokers. Materials and Methods: Data regarding general characteristics and smoking status was collected using a self-administered smoking questionnaire. The Fagerstr$\ddot{o}$m test for nicotine dependence (FTND) was used to determine nicotine dependence of the participants, and a total of 381 participants were classified into 3 groups of nicotine dependence: low (n=205, 53.8%), moderate (n=127, 33.3%), and high dependence groups (n=49, 12.9%). Stepwise multiple linear regression model and receiver operating characteristic (ROC) curves analyses were used to determine the validity of urinary cotinine for high nicotine dependence. Results: In correlation analysis, urinary cotinine levels increased with FTND score (r=0.567, P<0.001). ROC curves analysis showed that urinary cotinine levels predicted the high-dependence group with reasonable accuracy (optimal cut-off value=1,000 ng/mL; AUC=0.82; P<0.001; sensitivity=71.4%; specificity=74.4%). In stepwise multiple regression analysis, the total smoking period (${\beta}$=0.042, P=0.001) and urinary cotinine levels (${\beta}$=0.234, P<0.001) were positively associated with nicotine dependence, whereas an inverse association was observed between highest education levels (>16 years) and nicotine dependence (${\beta}$=-0.573, P=0.034). Conclusions: The results of this study support the validity of using urinary cotinine levels for assessment of nicotine dependence in active smokers.

• Journal of Periodontal and Implant Science
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• v.33 no.4
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• pp.729-738
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• 2003

Nicotine is one of the major components of cigarette smoking which causes various systemic and local diseases to human body. The purpose of the present study was to investigate the effects of nicotine on bone mineralization in human fetal osteoblasts cell line(hFOB1). To compare the alkaline ph-osphatase(ALP) synthesis, hFOBl were cultured with DMEM/F-12 1:1 Mixture and 100 pg/ml, 1 ng/ml, 10 ng/ml, 100 ng/ml, 1 ${\mu}g$/ml, 10 ${\mu}g$/ml, 100 ${\mu}g$/ml of nicotine. And to compare the calcium accumulation, hFOB1 cultured for 23 days were quantified and photographed. ALP activity of hFOB1 exposed to nicotine was not significantly changed at a lower concentrations of nicotine, but was significantly decreased at a higher concentrations (10 ${\mu}g$/ml, 100 ${\mu}g$/ml) of nicotine (p<0.05). A quantified calcium acculation in hFOB1 was significantly decreased at 1,10, and 100${\mu}g$/ml of nicotine (p<0.05). Significantly decreased calcium deposition was observed at 1, 10, and 100${\mu}$/ml of nicotine. These results indicate that a higher concentration of nicotine show a negative effects on mineralization of hFOB1.

• Journal of Korean Biological Nursing Science
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• v.16 no.3
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• pp.173-181
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• 2014

Purpose: The purpose of this study was to analyze the effects of a quit smoking program using the Web and short message service on exhaled carbon monoxide, self-efficacy, and depression according to nicotine dependency level in undergraduate students. Methods: In this study a non-equivalent control group pretest-posttest design was applied. The participants included 90 students (52 in the low nicotine dependency group and 38 in the high nicotine dependency group) who succeeded in quitting smoking. Data were collected on 3 occasions, that is, before the program, immediately after the program, and 3 weeks after the program. Collected data were analyzed using independent t-test, repeated measure ANOVA, and paired t-test with SPSS 20.0. Results: Exhaled carbon monoxide was higher in the high nicotine dependency group than in the low nicotine dependency group. Self-efficacy significantly increased 3 weeks after the program in the low nicotine dependency group and significantly increased immediately after the program in the high nicotine dependency group. Depression significantly decreased 3 weeks after the program in the low nicotine dependency group. Conclusion: Self-efficacy may be enhanced when it is dealt with during an early phase of the quit smoking program for the high nicotine dependency group. Long-term intervention and persistent intervention are needed with regard to depression during a quit smoking program.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.2
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• pp.829-833
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• 2016

Purpose: To investigate the work associated stress and nicotine dependence among law enforcement personnel in Mangalore, India. Materials and Methods: A cross-sectional questionnaire survey was conducted among law enforcement personnel in Mangalore, India. Demographic details, stress factors experienced at work and nicotine dependency were the variables studied. The extent of stress factors experienced at work was assessed using the Effort-Reward Imbalance scale (ERI). Nicotine dependence was measured using the Fagerstrom Test for Nicotine Dependence (FTND) and the Fagerstrom Test for Nicotine Dependence-Smokeless Tobacco (FTND-ST). Logistic regression was used for the statistical analysis. Results: Three hundred and four law enforcement personnel participated in the study, among whom 68 had the presence of one or more habits like tobacco smoking, tobacco chewing and alcohol use. The mean effort score was $15.8{\pm}4.10$ and the mean reward and mean overcommitment scores were $36.4{\pm}7.09$ and $17.8{\pm}5.32$ respectively. Effort/Reward ratio for the total participants was 1.0073 and for those with nicotine habit was 1.0850. Results of our study demonstrated no significant association between domains of ERI scale and presence of habits but work associated stress was associated with the presence of one or more habits. Compared to constables, head constables had 1.12 times higher risk of having a nicotine habit. Conclusions: Our study implies job designation is associated with nicotine habits. However, there was no association between work associated stress and nicotine dependence among law enforcement personnel in Mangalore.

• Environmental Analysis Health and Toxicology
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• v.19 no.2
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• pp.169-176
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• 2004

ETS (environmental tobacco smoke) is composed of exhaled mainstream smoke (MS) from the smoker, sidestream smoke (SS) emitted from the smoldering tobacco between puffs and contaminants that diffuse through the cigarette paper and mouth between puffs. These emissions contain both vapor phase and particulate contaminants. ETS is a complex mix of over 4,000 compounds. This mix contains many known or suspected human carcinogens and other toxic agents. More of these toxic compounds are found in SS than in MS. Workplace exposure to ETS can result in significant smoke intake, and passive smoke exposure may be related to impair respiratory function and an increase risk of lung cancer in nonsmokers. For nonsmokers sharing a work environment with cigarette smokers, the workplace must be considered hazardous independently of any specific industrial toxic exposure. The risk is particularly important when a high percentage of the workers smoke or where smokers and nonsmokers work in poorly ventilated areas. Nicotine is converted in the body to cotinine; cotinine therefore can be used as an indirect measure of a person's recent exposure to tobacco smoke. Levels of nicotine in hair and levels of cotinine in body fluids (saliva and urine) have been shown to increase with increasing environmental nicotine levels and with self-reported ETS exposure. The measurement of nicotine or cotinine in hair may be more appropriate for longer-term exposure to tobacco. The purpose of this study is to comparing airborne nicotine levels and hair cotinine level in restaurant workers. Concentration of airborne nicotine and hair nicotine (and cotinine) is closely related to exposed frequency of sidestream smoke in the workplace. Nicotine in hair is a better predictor of airborne nicotine than hair cotinine. Hair nicotine can be a useful tool to assess ETS exposure interventions. It may have limiting levels of ETS exposure by placing regulatory restrictions on smoking in workplaces and in public spaces.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.3
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• pp.257-262
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• 2015

It is well known that cigarette smoke can cause erectile dysfunction by affecting the penile vascular system. However, the exact effects of nicotine on the corpus cavernosum remains poorly understood. Nicotine has been reported to cause relaxation of the corpus cavernosum; it has also been reported to cause both contraction and relaxation. Therefore, high concentrations of nicotine were studied in strips from the rabbit corpus cavernosum to better understand its effects. The proximal penile corpus cavernosal strips from male rabbits weighing approximately 4 kg were used in organ bath studies. Nicotine in high concentrations ($10^{-5}{\sim}10^{-4}M$) produced dose-dependent contractions of the corpus cavernosal strips. The incubation with $10^{-5}M$ hexamethonium (nicotinic receptor antagonist) significantly inhibited the magnitude of the nicotine associated contractions. The nicotine-induced contractions were not only significantly inhibited by pretreatment with $10^{-5}M$ indomethacin (nonspecific cyclooxygenase inhibitor) and with $10^{-6}M$ NS-398 (selective cyclooxygenase inhibitor), but also with $10^{-6}M$ Y-27632 (Rho kinase inhibitor). Ozagrel (thromboxane $A_2$ synthase inhibitor) and SQ-29548 (highly selective TP receptor antagonist) pretreatments significantly reduced the nicotine-induced contractile amplitude of the strips. High concentrations of nicotine caused contraction of isolated rabbit corpus cavernosal strips. This contraction appeared to be mediated by activation of nicotinic receptors. Rho-kinase and cyclooxygenase pathways, especially cyclooxygenase-2 and thromboxane $A_2$, might play a pivotal role in the mechanism associated with nicotine-induced contraction of the rabbit corpus cavernosum.

• Journal of dental hygiene science
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• v.22 no.3
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• pp.164-170
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• 2022

Background: When cells are damaged by nicotine, cellular senescence due to oxidative stress accelerates. In addition, stress-induced inflammatory response and cellular senescence cause the accumulation of damaged organelles in cells, and autophagy appears to remove them. Conversely, when autophagy is reduced, harmful cell components accumulate, and aging is accelerated. This study aimed to determine the association between nicotine-induced cellular senescence and autophagy expression patterns in human gingival fibroblasts. Methods: Cells were treated with various concentrations of nicotine (0, 0.1, 0.5, 1, 2, and 5 mM) and 10 nM rapamycin was added to 1 mM nicotine to investigate the relationship between autophagy and cellular senescence. Cell viability was confirmed using WST-8 and the degree of cellular senescence was measured by SA-β-gal staining. The expression of the inflammatory proteins (COX-2 and iNOS) and autophagy markers (LC3-II, p62, and Beclin-1) was analyzed by western blotting. Results: The cell viability tended to decrease in a concentration-dependent manner. COX-2 showed no concentration-dependent expression and iNOS increased in the 0.5 mM nicotine treated group. The degree of cellular senescence was the highest in the 1 mM nicotine treatment group. In the group treated with rapamycin and nicotine, the conversion ratio of LC3-II to LC3-I was the highest, that of p62 was the lowest, and the level of Beclin-1 proteins was significantly increased. Furthermore, the degree of cellular senescence was reduced in the group in which rapamycin was added to nicotine compared to that in the group treated with nicotine alone. Conclusion: This study provides evidence that autophagy activated in an aging environment reduces cellular senescence to a certain some extent.