• Journal of the Korean Society of Tobacco Science
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• v.27 no.2
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• pp.219-225
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• 2005

Characterizing nicotine delivery from tobacco products is important in the understanding of their addictive potential. Most previous studies report total nicotine and have not differentiated between nicotine in its protonated or free-base form. The amount of free nicotine calculated by determining pH and nicotine contents. The pH and nicotine contents in smokeless tobacco product, tobacco products and tobacco leaves were analyzed by Health Canada-Official Method T-310 and CORESTA Recommended Method $N^{\circ}62$. The content of free nicotine was calculated according to the Henderson-Hasselbalch equation and the value of $\alpha_{fb}$(the fraction of nicotine that is in the free base form) by using a pKa value of 8.02 for nicotine. The percentage of free nicotine then was calculated by dividing the free nicotine content by total nicotine content. The pH value and percentage of free nicotine ranged from 5.01 to 5.45 and $0.10\%\;to\;0.27\%$ in cut tobacco and 5.10 to 7.10 and $0.12\%\;to\;10.73\%$ in tobacco leaves, respectively.

• The Korean Journal of Pharmacology
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• v.31 no.3
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• pp.313-321
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• 1995

Conflicting data have been reported on the effect of nicotine on gastric mucosal damage. To elucidate the effect of chronic intermittent nicotine on gastric mucosal damage, intragastric nicotine (5 mg/kg, 10 mg/kg) was administered twice per day for 9 days. Gastric mucosal damage was created by s.c. injection of a large dose (1.2 mg/kg) of pentagastrin followed by pylorus ligation for 6 hours. Nicotine treated rats showed reduced gastric mucosal damage about 50% of the control. To examine the mechanism of the protective effect of nicotine, gastric perfusion experiments were done. Basal acid secretion was not affected by intragastric or intravenous nicotine. However, pentagastrin-stimulated acid secretion markedly inhibited by a bolus injection of nicotine, and this response was dose-related. These data indicates that chronic intermittent administration of nicotine protects gastric mucosa against gastrin-induced gastric mucosal damage, and nicotine-induced inhibition of gastrin-stimulated acid secretion has an important role for the protective effect of nicotine. Considering reports concerning nicotine's aggravating effect on the gastric mucosal damage, it is suggested that the methods of administration of nicotine may be an important decisive factor of the divergent action of nicotine on the gastric mucosa.

• Clinical and Experimental Reproductive Medicine
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• v.28 no.1
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• pp.1-12
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• 2001

Objective: The present study was done to clarify the effects of nicotine and nicotine tartrate on the mouse oocyte maturation in vitro. Methods: GV (germinal vesicle) oocytes were isolated from Graafian follicle of ovaries with sharp needles under a stereomicroscope from female mouse of ICR strain (4 weeks old). Collected oocytes were cultured for 17 hours at $37^{\circ}C$, 5% $CO_2$ in air and 100% humidified condition in incubator. New MHBS was the basic medium used in which nicotine, nicotine tartrate, and mecamylamine (antagonist of nicotinic acetylcholine receptor) were added depending on the experimental group. GV oocytes were cultured in one of these media. Results: Nicotine ($300{\mu}M{\sim}5mM$) had no effects on GVBD (germinal vesicle breakdown) compared to the control, but increasing concentration of nicotine led to an decrease in the first polar body formation. However, nicotine ($10{\sim}500{\mu}M$) induced GVBD in a dose-dependent manner of GV oocytes in a medium containing dbcAMP. Nicotine tartrate ($50{\mu}M{\sim}5mM$) had no effects on GVBD compared to the control but, increasing concentration of nicotine tartrate led to an decrease in the first polar body formation. Mecamylamine $10{\mu}M$ added to the medium containing nicotine ($300{\mu}M{\sim}5mM$) showed higher percentage of the first polar body formation compared to the nicotine ($300{\mu}M{\sim}5mM$) treatment group. Mecamylamine $10{\mu}M$ added to the medium containing nicotine tartrate ($50{\mu}M{\sim}5mM$) showed higher percentage of the first polar body formation compared to the nicotine tartrate ($50{\mu}M{\sim}5mM$) treatment group. Conclusion: The present study suggest that nicotine and nicotine tartrate have the harmful effects on the meiotic maturation of the mouse oocytes in vitro. However, mecamylamine block harmful effects of nicotine and nictine tartrate.

• Korean Journal of Adult Nursing
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• v.18 no.5
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• pp.737-745
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• 2006

Purpose: The purpose of the study was to investigate the level of smoking, process of smoking cessation, and nicotine dependency, and urine nicotine among adults with diabetes which are smokers and to examine the relationship among those variables. Method: The subjects consisted of 62 adult men smokers with diabetes mellitus. FTQ and NicCheck 1 were used to measure the level of nicotine dependence. The amount of cigarette smoking was measured by the number of cigarette packs use per week. The stage of smoking cessation was measured by the Prochaska's method. Results: The Subjects smoked cigarettes with a mean of 5.97 packages per week. Seventy-seven percent of the subjects had a nicotine dependency. Fifty-two percent had a high level of nicotine dependency in urine nicotine. Nineteen percent were in the precontemplation stage. The level of cigarette consumption was related to nicotine dependence and urine nicotine. Also, nicotine dependency was related to urine nicotine. Conclusion: A tailored smoking cessation program is needed to prevent the chronic complication for diabetes smokers. Self-reported smoking and nicotine dependency seemed to do equally well as NicCheck 1 in assessing nicotine intake.

• Korean Journal of Health Education and Promotion
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• v.27 no.4
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• pp.123-129
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• 2010

Objectives: The aim of this study is to seek an effective way to support smoking cessation by analyzing any change to the pattern of nicotine dependence according to the change in time. Methods: The study was conducted with 800 male smokers who had participated in smoking cessation programs at public health centers from July 16, 2005 to July 15, 2008. Latent growth curve modeling approach was used for data analysis. Results: From the developmental trajectory of individual nicotine dependence, while nicotine dependence of smokers with high nicotine dependence in the first year was slightly decreased in the third year, smokers with low nicotine dependence in the year showed dramatically lower nicotine dependence in the third year. Compared with those who did not successfully quit smoking, the initial value of nicotine dependence of those who successfully quit smoking in the first and the second year was low. Over the years, nicotine dependence was decreased. Conclusion: From this study it was demonstrated that nicotine dependence was reduced through the practice of smoking cessation and reduced nicotine dependence was a factor which affects successful smoking cessation. These results indicate that multiple attempts to quit smoking finally reduces nicotine dependence. Reduced nicotine dependence is likely to increase the possibility of successful smoking cessation.

• Journal of Pharmacopuncture
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• v.23 no.1
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• pp.1-7
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• 2020

Nicotine, primary component of tobaco produces craving and withdrawal effect both in humans and animals. Nicotine shows a close resemblance to other addictive drugs in molecular, neuroanatomical and pharmacological, particularly the drugs which enhances the cognitive functions. Nicotine mainly shows its action through specific nicotinic acetylcholine receptors located in brain. It stimulates presynaptic acetylcholine receptors thereby enhancing Ach release and metabolism. Dopaminergic system is also stimulated by it, thus increasing the concentration of dopamine in nuclear accumbens. This property of nicotine according to various researchers is responsible for reinforcing behavioral change and dependence of nicotine. Various researchers have also depicted that some non dopaminergic systems are also involved for rewarding effect of nicotinic withdrawal. Neurological systems such as GABAergic, serotonergic, noradrenergic, and brain stem cholinergic may also be involved to mediate the actions of nicotine. Further, the neurobiological pathway to nicotine dependence might perhaps be appropriate to the attachment of nicotine to nicotinic acetylcholine receptors, peruse by stimulation of dopaminergic system and activation of general pharmacological changes that might be responsible for nicotine addiction. It is also suggested that MAO A and B both are restrained by nicotine. This enzyme helps in degradation dopamine, which is mainly responsible for nicotinic actions and dependence. Various questions remain uninsurable to nicotine mechanism and require more research. Also, various genetic methods united with modern instrumental analysis might result for more authentic information for nicotine addiction.

• Archives of Pharmacal Research
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• v.23 no.5
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• pp.488-494
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• 2000

Cerebellar granule and glial cells prepared from 7 day-old rat pups were used to investigate the effects of sub-acute nicotine exposure on the glutamatergic nervous system. These cells were exposed to nicotine in various concentrations for 2 to 10 days in situ. Nicotine-exposure did not result in any changes in cerebellar granule and glial cell viability at concentrations of up to 500 $\mu\textrm{M}$. In cerebellar granule cells, the basal extracellular levels of glutamate, aspartate and glycine were enhanced in the nicotine-exposed granule cells. In addition, the responses of N-methyl-D-aspartate (NMDA)-induced glutamate release were enhanced at low NMDA concentrations in the nicotine-exposed granule cells. However, this decreased at higher NMDA concentrations. The glutaminase activity was increased after nicotine exposure. In cerebellar glial cells, glutamate uptake in the nicotine-exposed glial cells were either increased at low nicotine exposure levels or decreased at higher levels. The inhibition of glutamate uptake by L-trans-pyrollidine-2,4-dicarboxylic acid (PDC) was lower in glial cells exposed to 50 $\mu\textrm{M}$ nicotine. Glutamine synthetase activity was lower in glial cells exposed to 100 or 500 $\mu\textrm{M}$ of nicotine. These results indicate that the properties of cerebellar granule and glial cells may alter after subacute nicotine exposure. Furthermore, they suggest that nicotine exposure during development may modulate glutamatergic nervous activity.

• Journal of The Korean Society of Clinical Toxicology
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• v.5 no.1
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• pp.53-56
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• 2007

Nicotine poisoning arising from the use of nicotine patches is rare. However, because nicotine patches are classified as an OTC drug, the risk of misuse or abuse is increasing. Nicotine poisoning using nicotine patches shows an unusual clinical presentation compared to that from oral ingestion of multiple doses of nicotine. We present a case of misused nicotine patches that cause a nicotine poisoning. A thirty-nine year-old healthy man visited the ER with complaints of an intermittent cramping abdominal pain with nausea and vomiting. Upon physical examination, there were no specific findings except increased bowel sounds, and the patient's initial laboratory findings were also unremarkable except for an increased bilirubin level. CT revealed a mild degree of fatty liver. The patient's symptoms did not improve any further with conservative management. During his ED stay, we meticulously took his history again, and we discovered that he had used nicotine patches for three days, six days before admission, and had misused the nicotine patches as NSAID patches. The patient's diagnosis of nicotine poisoning was confirmed by a urine cotinine level ten times the normal value. After a 12-hour stay in the ED, his symptoms disappeared without any specific management.

• Biomolecules & Therapeutics
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• v.11 no.4
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• pp.238-244
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• 2003

Nicotine is one of the major hazardous components in cigarettc smoke. Nicotine deals a harmful effect to smokers and passive smokers due to its rapid conversion to various carcinogenic metabolites. Nitrosamine-4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is believed to cause lung cancers among the nicotine-derived carcinogens. Recent studies report that NNK synthesis can be inhibited by the metabolism pathway to produce a stable metabolite cotinine from nicotine. Tea polyphenols have been known to contain factors to prevent cancers and to retard progression of cancers. This study aims to correlate tea polyphenol's potential for cancer prevention with an accelerated formation of cotinine. The conversion from nicotine to cotinine in the presence of tea extracts or three polyphenols (Catechin, epicatechin gallate, epigallocatechin gallate) was measured in established cell lines and in Xenopus oocytes. Among three lines of cell used, PLC/PRF5 and HEK293 cells showed a fast turnover from nicotine to cotinine while HepG2 cell line showed a marginal difference between groups treated and non-treated with tea polyphenols. When Xenopus oocytes were microinjected with nicotine, tea polyphenols appear to accelerate the conversion of nicotine to cotinine. Among the polyphenols tested in this study, (＋)－catechin showed the best efficiency overall in accelerating conversion from nicotine to cotinine both in the cell lines and in the oocytes. In summary, the present study indicated that tea polyphenols have a positive effect on conversion of nicotine to cotinine.

• Journal of Plant Biology
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• v.34 no.2
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• pp.101-106
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• 1991

Effects of two auxins, 2,4-dichlorophenoxyacetic acid (2,4-D) and a-napthaleneacetic acid (NAA) on nicotine production during callus culture of a wild tobacco (Nicotiana glauca) were investigated using a high performance liquid chromatography (HPLC). The high concentration ($11.5\;\mu\textrm{M}$)of 2,4-D and NAA had peaks of nicotine contents at 4th and 2nd week, respectively. Thereafter, the concents decreased and the nicotine was metabolized to other alkaloids. The low concentration ($1.5\;\mu\textrm{M}$) of 2,4-D on the medium supplemented with 0.1 mM of L-aspartic acid or L-arginine inhibited nicotine production. However, the low NAA promoted it only when the medium was supplemented with L-aspartic acid. From these results, it could be concluded that both auxins exhibit different action mechanisms on nicotine production pathway and the low NAA promotes the activities for the pathway with L-aspartic acid as a precursor.cursor.