• Archives of Pharmacal Research
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• v.16 no.2
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• pp.89-93
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• 1993

Incubation of $S(-)-^3H$-nicotine with rabbit lung microsomes in the presence of dioxygen and NADPH results in the formation of metabolities that bind covalently to microsomal macro-molecules. The addition of cytochrome P-450 monooxygenase inhibitors, $\alpha$-methylbenzyl ami-nobenzotriazole and aroclor 1260, inhibited both (S)-nicotine metabolism and covalent binding. The relative rates of oxidation of nicotine $\Delta^{1',5'}$ iminium ion to continine indicates that lung $100,000\times{g}$ supematant catalyzed this oxidation approximately 18 times slower than that of liver system based on mg of protein, and increased covalent interactions. Since than that of liver system based on mg of protein, nd increased covalent interactions. Since the activity of lung iminium oxidase appears much lowr than the liver, it is tempting to speculate that localized concentrations of nicotine $\Delta^{1',5'}$ iminium ion in the lung will survive for a longer period of time. These results support that cytochrome P-450 catalyzed oxidation of nicotine leads to the formation of reactive nad electrophilic intemediates capable of chemical interactions with biomacromolecules.

• Archives of Pharmacal Research
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• v.14 no.2
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• pp.130-136
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• 1991

Nicotine (100 .mu. M) was incubated with microsomes (1 mg/ml) prepared from New Zealand White rabbits. On the basis of microsomal weight, the rate of nicotine oxidation were calculated on the basis of cytochrome P-450 concentration, the specific activity of the metabolic oxidation catalyzed by lung was approximately 4 times greater than liver (6.4 vs 1, 65 nmoles nicotine oxidized. nmole cytochrome $P-450^{-1}\;min{-1})$. These studies employed several methods of altering activities of specific isozymes present in pulmonary microsomes, including the use of the isozyme2 and 6 specific inhibitor $\alpha$-methylbenzyl ABT, metabolite inhibitors, norbenzphetamine and N-hydroxyamphetamine. TCDD induction and Arochlor 1260 pretreatment. These results support the conclusion that nicotine metabolism by rabbit lung microsomes is mediated primarily by cytochrome P-450 isozyme 2.

• Nutritional Sciences
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• v.9 no.4
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• pp.288-294
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• 2006

In this study, the effects of smoking cessation and relative antioxidant activities on the oxidative stress were determined by using in vitro method. Thirty healthy smokers who were free of any disease and smoked more than 1 pack per day for the past 10 years participated in this study. For smoking cessation, smokers were asked to wear nicotine patch (21mg nicotine/ patch) everyday for 30 days and then to replace at the same time of the day. Smoking cessation program in conjunction with nicotine patch replacement was also conducted every week, one hour/each session, for 4 weeks. Canthaxanthin, $\beta-carotene$, and $\alpha-tocopherol$ were added into red blood cells at pre and post smoking cessation. As indicators of oxidative stress, hemoglobin degradation, lipid peroxidation, and percent hemolysis were determined at both pre and post smoking cessation. After 30 days of smoking cessation, the subjects gained an average of 5 pounds, varying 2 to 8 pounds, by suggesting that behavioral problems rather than nicotine itself are more important for gaining weight in ex-smokers. The total hemoglobin concentrations in blood were similar in pre and post smoking cessation, but smoking cessation resulted in a decrease in the percentage of methemoglobin from 0.96% to 0.85% Smoking cessation also caused to decease malondialdehyde (MDA) values ($26.7{\pm}7.8$ vs. $23.6{\pm}4.5$ (without oxidation), $179.3{\pm}21$ vs. $161.2{\pm}28$ nmol/ml (with oxidation) (p<0.05)), not percent hemolysis. Various antioxidants with smoking cessation significantly decreased MDA values(p<0.05), in contrast to marginal decrease of MDA in smoking cessation only. Three antioxidants used in this stu study were similarly effective in inhibiting MDA production, but relative effectiveness of canthaxanthin or $\alpha-tocopherol$ was greater than that of $\beta-carotene$ (p<0.05), in case of oxidation induced. The percent hemolysis was greatly decreased when antioxidants were added into the blood of ex-smokers (p<0.05) but no statistical significance in relative effectiveness of antioxidants was observed.

• Journal of Korean Society of Environmental Engineers
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• v.28 no.3
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• pp.316-322
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• 2006

The current study evaluated the technical feasibility of the application of $TiO_2$ photocatalysis for the removal of nocotine which has well known as a representative material of environmental tobacco smoke(ETS). Four different preliminary experiments were performed for the evaluation of nicotine removal using photocatalyst-coated construction materials. The photocatalytic removal of nicotine was investigated for five parameters: dry condition of coating tiles, type of coating sol, number of coatings, relative humidity(RH), and input concentrations. Prior to performing the parameter tests, adsorption of nicotine onto the current experimental system was surveyed. All the variables tested in the present study exhibited to influence the photocatalytic decomposition of Nicotine. A dry condition of high temperature and short dry period presented higher photocatalytic oxidation(PCO) efficiency compared to that of low temperature and long dry period. ST-KO3 sol showed higher decomposition efficiency than E-T Sol. The PCO efficiency increased as the number of coating increased. High humidity and low input concentrations exhibited higher PCO efficiency. Consequently, it is noted that the five parameters tested in the present study should be considered for the application of photocatalyst-coated construction materials in cleaning nicotine in ETS.

• Journal of the Korean Applied Science and Technology
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• v.29 no.1
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• pp.40-46
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• 2012

In vivo nicotine is associated with Alzheimer's, Parkinson's and lung cancer. Diagnostic assays of these diseases depend on very low analytical detection limits. In this study, a sensitive analytical method was examined using a voltammetric graphite pencil electrode (GPE) and a modified carbon nanotube paste electrode (CNE). The optimum analytical conditions for both electrodes were compared using square wave anodic stripping voltammetry (SW) and cyclic voltammetry (CV) obtaining 400 sec accumulation time and oxidation peak. Under optimum parameters, the stripping working range of GPE was $5.0-40.0{\mu}g/L$, CNE: 0.1-0.8 and $5-50{\mu}g/L$. Quantification limits were $5.0{\mu}g/L$ for GPE and $0.1{\mu}g/L$ for CNE, while detection limits were $0.6{\mu}g/L$ for GPE and $0.07{\mu}g/L$ for CNE. A standard deviation of $10.0{\mu}g/L$ was observed for 0.064 GPE and 0.095 CNE (n = 12) using 400 sec accumulation time. The results obtained can be applied to non.treated urine and ex vivo biological diagnostics.

• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.723-735
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• 1998

Background : Vitamin C has been reported to have a role in the decrease of airway hyperresponsiveness in animal models. This data is based on some metabolic actions of vitamin C, such as promotion of histamine degradation, producing more $PGE_2$ than $PGF_{2\alpha}$ in cyclooxygenase pathway, decrease of smooth muscle contraction, and acting as reducing agent of oxidant. It has been also known that heavy smokers have lower blood levels of vitamin C than nonsmokers and this deficiency in heavy smokers have been explained by several mechanisms, such as increased oxidation by oxidants and free radicals, increased biosynthesis of catecholamine and serotonin released by nicotine, and inadequate dietary intake. In this study, We attempted to assess effect of vitamin C on bronchial hyperresponsiveness in heavy smokers who have bronchial hyperresponsiveness and role of vitamin C on bronchial hyperresponsiveness. Method: To assess acute effect of vitamin C on airway hyperresponsiveness, blood sample for vitamin C level and spirometry, methacholine challenge test were done in 17 smokers and 8 nonsmokers, and one hour after oral administration of vitamin C 3 g, blood sample for vitamin C level and spirometry, methacholine challenge test were repeated. To assess chronic effect of vitamin C on airway hyperresponsiveness, after daily administration of vitamin C 1 g for one week in 17 smokers, blood sample for vitamin C level and spirometry, methacholine challenge test were done. To assess role of vitamin C, after oral administration of vitamin C 3 g plus indomethacin 100 mg in 12 of 15 smokers who were reactive to methacholine challenge test, spirometry and methacholine challenge test were done and after oral intake of indomethacin 100 mg in 12 smokers who were reactive to methacholine challenge test, spirometry and methacholine challenge test were repeated. Result: There were no significant differences in whole blood vitamin C levels between smokers($1.17{\pm}0.22$ mg/dL) and nonsmcikers($1.14{\pm}0.19$ mg/dL) (p>0.05). Fifteen of the 17 smokers(88.2%) were reactive to methacholine challenge test and 10 of the 15 smokers who were reactive to methacholine challenge test were less than 8 mg/dL in $PC_{20}FEV-2$, and 7 of the 8 nonsmokers(87.5%) were nonreactive to methacholine challenge test There were significant decrease in bronchial responsiveness after oral administration of vitamin C 3 g in 13 of the 15 smokers who were reactive to methacholine challenge test This significant decrease persisted with maintenance daily administration of 1 g for one week. $PC_{20}FEV-2$ were not correlated to vitamin C levels in smokers. After oral administration of indomethacin 100 mg, significant reduction of bronchial responsiveness that occured after oral administration of vitamin C 3 g in smokers were attenuated. Conclusion: Although there were no significant differences in whole blood vitamin C levels between smokers and nonsmokers. heavy smokers have significant increase in bronchial responsiveness than nonsmokers. This bronchial hyperresponsiveness of heavy smokers can be attenuated by vitamin C supplement. Disappearance of vitamin C effect by indomethacin supplement may suggest that vitamin C exert its effect via alteration of arachidonic acid metabolism.