Wyniki wyszukiwania - Biblioteka Nauki

1

Serum beta-glucuronidase in colon cancer patients dependent on alcohol and nicotine: preliminary report

100%

Waszkiewicz N. , Zalewska-Szajda B. , Repka B. , Szulc A. , Kępka A. , Chojnowska S. , Dadan J. , Ładny J. , Zwierz K. , Szajda S.

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nr 2

64-69

EN

Introduction: Beta-glucuronidase (GLU) is a lysosomal exoglycosidase involved in the catabolism of glycoconjugates. Excessive GLU activity may be a primary factor in the etiology of colon cancer. The stimulation of glycosidases and other degradative enzyme activity has been noted in cancers as well as in alcohol and nicotine addiction. Purpose: To compare the serum GLU activity between alcohol- and nicotine-dependent colon cancer patients and colon cancer patients without a history of alcohol- and nicotine-dependence. Materials and methods: Material was the serum of 22 colon cancer patients, 11 of whom met alcohol and nicotine dependence criteria. The activity of serum GLU (pKat/ml) was determined by the colorimetric method. Carcinoembryonic antigen (CEA) concentration (ng/ml) in the serum was determined by the immunoenzymatic method. Comparisons between groups were made using the Mann-Whitney “U” test. Spearman’s rank correlation coefficient was used to measure the association between two variables. Results: The activity of serum GLU was significantly higher in colon cancer patients with a history of alcohol and nicotine dependence, than in the colon cancer patients without a history of drinking and smoking (p=0.003). There was no significant difference in the CEA concentration between colon cancer patients with and without a history of drinking and smoking. Conclusion: Alcohol and nicotine addiction may increase the serum GLU activity in all cancer patients, as already seen in colon cancer patients. This may potentially be important for the degradation of pericancerous matrix, tumor growth, invasion and metastasis

2

Determination of nicotine and three minor alkaloids in tobacco by hydrophilic interaction chromatography-tandem mass spectrometry

88%

Taujenis L. , Olšauskaitė V. , Padarauskas A.

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tom Vol. 27, no. 2

373--385

EN

A reliable, sensitive and rapid method for determination of nicotine and three minor alkaloids (cotinine, anabasine and nornicotine) in tobacco by ultra-high performance liquid chromatography in hydrophilic interaction chromatography mode coupled with tandem mass spectrometry (HILIC-MS/MS) has been established. HILIC separation was performed on a BEH HILIC column using isocratic elution at 0.5 mL/min with acetonitrile:water (85:15, v/v) mobile phase containing 5 mmol/L ammonium acetate (pH 5.00). Separated analytes were determined by electrospray ionization MS/MS in the positive ion mode using multiple reaction monitoring. Alkaloids from tobacco were extracted in an ultrasonic bath for 10 min with acetonitrile:water mixture (8:2, v/v) containing 5 mmol/L ammonium acetate (pH 5.00). Limits of quantification were 10 μg/g for cotinine, 20 μg/g for anabasine and nornicotine, and 30 μg/g for nicotine. Mean recoveries from tobacco ranged between 94.8% and 104.1% for different analytes with relative standard deviations within 5%. The performance of the proposed method was tested for the extraction and determination of the four alkaloids in cigarette tobacco fillers, and satisfactory results were achieved.

3

Effects of nicotine on the concentration of native and cryptic Met- and Leu-enkephalin in peripheral tissues

88%

Pierzchala-Koziec K. , Van Loon G. R.

Journal of Physiology and Pharmacology

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1994

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tom 45

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nr 2

4

Protective effects of nicotine against glutamate-induced neurotoxicity in PC12 cells

88%

Sun X. , Liu Y. , Hu G. , Wang H.

Cellular and Molecular Biology Letters

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2004

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tom 09

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nr 3

EN

This study aimed to assess whether nicotine prevented glutamate neurotoxicity in PC12 cells, and to identify the molecular mechanisms of any effects. The results showed that glutamate neurotoxicity in PC12 cells could be prevented by treatment with nicotine at concentrations of 10 nmol.l-1-1 mmol.l-1. This effect was in turn found to be inhibited by the application of the nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine. Nicotine significantly decreased the basal level of intracellular free Ca2+ and enhanced the buffering action on Ca2+ overload induced by high concentrations of glutamate (5 mmol.l-1). In addition, nicotine treatment up-regulated the mRNA and protein expression of apoptosis-related factors including bcl-2 mRNA and protein, but down-regulated the expression of bax mRNA and protein. It is concluded that the protective effects of nicotine against the neurotoxicity induced by glutamate are mediated by nAChRs, due to the increased buffering action on Ca2+ and the modulation of apoptotic processes.

5

Role of nitric oxide in the nicotine-induced pituitary-adrenocortical response

88%

Gadek-Michalska A. , Bugajski J.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 2

EN

Nitric oxide (NO) is a major signaling molecule and biological mediator of the hypothalamic-pituitary-adrenal (HPA) axis. We investigated the role of NO formed by endothelial (e), neuronal (n) and inducible (i) nitric oxide synthase (NOS) in the stimulatory effect of nicotine on the HPA axis in rats under basal conditions. Also possible interaction of NOS systems with endogenous prostaglandins (PG) in that stimulation was assessed. NOS and cyclooxygenase inhibitors were administered i.p. 15 min prior to nicotine (2, 5 mg/kg i.p.). Plasma ACTH and serum corticosterone levels were measured 1 h after nicotine injection. NOS blockers given alone did not markedly affect the resting ACTH and corticosterone levels. L-NAME (2-10 mg/kg), a broad spectrum NOS inhibitor considerably and dose dependently enhanced the nicotine-induced ACTH and corticosterone secretion. L-NNA (2 mg/kg) and 7-nitroindazole (7-NI 20 mg/kg), neuronal NOS inhibitors in vivo also significantly augmented the nicotine-induced ACTH and corticosterone levels. L-arginine greately impaired the nicotine-induced hormone responses and reversed the L-NNA elicited enhancement of the nicotine-evoked ACTH and corticosterone response. In contrast to the constitutive eNOS and nNOS antagonists, an inducible NOS antagonist guanethidine (50-100 mg/kg i.p.) did not substantially affect the nicotine-elicited pituitary-adrenocortical responses. Indomethacin (2 mg/kg i.p.), a non-selective cyclooxygenase blocker abolished the L-NAME and L-NNA-induced enhancement of the nicotine-evoked ACTH and corticosterone response. These results indicate that NO is an inhibitory mediator in the HPA axis activity. Inhibition of its generation by eNOS and nNOS significantly enhances the nicotine-induced HPA response. Under basal conditions iNOS is not involved in the nicotine-induced ACTH and corticosterone secretion. Prostaglandins play an obligatory role in the response of HPA axis to systemic nicotine administration.

6

Papieros przed sniadaniem

75%

Kolodziejczyk M.

Żywność, Żywienie, Życie. Szkoła Główna Gospodarstwa Wiejskiego w Warszawie

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2002

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nr 1

38-39

7

Nikotyna

75%

Szymańska J. , Frydrych B. , Bruchajzer E.

Podstawy i Metody Oceny Środowiska Pracy

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2007

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tom Nr 2 (52)

121--154

PL

Nikotyna jest bezbarwną, bezwonną i oleistą cieczą otrzymywaną z liści tytoniu przez destylację z parą wodną w środowisku zasadowym i ekstrakcję eterem. Największe zużycie nikotyny jest związane z produkcją wyrobów tytoniowych, a także z produkcją środków, których zażywanie ma na celu odzwyczajenie się od palenia. Nikotyna jest składnikiem niektórych pestycydów. Narażenie zawodowe na nikotynę możliwe jest przy produkcji i suszeniu tytoniu. Zatrucia śmiertelne zdarzały się w latach 20. i 30. XX w. w trakcie opryskiwania roślin preparatami z nikotyną. Obecnie w Polsce tylko 8 osób było narażonych na nikotynę o stężeniu w powietrzu przekraczającym wartość NDS, tj. 0,5 mg/m3 (dane z 2002 r.). Do śmiertelnego zatrucia zawodowego nikotyną dochodzi bardzo rzadko. Objawami ostrego zatrucia małymi dawkami nikotyny są: pobudzenie oddechu, nudności, wymioty, bóle i zawroty głowy, biegunka, częstoskurcz, wzrost ciśnienia krwi oraz pocenie i ślinienie się. Po dużych dawkach nikotyny stwierdzono ponadto pieczenie w jamie ustnej, gardle i żołądku. Później następowało wyczerpanie, drgawki, osłabienie czynności oddechowej, zaburzenie rytmu serca oraz zaburzenia koordynacji ruchowej i śpiączka. Śmierć może wtedy nastąpić w czasie od 5 min do 4 h. Zatrucia przewlekłe nikotyną prowadzą do zaburzeń układu krążenia. Zmiany naczyniowe sprzyjają powstawaniu dusznicy bolesnej oraz zawałom serca, a także powodują: osłabienie pamięci, zwolnienie procesów psychicznych i koordynacji myśli, brak energii oraz ogólne wyczerpanie. Obserwuje się również zaburzenia ze strony przewodu pokarmowego. Nikotyna jest związkiem, który powoduje uzależnienie fizyczne i psychiczne. W dostępnym piśmiennictwie nie znaleziono danych epidemiologicznych dotyczących zawodowego narażenia na nikotynę w postaci czystej. Nikotyna jest substancją o dużej toksyczności ostrej dla zwierząt – po podaniu dożołądkowym wartość DL50 mieści się w granicach 3,34 ÷ 188 mg/kg masy ciała. Informacje na temat toksyczności nikotyny wskazują na jej wielokierunkowe działanie. Narażenie drogą pokarmową szczurów na dawkę 1 mg/kg/dzień nikotynę przez 9 dni nie spowodowało żadnych zmian. Podobnie żadnych skutków nie zanotowano po podawaniu nikotyny szczurom w dawce 1,14 mg/kg/dzień przez 34 tygodnie. Dawka czterokrotnie większa powodowała wzrost aktywności niektórych enzymów w sercu szczurów narażonych przez 34 tygodnie. Podobna dawka podawana przez 9 dni wywoływała zmiany w zapisie EEG. Narażenie szczurów na nikotynę w dawce 3,5 mg/kg/dzień przez 90 dni oraz na nikotynę w dawce 12,5 mg/kg/dzień przez 28 dni (dawka skumulowana wynosiła odpowiednio: 315 lub 350 mg/kg) powodowało u zwierząt zaburzenia w gospodarce lipidowej i węglowodanowej. Z obserwacji zależności efektu toksycznego od wielkości narażenia po podaniu dożołądkowym nikotyny można przyjąć za wartość NOAEL dawkę 1,14 mg/kg/dzień, a za wartość LOAEL dawkę 4,56 mg/kg/dzień. Nikotyna nie wykazuje działania mutagennego, ale jest jednak genotoksyczna (wymiana chromatyd siostrzanych i aberracje chromosomowe) oraz fetotoksyczna. Udowodnione działanie rakotwórcze wykazują nitrozoaminy – związki powstające w wyniku palenia się tytoniu (NNN i NNK). Nikotyna dobrze wchłania się przez drogi oddechowe, przewód pokarmowy i skórę. Największe stężenia nikotyny stwierdzono w mózgu, nerkach, błonie śluzowej żołądka, rdzeniu nadnerczy, błonie śluzowej nosa i śliniankach. Nikotyna wiąże się z białkami osocza w 5 20% i przenika przez łożysko oraz do mleka matek karmiących. W trakcie metabolizmu nikotyna może ulegać: C-oksydacji, demetylacji połączonej z C-oksydacją, N-oksydacji oraz N-metylacji. Jej głównymi metabolitami są: kotynina i nikotyno-1’-N-tlenek. Nikotyna i jej metabolity są szybko wydalane przez nerki. Mechanizm działania nikotyny jest wypadkową aktywacji cholinergicznych receptorów nikotynowych powodujących pobudzenie komórek nerwowych i desensytyzacji powodującej zablokowanie przekaźnictwa sympatycznego. Działania obwodowe wywołane małymi dawkami nikotyny są wynikiem pobudzenia zwojów autonomicznych i obwodowych receptorów czuciowych, głównie w sercu i płucach. Pobudzenie tych receptorów wywołuje częstoskurcz, zwiększenie wyrzutu serca, wzrost ciśnienia tętniczego, zmniejszenie perystaltyki przewodu pokarmowego i pocenie się. Najbardziej rozpowszechnionym wśród ludzi przykładem działania łącznego nikotyny z innymi związkami jest palenie papierosów, w których – oprócz nikotyny – znajdują się setki innych substancji. Jednoczesnemu narażeniu szczurów na nikotynę i etanol towarzyszyło znaczące zmniejszenie ich płodności oraz zaburzenie reakcji immunologicznych u potomstwa. Nikotyna nasila hepatotoksyczne działanie CCl4. Na podstawie danych literaturowych przyjęto dawkę 1,14 mg/kg/dzień (po której nie zaobserwowano żadnych szkodliwych skutków) za wartość NOAEL nikotyny, zaś dawkę 4,56 mg/kg/dzień – za jej wartość LOAEL Po analizie danych literaturowych i wykonanych obliczeniach pozostano przy obowiązującej w Polsce wartości najwyższego dopuszczalnego stężenia (NDS) nikotyny wynoszącej 0,5 mg/m3 z oznaczeniami związku literami „Sk” i „Ft”. W dostępnym piśmiennictwie nie znaleziono informacji uzasadniających wyznaczenie dla nikotyny wartości najwyższego dopuszczalnego stężenia chwilowego (NDSCh).

EN

Nicotine is an oily, colourless and odourless liquid obtained from leaves of tobacco plants. The most widespread use of nicotine is in tobacco as well as in remedies for nicotine abuse. Nicotine is a component of certain pesticides. Occupational exposure to nicotine is possible during its production and the tobacco drying process. To date only 8 people have been exposed in Poland to nicotine concentration in the air exceeding the TWA value which is 0.5 mg/m3 (data from 2002). Deadly occupational nicotine intoxication is very rare. The symptoms of severe nicotine intoxication with its small doses are: increased breath stimulation, nausea, vomitting, headache and vertigo, diarrhea, tachycardia, high blood pressure as well as sweating and excessive saliva production. After the administration of high doses of nicotine the following symptoms occured: burning sensations in the oral cavity, throat and stomach, fatigue, palpitations, weakening of the respiratory functions, disturbances of cardiac rhythm, dizziness, weakness, lack of coordination and coma. Death can then occur within 5 minutes up to 4 hours. Chronic nicotine intoxication leads to disturbances in the circulatory system. Vascular changes may lead to angina pectoris and heart attacks; they also cause: a weakening of memory, a slowdown of physical processes and thought coordination, lack of energy and exhaustion. Disturbances in the digestive system may also occur. Nicotine causes both physical and mental abuse. No epidemiological data was found concerning occupational exposure to nicotine in pure form. Nicotine is a substance of high acute toxicity to animals. After intragastrical administration the LD50 value is between 3.34 ÷ 188 mg/kg of body weight. Information concerning toxicity of nicotine indicates its multidirectional influence. Exposure of rats at oral doses (1 mg/kg/day, 9 days or 1.14 mg/kg/day, 34 weeks) caused no changes. When fourfold higher doses were administered to rats, after 34 weeks they caused an increase in the activity of certain enzymes in the heart, and the EEG changed after 9 days. Exposure to nicotine for 28 and 90 days (the accumulated dose was 350 or 315 mg/kg respectively) caused a disturbances in lipid and carbohydrate metabolism. Nicotine has no mutagenic potential, yet it is genotoxic (sister chromatid exchanges and chromosomal aberrations) as well as fetotoxic. Nitrosoamines (compounds produced due to tobacco smoking) have proved to show carcinogenic potential. Nicotine is well absorbed via respiratory tracts, the alimentary canal and the skin. The highest concentrations were detected in the brain, kidneys, stomach mucosa, adrenal medulla, nasal mucosa and salivary glands. Nicotine binds with plasma proteins in 5 - 20%. It penetrates through placenta and gets to the milk of nursing mothers. During metabolism nicotine can undergo: C-oxidation, demethylation with z C-oxidation, N-oxidation and N-methylation. Nicotine’s core metabolites are: cotinine and nicotine-1’-N-oxide. Nicotine and its metabolites are rapidly discharged by the kidneys. Smoking cigarettes is the most common example of nicotine activity together with many other compounds. In addition to nicotine, they include hundreds of other substances. Rats simultaneously exposured to ethanol and nicotine have shown impaired fertility and disturbance of immunological reactions occured in the offspring. Nicotine increases the hepatotoxic activeness of CCl4. Basing on the literature data 1.14 mg/kg/day has been accepted as a NOAEL value of nicotine (no negative results have been observed) whereas 4.56 mg/kg/day has been taken as its LOAEL value. After an analysis of published data and after conducting necessary calculations the MAC of nicotine in Poland remains unchanged: 0.5 mg/m3 with ‘Sk’ and ‘Ft’ compound symbols.

8

Środowiskowy dym tytoniowy

75%

Demkowska I. , Polkowska Ż. , Namieśnik J.

Analityka : nauka i praktyka

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2007

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tom nr 3

35-38

9

New ideas, old problems? Heated tobacco products – a systematic review

75%

Jankowski M. , Brożek G. M. , Lawson J. , Skoczyński S. , Majek P. , Zejda J. E.

International Journal of Occupational Medicine and Environmental Health

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2019

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tom 32

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nr 5

595-634

EN

Heated tobacco products (HTPs) are a form of nicotine delivery intended to provide an alternative to traditional cigarettes. The aim of this systematic review was to present the current state of knowledge on HTPs with an emphasis on the potential impact of HTP use on human health. During the preparation of this systematic review, the literature on HTPs available within Medline/PubMed, EMBASE, CINAHL, ScienceDirect, and Google Scholar was retrieved and examined. In the final review, 97 research papers were included. The authors specifically assessed the construction and operation of HTPs, as well as the chemical composition of HTP tobacco sticks and the generated aerosol, based on evidence from experimental animal and cellular studies, and human-based studies.Heated tobacco products were found to generate lower concentrations of chemical compounds compared to traditional cigarettes, except for water, propylene glycol, glycerol, and acetol. The nicotine levels delivered to the aerosol by HTPs were 70–80% as those of conventional combustion. The results of in vitro and in vivo assessments of HTP aerosols revealed reduced toxicity, but these were mainly based on studies sponsored by the tobacco industry. Independent human-based studies indicated that there was a potentially harmful impact of the active and passive HTP smoking on human health. Currently, a large body of knowledge on HTP exposures and health effects is provided by the tobacco industry (52% of identified studies). Based on the available evidence, HTPs produce lower levels of toxic chemicals, compared to conventional cigarettes, but they are still not risk-free. Int J Occup Med Environ Health. 2019;32(5):595–634

10

E-smoking: Emerging public health problem?

75%

Jankowski M. , Brożek G. , Lawson J. , Skoczyński S. , Zejda J. E.

International Journal of Occupational Medicine and Environmental Health

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2017

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tom 30

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nr 3

329-344

EN

E-cigarette use has become increasingly popular, especially among the young. Its long-term influence upon health is unknown. Aim of this review has been to present the current state of knowledge about the impact of e-cigarette use on health, with an emphasis on Central and Eastern Europe. During the preparation of this narrative review, the literature on e-cigarettes available within the network PubMed was retrieved and examined. In the final review, 64 research papers were included. We specifically assessed the construction and operation of the e-cigarette as well as the chemical composition of the e-liquid; the impact that vapor arising from the use of e-cigarette explored in experimental models in vitro; and short-term effects of use of e-cigarettes on users’ health. Among the substances inhaled by the e-smoker, there are several harmful products, such as: formaldehyde, acetaldehyde, acroleine, propanal, nicotine, acetone, o-methyl-benzaldehyde, carcinogenic nitrosamines. Results from experimental animal studies indicate the negative impact of e-cigarette exposure on test models, such as ascytotoxicity, oxidative stress, inflammation, airway hyper reactivity, airway remodeling, mucin production, apoptosis, and emphysematous changes. The short-term impact of e-cigarettes on human health has been studied mostly in experimental setting. Available evidence shows that the use of e-cigarettes may result in acute lung function responses (e.g., increase in impedance, peripheral airway flow resistance) and induce oxidative stress. Based on the current available evidence, e-cigarette use is associated with harmful biologic responses, although it may be less harmful than traditional cigarettes. Int J Occup Med Environ Health 2017;30(3):329–344

11

A simultaneous measurement of nicotine and cotinine in the urine of smokers and passive smokers by high-performance liquid chromatography

75%

Głowacki R. , Brózik H. , Sabanty W. , Bald E.

Chemia Analityczna

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2000

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tom Vol. 45, No. 2

205-214

EN

This paper describes a sensitive and reliable high-performance liquid chromatographic method with ultraviolet detection for the simultaneous analysis of nicotine and cotinine in urine of smokers and passive smokers. The method involves an internal standard approach with the use of nikethamide, and consists of two essential steps: solid-phase extraction on Extrelut-1 column, and separation and quantitation by reversed-phase ion-pair liquid chromatography. The calibration'graphs for nicotine and cotinine were linear over the range from 20 to 2000 ng ml(-1) and from 10 to 1600 ng ml(-1), respectively. The relative standard deviations for above calibration ranges were from 6.46 to 2.09% and from 15.80 to 1.01 %, respectively. The method described represents an improvement on different liquid chromatography procedures previously published and it has significant advantages mostly in terms of final HPLC separation conditions.

PL

Opisano czułą i pewną metodę jednoczesnego oznaczania nikotyny i kotyniny w moczu palaczy i biernych palaczy, techniką wysokosprawnej chromatografii cieczowej z detekcją w zakresie nadfioletu. Zastosowano niketamid jako standard wewnętrzny. Metoda składa się z dwóch zasadniczych etapów: ekstrakcji do fazy stałej na kolumnie Extre-lut-1 oraz separacji i oznaczania techniką chromatografii par jonowych w odwróconym układzie faz. Krzywe kalibracyjne wykazały liniową zależność między zawartością analitów w próbce, a wskazaniem detektora, w zakresie stężeń od 20 do 2000 ng ml(-1) dla nikotyny i od 10 do 1600 ng ml(-1) dla kotyniny. Względne odchylenie standardowe dla tych zakresów kalibracyjnych były odpowiednio od 6,46 do 2,09% i od 15,80 do 1,01%. Opisana metoda jest udoskonaleniem publikowanych wcześniej procedur analitycznych wykorzystujących technikę chromatografii cieczowej i posiada szereg zalet szczególnie w aspekcie finalnej separacji na drodze HPLC.

12

Simple HPLC method for simultaneous quantification of nicotine and cotinine levels in rat plasma after exposure to two different tobacco products

75%

Alhusban A. A. , Hammad A. M. , Alzaghari L. F.

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tom Vol. 35, no. 1

106--114

EN

Purpose: Development and validation of a selective analytical method to accurately and precisely quantify nicotine and cotinine levels in rat's plasma after exposure to tobacco cigarettes and tobacco water-pipe. Methods: An easy HPLC-Photodiode-Array Detection (PDA) method was developed and validated for simultaneous determination of nicotine and cotinine levels in plasma of 15 rats (10 rats after tobacco products exposure and 5 control rats). Nicotine and cotinine were extracted in one step from plasma using acetonitrile and concentrated to lowest volume using nitrogen stream. Results: The developed method offered a rapid analysis time of 14 min with single step of analytes extraction from rat's plasma with recovery percentage range between 93 and 95% and excellent linearity with correlation factor more than 0.994 with analytical range between 50 and 1000 ng mL⁻¹ and LOD of 25 ng mL⁻¹ and 23 ng mL⁻¹ for nicotine and cotinine, respectively. The analysis of rat's plasma after 28 days of exposure to tobacco cigarettes and tobacco water-pipe revealed that the average concentrations of 376 ng mL⁻¹ for cotinine and 223 ng mL⁻¹ for nicotine were obtained after tobacco cigarettes exposure, and 220 ng mL⁻¹ for cotinine and 192 ng mL⁻¹ for nicotine after tobacco water-pipe exposure. Conclusion: Higher nicotine and cotinine levels were found in plasma after tobacco cigarettes exposure than water-pipe exposure which may have potential undesirable effects on passive smokers in both cases.

13

Oddziaływanie nikotyny z melaniną

75%

Delijewski M. , Buszman E. , Wrześniok D.

Annales Academiae Medicae Silesiensis

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2013

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tom 67

|

nr 6

361-366

EN

BACKGROUND The available literature suggests that nicotine may accumulate in human tissues containing melanin, which increases the biosynthesis of this pigment. Studies conducted on the interaction between nicotine and melanin do not explain the impact of this binding on the metabolism and distribution of nicotine, level of dependence, effectiveness of smoking cessation therapies and potential adverse effects of nicotine. The role of these interactions may be important for people with a high degree of skin pigmentation. It is necessary to answer questions concerning the nature of nicotine–melanin interaction as well as the effect of nicotine on human cells, tissues and organs containing melanin pigment. The aim of this study was to examine the ability of nicotine to bind to synthetic melanin and to evaluate the kinetics and the nature of these interactions. MATERIAL AND METHODS Nicotine–melanin complexes were analyzed by use of the Scatchard method. The amounts of nicotine bound to melanin were determined spectrophotometrically. RESULTS It has been demonstrated that nicotine forms complexes with melanin. The amounts of nicotine bound to melanin increase with rising initial concentrations and prolongation of incubation time. For the studied complexes, two classes of independent binding sites with association constants K1 = 2.44 × 104 M-1 and K2 = 7.72 × 102 M-1 have been found. CONCLUSIONS The obtained results indicate the possible role of melanin in side effects of nicotine and in smoking cessation therapies effectiveness among people with high levels of pigmentation.

PL

WSTĘP Dostępna literatura sugeruje, że nikotyna może kumulować się w ludzkich tkankach zawierających melaninę, co powoduje zwiększenie biosyntezy tego barwnika. Dotychczasowe badania nad oddziaływaniem nikotyny z melaniną nie wyjaśniają wpływu wiązania na metabolizm i dystrybucję nikotyny, poziom uzależnienia, zdolność do zaprzestania palenia czy zwiększenie ewentualnych działań niepożądanych nikotyny. Rola tych oddziaływań może mieć duże znaczenie w przypadku osób o wysokim stopniu pigmentacji skóry. Odpowiedzi wymagają pytania dotyczące charakteru wiązań między nikotyną a melaniną oraz zmian, jakie nikotyna może wywierać w komórkach, tkankach i narządach ludzkiego ciała, w których występuje melanina. Celem badań była ocena zdolności nikotyny do wiązania się z melaniną syntetyczną, a także ocena kinetyki wiązania i trwałości powstałych kompleksów. MATERIAŁ I METODY Kompleksy nikotyna–melanina oceniano metodą Scatcharda. Ilość nikotyny związanej z melaniną wyznaczono techniką spektrofotometrii UV-VIS. WYNIKI Wykazano, że nikotyna tworzy kompleksy z melaniną. Ilość nikotyny związanej z melaniną wzrasta wraz ze wzrostem stężenia początkowego oraz z wydłużaniem czasu inkubacji. Dla badanych kompleksów stwierdzono występowanie dwóch klas niezależnych miejsc wiążących o wartościach stałych trwałości K1 = 2,44 × 104 M-1 oraz K2 = 7,72 × 102 M-1. WNIOSKI Uzyskane wyniki wskazują na możliwą rolę melaniny w działaniach niepożądanych nikotyny oraz w problematyce zaprzestania palenia u osób o wysokim stopniu pigmentacji.

14

Nikotyna - metoda oznaczania

75%

Kucharska M. , Wesołowski W.

Podstawy i Metody Oceny Środowiska Pracy

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2003

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tom Nr 4 (38)

149--155

PL

Metodę stosuje się do oznaczania stężeń par nikotyny w powietrzu na stanowiskach pracy podczas przeprowadzania kontroli warunków sanitarnohigienicznych. Metoda polega na adsorpcji par nikotyny na żywicy XAD-2, wyekstrahowaniu jej octanem etylu i analizie chromatograficznej otrzymanego roztworu. Oznaczalność metody wynosi 0,02 mg/m3.

EN

The method is based on the adsorption of nicotine on XAD-2, desorption with ethyl acetate and gas chromatographic (GC-MSD) analysis of the resulting solution. The determination limit of the method is 0.02 mg/m3.

15

A therapeutic potential of nicotine: reassessing the current paradigm of nicotine pharmacotherapy, literature review.

75%

Delijewski M. , Kośmider L. , Balwierz R. J. , Tomas M. B. , Yi D. , Koszowski B. , Marciniak D. , Karolewicz B.

Acta Poloniae Pharmaceutica - Drug Research

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2018

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tom 75

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nr 5

1053-1061

EN

Introduction: Nicotine is a widely known alkaloid synthesized from tobacco plants, being a main constituent of tobacco smoke and cigarettes. Nicotine has also gained eminence as the therapeutic option in managing smoking cessation and even other health conditions. However, the therapeutic potential of nicotine in other diseases has yet to be completely assessed. This information void stems from an inherent aversion from researchers in assessing nicotine’s risk-benefit, due to its toxicities. We present information on the current body of evidence relating to non-traditional therapeutic applications of nicotine to fill this literature void. The purpose of this work is to present current literature on the therapeutic uses of nicotine in treating various diseases. Methods: Electronic search in PubMed for relevant research relating to the therapeutic potential of nicotine in various diseases. Results/conclusions: Nicotine has gained therapeutic significance as an active compound of the nicotine replacement therapy. Research show nicotine may have other therapeutic applications in some diseases. We discussed application of nicotine in diminished prevalence of Parkinson’s disease, decreasing symptoms of the Tourette’s syndrome, psychiatric diseases like chizophrenia, depression and management of pain. We also reviewed nicotine dosing, type of formulations, and compliance which are crucial factors in the therapeutic applications of nicotine.

16

Green tobacco sickness – A brief review

75%

Reddy M. N. T. , Ashok N.

|

tom 24

209-214

EN

Green Tobacco Sickness (GTS) has been one of the unexplored areas of occupational health safety. Green Tobacco Sickness is caused by the absorption of nicotine through the skin from wet tobacco plants who have direct contact with tobacco plants during cultivation and harvesting. The present review was carried out to discuss the etiology, symptoms, diagnosis, treatment and prevention of GTS. It is caused by the absorption of nicotine through the skin while the workers are engaged in handling the uncured tobacco leaves. The symptoms include nausea, vomiting, pallor, dizziness, headaches, increased perspiration, chills, abdominal pain, diarrhea, increased salivation, prostration, weakness, breathlessness, and occasional lowering of blood pressure. The use of personal protective equipment like water‑resistant clothing, chemical‑resistant gloves, plastic aprons, and rain‑suits with boots should be used by the tobacco farmers to prevent its occurrence. An international‑level awareness campaign has to be taken up and more stringent workers safety regulations have to be formulated.

17

Simple HPLC method for rapid quantification of nicotine content in e-cigarettes liquids

75%

Alhusban A. A. , Ata S. A.

Acta Chromatographica

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2021

|

tom Vol. 33, no. 3

302--307

EN

Electronic nicotine delivery systems (ENDs) are gaining popularity in Jordan as alternatives to tobacco cigarettes with an estimation of 10% of tobacco smokers switching to ENDs. Since nicotine is toxic and highly addictive substance, it is important to develop and validate an easy and rapid analytical method to accurately measure nicotine level in e-liquids. A simple high performance liquid chromatography–photodiode array detection (HPLC–PDA) method was developed and validated for rapid determination of the actual nicotine content in 11 of the most popular e-liquids brands available in the Jordanian market and compared to the nicotine levels appeared in the labeled packaging. The new method of analysis showed an excellent linearity with correlation factor equal to 0.9994 with analytical range between 100 and 1,000 µg/mL, and Limit of detection (LOD) and Limit of quantification (LOQ) of 32.6 µg/mL and 98.9 µg/mL, respectively. The results showed that the actual measured nicotine concentrations ranged from 0 to 25.81 mg/mL with percent deviation ranged from 63.1% less than to 3.24% more than the labeled concentration on packaging. And more than 10% deviation difference in actual nicotine concentrations versus labeled were found in 9 of the 11 e-liquid products (82%). In conclusion, nicotine labelling among e-liquids products have not accurately reflect the actual content which may have potential negative impact on users.

18

Effect of adrenergic antagonists and cyclooxygenase inhibitors on the nicotine-induced hypothalamic-pituitary-adrenocortical activity

75%

Gadek-Michalska A. , Bugajski J. , Bugajski A. J. , Glod R.

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nr 2

EN

Nicotine is a potent stimulus for the hypothalamic-pituitary-adrenal (HPA) axis. Systemic nicotine acts via central mechanisms to stimulate by multiple pathways the release of ACTH from the anterior pituitary corticotrops and corticosterone from the adrenal cortex. Nicotine may stimulate indirectly the hypothalamic paraventricular nucleus, the site of the corticotropin-releasing hormone (CRH) neurons which activates ACTH release. In the present studies an involvement of adrenergic system and prostaglandins synthesized by constitutive cyclooxygenase (COX-1) and inducible cyclooxygenase (COX-2) in the nicotine-induced HPA response in rats was investigated. Nicotine (2.5-5 mg/kg i.p.) significantly increased plasma ACTH and corticosterone levels measured 1 hr after administration. Adrenergic receptor antagonists or COX inhibitors were injected i.p. 15 min prior to nicotine and the rats were decapitated 1 hr after the last injection. Prazosin (0.01-0.1 mg/kg), an alpha1-adrenergic antagonist, significantly decreased the nicotine-evoked ACTH and corticosterone secretion. Yohimbine (0.1-1.0 mg/kg), an alpha2-adrenergic antagonist, moderately diminished ACTH response, and propranolol (0.1-10 mg/kg), a ß-adrenergic antagonist, did not significantly alter the nicotine-induced hormones secretion. Pretreatment with piroxicam (0.2-2.0 mg/kg), a COX-1 inhibitor, considerably impaired the nicotine-induced ACTH and corticosterone secretion. Compound NS-398 (0.2-5.0 mg/kg), a selective COX-2 blocker did not markedly alter these hormones secretion, and indomethacin (2 mg/kg), a non-selective COX inhibitor significantly diminished ACTH response. These results indicate that systemic nicotine stimulates the HPA axis indirectly, and both adrenergic system and prostaglandins are significantly involved in this stimulation. Noradrenaline, stimulating postsynaptic aplha1-adrenergic receptors, and prostaglandins, synthesized by COX-1 isoenzyme, are of crucial significance in the nicotine-induced ACTH and corticosterone secretion.

19

Differential effects of nicotine on the activity of substantia nigra and ventral tegmental area dopaminergic neurons in vitro

75%

Teo M. Y. , Van Wyk M. , Lin J. , Lipski J.

|

2004

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tom 64

|

nr 2

20

Average quantitative concentration of cotinine within the system pregnant woman-baby

75%

Dobek D. , Karmowski A. , Sobiech K. A. , Terpilowski L. , Mis-Michalek M.

|

tom 46

|

nr 1