Nicotine Metabolites and Chemistry

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1. The Papers
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The Papers (28)

Newest first. Study types on this page — Human trial: 1 · Human observational study: 7 · Review: 7 · Animal study: 5 · Cell study: 1 · Chemistry / laboratory method: 6 · Other: 1. Each summary is written from the paper’s own abstract; follow the PubMed link for the full record.

The Distinct Biological Effects of 6-Hydroxy-L-Nicotine in Representative Cancer Cell Lines

Cell study, 2024. Researchers tested 6-hydroxy-L-nicotine, a compound made from nicotine, on three kinds of cancer cells grown in the lab (lung, breast and brain-tumour cells) and on two kinds of normal lung and breast cells. Computer modelling suggested the compound may bind to nicotinic receptors, the same receptor family nicotine acts on. In the lab dishes it made the brain-tumour (glioblastoma) cells grow more, held back the breast cancer cells, and had no effect on the lung cancer cells. The normal cells stayed alive at the same rate, but all of these results come from cells in dishes and computer models, not from animals or people.

Postu PA, Boiangiu RS, Mihasan M et al. (2024). The Distinct Biological Effects of 6-Hydroxy-L-Nicotine in Representative Cancer Cell Lines. Molecules. — PubMed PMID: 39683752 · doi:10.3390/molecules29235593

Analyses of nicotine metabolism biomarker genetics stratified by sex in African and European Americans

Human observational study, 2021. This genetic study looked at how fast people who smoke break down nicotine. The body converts nicotine to cotinine and then to 3'hydroxycotinine using an enzyme called CYP2A6, and the ratio of these two breakdown products is an inherited marker of nicotine metabolism. Researchers scanned the genomes of European American women (389) and men (541) and African American women (503) and men (352) who smoke, analyzing each sex separately. In every group the strongest genetic signal sat in or near the CYP2A6 gene on chromosome 19, explaining about 16% to 26% of the variation, though the top variant differed between African American women and men. Other regions found only in African American women (chromosome 12) or men (chromosomes 6 and 16) did not replicate and need more study.

Chenoweth MJ, Cox LS, Nollen NL et al. (2021). Analyses of nicotine metabolism biomarker genetics stratified by sex in African and European Americans. Sci Rep. — PubMed PMID: 34599228 · doi:10.1038/s41598-021-98883-z

Differential effects of alkaloids on memory in rodents

Animal study, 2021. This study tested three natural compounds that act on nicotinic receptors in the brain (nicotine, its breakdown product cotinine, and a related tobacco compound, anatabine) to see whether they could block memory problems caused by the drug scopolamine in mice and rats. All three compounds reduced the drug-induced loss of spatial memory in a maze test in mice. Only nicotine reduced the loss of short-term memory for objects in rats, even though the other two compounds were given at higher doses. These results are only in rodents, and the authors conclude that these compounds may help different kinds of memory in different ways.

Callahan PM, Terry AV, Peitsch MC et al. (2021). Differential effects of alkaloids on memory in rodents. Sci Rep. — PubMed PMID: 33972592 · doi:10.1038/s41598-021-89245-w

Impact of E-Cigarette Liquid Flavoring Agents on Activity of Microsomal Recombinant CYP2A6, the Primary Nicotine-Metabolizing Enzyme

Chemistry / laboratory method, 2020. This lab study tested whether flavored e-cigarette liquids slow down CYP2A6, the liver enzyme that breaks down about 80% of the nicotine in the body. The work used the purified enzyme in test tubes, not people or animals. Two of the three flavored liquids tested reduced the enzyme's activity, and more liquid reduced it more. Two flavoring chemicals, cinnamaldehyde (a cinnamon flavor) and benzaldehyde (an almond or cherry flavor), were the strongest blockers, with half-blocking concentrations of 1.1 μM and 3.0 μM. The authors say this could slow nicotine breakdown in the body, but that still needs to be studied in living people.

Winters BR, Kochar TK, Clapp PW et al. (2020). Impact of E-Cigarette Liquid Flavoring Agents on Activity of Microsomal Recombinant CYP2A6, the Primary Nicotine-Metabolizing Enzyme. Chem Res Toxicol. — PubMed PMID: 32496054 · doi:10.1021/acs.chemrestox.9b00514

The Novel CYP2A6 Inhibitor, DLCI-1, Decreases Nicotine Self-Administration in Mice

Animal study, 2020. This study in male and female mice tested a new experimental compound, DLCI-1, that blocks CYP2A6, the main liver enzyme that breaks down nicotine. Mice trained to give themselves nicotine through a vein took significantly less nicotine after the lower 25 mg/kg and moderate 50 mg/kg doses of DLCI-1. DLCI-1 cut nicotine intake more than a moderate 1 mg/kg dose of bupropion did, and it did not cause the side effects on behavior seen with a high 75 mg/kg dose of bupropion. DLCI-1 did not change how much food the mice worked for, and the authors suggest it could one day help people quit tobacco and nicotine products, but these results so far come only from mice.

Chen YC, Fowler JP, Wang J et al. (2020). The Novel CYP2A6 Inhibitor, DLCI-1, Decreases Nicotine Self-Administration in Mice. J Pharmacol Exp Ther. — PubMed PMID: 31628204 · doi:10.1124/jpet.119.260653

Evaluating metronidazole as a novel, safe CYP2A6 phenotyping probe in healthy adults

Human trial, 2019. This randomized crossover study in 16 healthy non-smoking adults tested whether the antibiotic metronidazole could replace nicotine as a safe test of CYP2A6, the liver enzyme that breaks down nicotine. Each person took a single 500 mg dose of metronidazole and, at least 2 weeks apart, one 2 mg piece of nicotine gum. The researchers then compared the blood ratios of each drug's breakdown products, including the ratio of two nicotine metabolites (trans-3-hydroxycotinine to cotinine). The two ratios matched closely (correlation of 0.9 or higher at several time points), and people whose genes predicted lower enzyme activity had ratios of 58% or less with metronidazole and 56% or less with nicotine, compared with people predicted to have full activity. No side effects were reported after metronidazole, while 38% of participants (6 people) reported mild side effects after the nicotine gum.

Stancil SL, Pearce RE, Tyndale RF et al. (2019). Evaluating metronidazole as a novel, safe CYP2A6 phenotyping probe in healthy adults. Br J Clin Pharmacol. — PubMed PMID: 30706508 · doi:10.1111/bcp.13884

Nicotine-N'-Oxidation by Flavin Monooxygenase Enzymes

Human observational study, 2019. The body breaks down nicotine mainly with a liver enzyme called CYP2A6, but a second family of enzymes, called FMOs, can also turn nicotine into a breakdown product called nicotine-N'-oxide. Researchers measured nicotine breakdown products in the urine of 106 current smokers in China. Smokers with lower CYP2A6 activity had more nicotine-N'-oxide in their urine. In lab-grown human cells, the researchers also found that FMO1, FMO3 and one working form of FMO2 could process nicotine, while FMO4 and FMO5 did very little, and several common genetic variants of these enzymes were less active or, in one case, not active at all.

Perez-Paramo YX, Chen G, Ashmore JH et al. (2019). Nicotine-N'-Oxidation by Flavin Monooxygenase Enzymes. Cancer Epidemiol Biomarkers Prev. — PubMed PMID: 30381441 · doi:10.1158/1055-9965.EPI-18-0669

Use of polygenic risk scores of nicotine metabolism in predicting smoking behaviors

Human observational study, 2018. Researchers tested whether genetic risk scores, built from large earlier studies of the genes linked to how fast the body breaks down nicotine, could predict nicotine metabolism and smoking habits in a separate group of people. The scores predicted blood markers of nicotine metabolism, explaining about 9.2% to 16% of the differences between people, and a single top gene variant explained about 14% to 17%. There was not enough evidence that the scores predicted how much people smoked or whether they quit. The authors say more research is needed to build a fuller genetic score for predicting smoking behaviors.

Chen LS, Hartz SM, Baker TB et al. (2018). Use of polygenic risk scores of nicotine metabolism in predicting smoking behaviors. Pharmacogenomics. — PubMed PMID: 30442082 · doi:10.2217/pgs-2018-0081

Slower nicotine metabolism among postmenopausal Polish smokers

Human observational study, 2018. Researchers studied 180 adults in Poland who smoked cigarettes daily (42% men, average age 34.6). They measured two nicotine breakdown products in urine to estimate how fast each person clears nicotine from the body. Women younger than 51 broke down nicotine faster than everyone else (an average ratio of 6.4 compared with 4.3), and there was no difference between age groups among men. The authors link this to estrogen, which is known to speed up the liver enzyme that breaks down nicotine, and suggest that younger women trying to quit may need higher doses of nicotine replacement or medicines that contain no nicotine.

Kosmider L, Delijewski M, Koszowski B et al. (2018). Slower nicotine metabolism among postmenopausal Polish smokers. Pharmacol Rep. — PubMed PMID: 29627689 · doi:10.1016/j.pharep.2017.11.009

Interaction between cytochrome P450 2A6 and Catechol-O-Methyltransferase genes and their association with smoking risk in young men

Human observational study, 2017. Researchers studied 500 young men in Taiwan. They looked at variants in two genes: one makes the main liver enzyme that breaks down nicotine (CYP2A6), and the other makes an enzyme that breaks down dopamine (COMT). They also measured nicotine and its breakdown product, cotinine, in urine and asked the men about their smoking. Men who carried both a slow version of the nicotine-breakdown gene and a particular COMT variant had lower odds of having started smoking (odds ratio 0.44). Nicotine dependence and withdrawal scores did not differ between gene groups, and neither did urine nicotine, but urine cotinine was higher in men with the COMT rs4680 variant (median 118.24 vs. 92.46 ng/μL).

Ou WC, Huang YC, Huang CL et al. (2017). Interaction between cytochrome P450 2A6 and Catechol-O-Methyltransferase genes and their association with smoking risk in young men. Behav Brain Funct. — PubMed PMID: 28472995 · doi:10.1186/s12993-017-0127-2

CYP2A6 Genetic Variation Alters Striatal-Cingulate Circuits, Network Hubs, and Executive Processing in Smokers

Human observational study, 2017. Researchers used brain scans to study how variation in the CYP2A6 gene affects the brain in 66 smokers and 92 nonsmokers. This gene controls how fast the body breaks down nicotine. Among smokers, people with the normal-speed version of the gene had stronger connections in two brain areas involved in reward and self-control than people with the slow version. No such difference appeared in nonsmokers. In a smaller group of 23 smokers and 20 nonsmokers who did reward and self-control tasks with and without a nicotine patch, smokers' reduced brain activity during abstinence returned toward normal after nicotine. In nonsmokers, the same brain activity went up after nicotine. The authors conclude that how fast a person breaks down nicotine, and so how much nicotine reaches the brain over years of addiction, shapes brain circuits for reward and impulsivity.

Li S, Yang Y, Hoffmann E et al. (2017). CYP2A6 Genetic Variation Alters Striatal-Cingulate Circuits, Network Hubs, and Executive Processing in Smokers. Biol Psychiatry. — PubMed PMID: 27865452 · doi:10.1016/j.biopsych.2016.09.013

Effects of nicotine and minor tobacco alkaloids on intracranial-self-stimulation in rats

Animal study, 2015. This rat study compared nicotine with several other natural chemicals found in tobacco (nornicotine, anabasine, myosmine, anatabine and cotinine, a breakdown product of nicotine). It used brain self-stimulation, a lab test of how strongly a drug acts on the brain's reward system and so of its addiction potential. At low to moderate doses nicotine boosted the reward response, and at high doses it dampened it or acted as something unpleasant; nornicotine and anabasine had the same two-sided effect but were weaker than nicotine, myosmine had an effect only at fairly high doses, and anatabine and cotinine had no effect at any dose tested. The authors say some of these minor tobacco chemicals can partly or fully copy nicotine's addiction-related effects, and that these results come only from rats and need more study.

Harris AC, Tally L, Muelken P et al. (2015). Effects of nicotine and minor tobacco alkaloids on intracranial-self-stimulation in rats. Drug Alcohol Depend. — PubMed PMID: 26094184 · doi:10.1016/j.drugalcdep.2015.06.005

Nicotine metabolite ratio (3-hydroxycotinine/cotinine) in plasma and urine by different analytical methods and laboratories: implications for clinical implementation

Chemistry / laboratory method, 2015. The body breaks nicotine down into cotinine, and then cotinine into 3-hydroxycotinine, mainly through a liver enzyme called CYP2A6. The ratio between these two breakdown products, called the nicotine metabolite ratio, shows how fast a person clears nicotine. Researchers sent blood samples (35) and urine samples (35) from people who smoke to eight different laboratories, which measured the ratio using similar and different methods. Blood results agreed closely across laboratories and were highly correlated (correlations above 0.96), while urine results agreed less well (correlations of 0.66 to 0.98). The authors concluded that blood is a very reliable sample for measuring this ratio, whichever laboratory or method is used.

Tanner JA, Novalen M, Jatlow P et al. (2015). Nicotine metabolite ratio (3-hydroxycotinine/cotinine) in plasma and urine by different analytical methods and laboratories: implications for clinical implementation. Cancer Epidemiol Biomarkers Prev. — PubMed PMID: 26014804 · doi:10.1158/1055-9965.EPI-14-1381

Pharmacogenetics of nicotine and associated smoking behaviors

Review, 2015. This review chapter looks at how differences in people's genes change the way their bodies break down nicotine and how nicotine acts on the brain, and how that affects smoking behavior. Nicotine is broken down by several liver enzymes, especially one called CYP2A6, and gene variants that make nicotine break down faster are linked to smoking more cigarettes, stronger nicotine dependence and lower quit rates. Nicotine works by attaching to nicotinic acetylcholine receptors in the brain, which release chemical messengers such as dopamine and serotonin, and gene differences in these receptors and related systems are also tied to different smoking patterns. The authors say the exact mechanisms behind many of these findings are still unknown, and that studying many genes together with environmental factors may lead to more personalized ways to help people quit smoking.

Tanner JA, Chenoweth MJ, Tyndale RF (2015). Pharmacogenetics of nicotine and associated smoking behaviors. Curr Top Behav Neurosci. — PubMed PMID: 25655887 · doi:10.1007/978-3-319-13665-3_3

Differential effects of non-nicotine tobacco constituent compounds on nicotine self-administration in rats

Animal study, 2014. This study used young adult female rats that had learned to give themselves nicotine. Researchers tested whether seven other compounds found in tobacco changed how much nicotine the rats took. The seven were anabasine, anatabine, nornicotine, myosmine, harmane, norharmane and tyramine. A low dose of anabasine (0.02 mg/kg) increased nicotine self-administration by 25%. A high dose of anabasine (2.0 mg/kg) cut nicotine intake by over 50%, and anatabine at 2.0 mg/kg cut it by nearly half. These results come from rats only. The authors suggest that some of these compounds could make nicotine more or less rewarding, and that some might be studied as possible aids for quitting smoking.

Hall BJ, Wells C, Allenby C et al. (2014). Differential effects of non-nicotine tobacco constituent compounds on nicotine self-administration in rats. Pharmacol Biochem Behav. — PubMed PMID: 24560911 · doi:10.1016/j.pbb.2014.02.011

Anatabine significantly decreases nicotine self-administration

Animal study, 2014. This study tested whether anatabine, a minor natural chemical found in tobacco, changes how much nicotine 7 rhesus monkeys chose to give themselves. Anatabine injections lowered nicotine self-administration in a dose-dependent way, and only the highest dose also reduced how hard the monkeys worked for food. The monkeys did not self-administer anatabine itself more than saline, which suggests it has little abuse potential. The results are only in monkeys, and the authors suggest anatabine could be studied as a possible treatment for nicotine addiction.

Mello NK, Fivel PA, Kohut SJ et al. (2014). Anatabine significantly decreases nicotine self-administration. Exp Clin Psychopharmacol. — PubMed PMID: 24490707 · doi:10.1037/a0035409

Molecular genetics of alkaloid biosynthesis in Nicotiana tabacum

Review, 2013. This review covers how the tobacco plant makes nicotine and related compounds called alkaloids, focusing on the genes and enzymes involved. Nicotine makes up about 90% of the alkaloids in a typical commercial tobacco plant, and most of the rest is nornicotine, anatabine and anabasine. Scientists have identified most of the genes that build nicotine and nornicotine, as well as some genes that control how nicotine is produced and moved around in the plant, but parts of the anatabine and anabasine pathways are still unknown. The authors say this knowledge can be used to change how much nicotine the leaf contains, or to lower the level of a potent cancer-causing nitrosamine that forms in tobacco.

Dewey RE, Xie J (2013). Molecular genetics of alkaloid biosynthesis in Nicotiana tabacum. Phytochemistry. — PubMed PMID: 23953973 · doi:10.1016/j.phytochem.2013.06.002

CYP2A6- and CYP2A13-catalyzed metabolism of the nicotine Δ5'(1')iminium ion

Chemistry / laboratory method, 2012. This laboratory study used purified enzymes, not people or animals, to look at how the body breaks down nicotine. Nicotine is mainly processed by a liver enzyme called CYP2A6, and a closely related enzyme, CYP2A13, works outside the liver. The researchers found that one of nicotine's breakdown products, the nicotine iminium ion, permanently switches off both enzymes. They also confirmed that both enzymes turn this breakdown product into cotinine, and that some of that cotinine may be processed further into 3'-hydroxycotinine before the enzyme releases it.

von Weymarn LB, Retzlaff C, Murphy SE (2012). CYP2A6- and CYP2A13-catalyzed metabolism of the nicotine Δ5'(1')iminium ion. J Pharmacol Exp Ther. — PubMed PMID: 22869927 · doi:10.1124/jpet.112.195255

Biomarkers to optimize the treatment of nicotine dependence

Review, 2011. This review looks at whether biological markers, mainly genetic differences between people, could help doctors choose the best treatment for nicotine dependence. It covers the brain biology of nicotine dependence, the evidence that it is partly inherited, and studies of genes that affect how the body processes nicotine and how people respond to treatment. The authors report that two kinds of markers look promising for guiding treatment choice: how quickly a person breaks down nicotine (measured as the nicotine metabolite ratio) and differences in dopamine-related genes. They also discuss what still stands in the way of using this research in everyday care, and where future research should go.

Schnoll RA, Leone FT (2011). Biomarkers to optimize the treatment of nicotine dependence. Biomark Med. — PubMed PMID: 22103610 · doi:10.2217/bmm.11.91

Simultaneous quantification of nicotine and metabolites in rat brain by liquid chromatography-tandem mass spectrometry

Chemistry / laboratory method, 2011. Researchers developed and checked a laboratory test that can measure nicotine and ten related compounds, including cotinine and nornicotine (substances the body makes as it breaks nicotine down), in rat brain tissue at the same time. They tried the test on rats that got a single 0.8 mg/kg injection of nicotine under the skin and were killed 2 hours later. In the striatum, a brain region, nicotine measured about 204.8 pg/mg, cotinine 138.2 pg/mg and nornicotine 36.1 pg/mg, with similar levels in the rest of the brain. In the blood the pattern was different: cotinine was much higher than nicotine (194.6 versus 52.7 ng/mL), and the authors conclude the test is sensitive and selective enough to measure nicotine markers in rat brain.

Vieira-Brock PL, Miller EI, Nielsen SM et al. (2011). Simultaneous quantification of nicotine and metabolites in rat brain by liquid chromatography-tandem mass spectrometry. J Chromatogr B Analyt Technol Biomed Life Sci. — PubMed PMID: 21963483 · doi:10.1016/j.jchromb.2011.09.026

Molecular genetics of nicotine metabolism

Review, 2009. This book chapter reviews how inherited differences in the body's enzymes change the way people break down nicotine, drawing on human research and briefly on studies in monkeys, mice and rats. Twin studies show that much of the large person-to-person and between-ethnic-group difference in nicotine breakdown is genetic, though environment also plays a part. The main enzyme that breaks down nicotine, CYP2A6, comes in several common genetic variants that strongly affect how fast nicotine is cleared. People who break down nicotine more slowly need to take it in less often, which affects their smoking behavior.

Mwenifumbo JC, Tyndale RF (2009). Molecular genetics of nicotine metabolism. Handb Exp Pharmacol. — PubMed PMID: 19184652 · doi:10.1007/978-3-540-69248-5_9

Nicotine chemistry, metabolism, kinetics and biomarkers

Review, 2009. This review looks at how nicotine is absorbed, spread through the body and cleared, both from tobacco and from medicinal nicotine products used to help people quit smoking. Nicotine is broken down mainly in the liver by the enzymes CYP2A6, UGT and FMO, and how fast this happens depends on genes, diet and meals, age, sex, estrogen-containing hormone products, pregnancy, kidney disease, other medicines and smoking itself, with large differences between racial and ethnic groups. Cotinine, a breakdown product of nicotine, is the most widely used marker of nicotine intake and can be measured in blood, urine, saliva, hair or nails. The authors report that the best blood cotinine cut-off to tell smokers from non-smokers in the general US population is now 3 ng/ml, much lower than the cut-off set 20 years earlier, which they link to less secondhand smoke exposure and more light or occasional smoking.

Benowitz NL, Hukkanen J, Jacob P (2009). Nicotine chemistry, metabolism, kinetics and biomarkers. Handb Exp Pharmacol. — PubMed PMID: 19184645 · doi:10.1007/978-3-540-69248-5_2

A novel duplication type of CYP2A6 gene in African-American population

Human observational study, 2007. Researchers looked at CYP2A6, the gene for the liver enzyme that breaks down nicotine, and found a new kind of extra copy (duplication) of this gene. The extra copy turned up in African Americans (176 people tested) at an allele frequency of 1.7%, and was not found in the European-American (187), Korean (209) or Japanese (184) people tested. In blood, the cotinine-to-nicotine ratio (a measure of how fast nicotine is broken down) was 10.8 in the 4 people carrying the extra copy, compared with 8.0 in 87 people with the usual gene, about 1.4 times higher, but this difference was not statistically significant. The authors suggest this gene variant may speed up nicotine breakdown and may affect smoking behavior.

Fukami T, Nakajima M, Yamanaka H et al. (2007). A novel duplication type of CYP2A6 gene in African-American population. Drug Metab Dispos. — PubMed PMID: 17267622 · doi:10.1124/dmd.106.013557

Prediction methods for nicotine clearance using cotinine and 3-hydroxy-cotinine spot saliva samples II. Model application

Other, 2007. This was a computer simulation study, not a study of real patients. Using a model of how the body breaks down nicotine, the researchers simulated saliva levels of two nicotine breakdown products, cotinine and 3-hydroxy-cotinine, in smokers. They then compared four ways of using a single saliva sample to estimate how fast a person clears nicotine, which reflects the activity of the liver enzyme CYP2A6. A simple method based on the natural logarithm of the ratio of the two breakdown products did better than using the plain ratio. It had a bias of about -10%, a precision of about 60%, and 43% of its estimates fell within 25% of the true value. Smoking pattern did not change the breakdown-product levels, and the authors say the results support using this method in smokers in the clinical setting.

Levi M, Dempsey DA, Benowitz NL et al. (2007). Prediction methods for nicotine clearance using cotinine and 3-hydroxy-cotinine spot saliva samples II. Model application. J Pharmacokinet Pharmacodyn. — PubMed PMID: 17206525 · doi:10.1007/s10928-006-9026-0

Metabolism and disposition kinetics of nicotine

Review, 2005. This review covers what is known about how the body absorbs, distributes, breaks down and gets rid of nicotine, along with some related tobacco alkaloids and nicotine-like compounds being developed as medicines. It mainly covers studies in people, and brings in animal data where it helps explain the human findings. It describes the enzymes that break down nicotine, with a special focus on the liver enzyme CYP2A6, which does most of the work of clearing nicotine. It also looks at what changes how fast nicotine is broken down, including genetic differences, diet, age, sex, pregnancy, liver and kidney disease, racial and ethnic background, smoking, and medicines such as oral contraceptives.

Hukkanen J, Jacob P, Benowitz NL (2005). Metabolism and disposition kinetics of nicotine. Pharmacol Rev. — PubMed PMID: 15734728 · doi:10.1124/pr.57.1.3

CYP2A6 genetic variation and potential consequences

Review, 2002. This review looks at CYP2A6, a liver enzyme that breaks down nicotine and its main breakdown product, cotinine, and also processes several cancer-causing chemicals in tobacco, coumarin and many toxins. The authors describe 13 known genetic variants of the gene. Some variants make the enzyme inactive, some lower its activity, and gene duplications raise it, so people differ widely in how fast they process nicotine. These variants are more or less common in different ethnic groups, which may partly explain group differences in nicotine metabolism, smoking behavior and lung cancer. The authors note that research on these variants and their health effects was still at a fairly early stage.

Xu C, Goodz S, Sellers EM et al. (2002). CYP2A6 genetic variation and potential consequences. Adv Drug Deliv Rev. — PubMed PMID: 12406643 · doi:10.1016/s0169-409x(02)00065-0

Optimization study for the reversed-phase ion-pair liquid chromatographic determination of nicotine in commercial tobacco products

Chemistry / laboratory method, 1999. This laboratory study looked at how to measure nicotine accurately in commercial tobacco products using a technique called liquid chromatography, which separates the chemicals in a sample. The researchers studied how nicotine and several related tobacco alkaloids (anatabine, nornicotine, anabasine and cotinine) behave in this test, noting that nicotine is a base with two acid-base values of 3.12 and 8.02. They used what they learned about each chemical's size, structure and acid-base strength to explain the order in which the chemicals come out of the test, and to choose the best test conditions for measuring nicotine. No people or animals were involved; this was a chemistry method study.

Ciolino LA, Turner JA, McCauley HA et al. (1999). Optimization study for the reversed-phase ion-pair liquid chromatographic determination of nicotine in commercial tobacco products. J Chromatogr A. — PubMed PMID: 10481983 · doi:10.1016/s0021-9673(99)00639-1

Increasing urinary cotinine concentrations at elevated temperatures: the role of conjugated metabolites

Chemistry / laboratory method, 1997. This laboratory study tested whether cotinine, a breakdown product of nicotine that urine tests use to tell smokers from nonsmokers, stays stable in stored urine. Urine samples from smokers were kept at temperatures from 5 to 60 degrees C for 30 days. At higher temperatures, the amount of free cotinine went up, nearly doubling at 60 degrees C (from 1301 to 2476 ng/ml), and the evidence pointed to a bound form, cotinine-N-glucuronide, breaking back down into free cotinine. The authors warn that if urine is not kept cool during handling and shipping, a sample just below the cutoff could wrongly test positive for smoking.

Hagan RL, Ramos JM, Jacob PM (1997). Increasing urinary cotinine concentrations at elevated temperatures: the role of conjugated metabolites. J Pharm Biomed Anal. — PubMed PMID: 9408833 · doi:10.1016/s0731-7085(97)00021-6

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1. PubMed: Metabolites and Chemistry and nicotine (the search this page is built from)

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Connections

• Nicotine: The Research
• The Nicotine Patch, animated
• Nicotinic Acetylcholine Receptors
• Cigarette Smoke — what burnt tobacco adds that nicotine alone does not
• Brain and Memory
• Mood and Mental Health
• Inflammation and Immunity
• Cancer Research
• Heart and Blood Vessels
• Metabolism and Weight
• Addiction and Withdrawal
• Patches, Gum and Delivery

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