Nicotine: Potentially a Multifunctional Carcinogen?

Campain, Julie A.

doi:10.1093/toxsci/kfh106

Cited by 50 publications

(29 citation statements)

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“…Nicotine is not a direct cause of most tobacco-related diseases, but it is highly addictive (Djordjevic et al, 1989;Benowitz, 1992;Shihadeh & Saleh, 2005). The addictiveness of nicotine is the cause of the continuing use of tobacco products, which in turn results in exposure to the diverse array of carcinogens and other bioactive compounds in tobacco (Brown et al, 2001;Campain, 2004). Nicotine is an amine composed of pyridine and pyrrolidine rings (Trushin & Hecht, 1999).…”

Section: Introductionmentioning

confidence: 99%

Effects of Oral Nicotine on Rat Liver Stereology

2008

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SUMMARY:Nicotine is the more abundant component in cigarette smoke. Because nicotine is first metabolized in the liver, our aim was to investigate the effects of nicotine on this organ by biochemical and stereological methods. Male Wistar rats were treated with oral nicotine (ON) diluted in drinking water during 32 days. The control group was treated with drinking water in the same period. Rats were sacrificed 24 hours after last day, the blood was collected and the liver was removed. Lipidogram was performed by enzymatic method and collagen fibers, fat globules and hepatocytes were count in the liver by stereological methods. We observed in control group preserved hepatocytes, with no presence of inflammatory cells. However in the ON group was possible to observe varied size of hepatocytes with cloudy cellular limits and histoarchitecture loss. Capillaries were fully of red blood cells. We observed also an increase of fat globules with small size. We observed in leucogram a reduction of leukocytes number (lymphocytes, neutrophils and monocytes) in the ON group in comparison to control group. The lipidogram showed an increase of triglycerides and total cholesterol for ON group when compared to control group. Moreover, a reduction of HDL-cholesterol was observed in ON group when compared to control group. Numerical density of hepatocytes was lesser in ON group when compared to control group. We suggest harmful effects of oral nicotine in liver induced by toxic mechanism with reduction of hepatocytes number and disturbance in lipid metabolism.

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Section: Introductionmentioning

confidence: 99%

Effects of Oral Nicotine on Rat Liver Stereology

2008

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“…Nicotine, a major toxic component of tobacco, can cross biological membranes and the blood-brain barrier easily (3,9,16). During cigarette manufacturing, large quantities of tobacco waste with high concentrations of nicotine are produced, and the disposal of these wastes is a serious ecological problem (4,14).…”

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confidence: 99%

Novel Nicotine Oxidoreductase-Encoding Gene Involved in Nicotine Degradation by Pseudomonas putida Strain S16

Tang

Wang

Meng

et al. 2009

Appl Environ Microbiol

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There are quite a few ongoing biochemical investigations of nicotine degradation in different organisms. In this work, we identified and sequenced a gene (designated nicA) involved in nicotine degradation by Pseudomonas putida strain S16. The gene product, NicA, was heterologously expressed and characterized as a nicotine oxidoreductase catalyzing the initial steps of nicotine metabolism. Biochemical analyses using resting cells and the purified enzyme suggested that nicA encodes an oxidoreductase, which converts nicotine to 3-succinoylpyridine through pseudooxynicotine. Based on enzymatic reactions and direct evidence obtained using H 2 18 O labeling, the process may consist of enzyme-catalyzed dehydrogenation, followed by spontaneous hydrolysis and then repetition of the dehydrogenation and hydrolysis steps. Sequence comparisons revealed that the gene showed 40% similarity to genes encoding NADH dehydrogenase subunit I and cytochrome c oxidase subunit I in eukaryotes. Our findings demonstrate that the molecular mechanism for nicotine degradation in strain S16 involves the pyrrolidine pathway and is similar to the mechanism in mammals, in which pseudooxynicotine, the direct precursor of a potent tobacco-specific lung carcinogen, is produced.

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“…Nikotin adalah bahan alkaloid terbanyak yang dikesan dalam tembakau dan asap rokok serta merupakan bahan yang menyebabkan ketagihan melampau pada perokok (Campain 2004). Ia boleh meresap ke dalam tubuh melalui kulit dan saluran respiratori dan dioksidakan dengan cepat di hepar kepada metabolit utamanya iaitu kotinin (Tundulawessa et al 2010).…”

Section: Pengenalanunclassified