Tobacco alkaloids

Nicotine is a stimulant and potent parasympathomimetic alkaloid that accounts for 96–98% of alkaloid content. A reduction in the amount of nicotine in cigarettes to achieve a non-addictive level is necessary.

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Consensus of opinion in literature regarding tobacco research has shown that cigarette smoke can cause irreparable damage to the genetic material, cell injury, and general respiratory landscape.

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Nicotine catabolism, linked inArthrobacter nicotinovorans to the presence of the megaplasmid pAO1, leads to the for-mation ofc-N-methylaminobutyrate from the pyrrolidine ring of the alkaloid. Until now the metabolic fate of c-N-methylaminobutyrate has beenunknown. pAO1 carries a cluster of ORFs with similarity to sarcosine and dimeth-ylglycine dehydrogenases and oxidases, to the bifunctional enzyme methylenetetrahydrofolate dehydrogenase/cyclo-hydrolase and to formyltetrahydrofolate deformylase.

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New enzymes of nicotine catabolism instrumental in the detoxification of the tobacco alkaloid by Arthrobacter nicotinovoranspAO1 have been iden-tified and characterized. Nicotine breakdown leads to the formation of nicotine blue from the hydroxylated pyridine ring and of c-N-methyl-aminobutyrate (CH3-4-aminobutyrate) from the pyrrolidine ring of the molecule.

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Acetylcholine is a widespread chemotransmitter in the body, mediating a broad range of physiological effects.There are two distinct classes of receptor for acetylcholine defined on the basis of their preferential activation by the alkaloids, nicotine (from tobacco) and muscarine (from a fungus, Amanita muscaria). Cholinergic drugs (acetylcholine agonists) mimic acetylcholine at all sites although the balance of nicotinic and muscarinic effects is variable.

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Introduction: Nicotine is a main water-soluble alkaloid being contained in the tobacco plant (Nicotiana tabacum), which acts as an inducing compound for smoking-dependence. Twelve kinds of nicotine metabolites are known in rats [1]. Among them, cotinine is the major metabolite of nicotine; the half-life (T1/2) of cotinine is much longer (10–20 h) than that of nicotine (24–84 min). The qualitative analysis of cotinine in urine and saliva is being thus carried out as indicators for smoking during its abstinence therapy and for confirming passive smoking.

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