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Nicotine oxidase

Dai VD, K Decker, H Sund (1968) Purification and properties of L-6-hydroxy nicotine oxidase. Eur J Biochem 4 95-102. [Pg.137]

Whereas many coenzymes form noncovalent complexes with their respective apoenzymes, various flavoenzymes are characterized by covalently bound FMN (25) or FAD (Fig. 3). Covalent linkage involves the position 8a methyl group or the benzenoid carbon atom 6 of the flavin and a cysteine or histidine residue of the protein. The covalent CN or CS bond can be formed by autoxidation of the noncovalent apoen-zyme/coenzyme precursor complex as shown in detail for nicotine oxidase (59). [Pg.254]

Koetter JW, Schulz GE. Crystal structure of 6-hydroxy-D-nicotine oxidase from Arthrobacter nicotinovorans. J. Mol. Biol. 2005 352 418-128. [Pg.259]

FIGURE 2. Alignment of the deduced amino acid sequences of GLO, 6-hydroxy-D-nicotine oxidase (6-HDNO), mcrA protein (MCRA), and berberine bridge enzyme (reticuline oxidase) (BBE). Identical residues are boxed. Arrowhead indicates the position of the histidyl residue to which FAD is covalently bound in 6-hydroxy-D-nicotine oxidase. Adapted from Brandsch (1994) and August et al. (1994). [Pg.27]

The aerobic degradation of nicotine produces an A-methylpyrrolidine as the first metabolite by dehydrogenation. This is then hydroxylated at the benzylic carbon atom by an FAD-containing oxidase (Dai et al. 1968), and the y-A-methylaminobutyrate that is produced by fission of the A-methylpyrolidine ring is demethylated by an oxidase to 4-aminobutyrate (Chiribau et al. 2004). [Pg.132]

Chiribau CB, C Sandu, M Eraaije, E Schiltz, R Bradsch (2004) A novel y-A-methylaminohutyrate demethyl-ating oxidase involved in catabolism of the tobacco alkaloid nicotine by Arthrobacter nicotinovorans pAOl. Eur JBiochem 271 4677-4684. [Pg.137]

Villegier, A.S., Blanc, G., Glowinski, J., Tassin, J.P. Transient behavioral sensitization to nicotine becomes long-lasting with monoamine oxidases inhibitors. Pharmacol. Biochem. Behav. 76 267, 2003. [Pg.49]

Increased bilirubin levels are caused due to the intake of large doses of such drugs as chloroquine, vitamin K, sulpha-drugs, tetracyclines, paracetamol, nicotinic acid and monoamine oxidase inhibitors (e.g., iproniazid RP 1.0 nialamide RP 1.8 isocarboxazid RP 3.1 phenelzine RP 18 pheniprazine RP31 and tranylcypromine RP 45), where RP designates the Relative Potency based on the tiyptamine potentiation test. The elevated levels are due to hepatic injury, and... [Pg.57]

Nicotine is extensively metabolized to a nnmber of metabolites (Fig. 3) by the liver. Six primary metabolites of nicotine have been identified. Qnantitatively, the most important metabolite of nicotine in most mammalian species is the lactam derivative, cotinine. In humans, about 70-80% of nicotine is converted to cotinine. This transformation involves two steps. The first is mediated primarily by CYP2A6 to produce nicotine-A -iminium ion, which is in equilibrium with 5 -hydroxynicotine. The second step is catalyzed by a cytoplasmic aldehyde oxidase. Nicotine iminiiim ion has received considerable interest since it is an alkylating agent and, as such, could play a role in the pharmacology of nicotine (Shigenaga etal. 1988). [Pg.35]

Benwell ME, Balfour DJK, Anderson JM (1988) Evidence that tobacco smoking increases the density of (-)-[ H]nicotine binding sites in human brain. J Neurochem 50 1243-1247 Berlin 1, Anthenelli RM (2001) Monoamine oxidases and tobacco smoking. Int J Neuropsy-chopharmacol 4 33 2... [Pg.162]

Brandange S, Lindblom L (1979) The enzyme aldehyde oxidase is animinium oxidase. Reaction with nicotine delta 1(5 ) iminium ion. Biochem Biophys Res Commun 91 991-996 Byrd GD, Chang KM, Greene JM, deBethizy JD (1992) Evidence for urinary excretion of glu-curonide conjugates of nicotine, cotinine, and trans-3 -hydroxycotinine in smokers. Drug Metab Dispos 20 192-197... [Pg.252]

Villegier AS, Salomon L, et al (2006) Monoamine oxidase inhibitors allow locomotor and rewarding responses to nicotine. Neuropsychopharmacology 31(8) 1704-1713 von Ziegler NI, Schlumpf M, et al (1991) Prenatal nicotine exposure selectively affects perinatal forebrain aromatase activity and fetal adrenal function in male rats. Brain Res Dev Brain Res 62(1) 23-31... [Pg.294]

Wiley JL, LaVecchia KL, Martin BR, Damaj MI (2002) Nicotine-like discriminative stimulus effects of bupropion in rats. Exp Clin Psychopharmacol 10 129-135 Williams M, Robinson JL (1984) Binding of the nicotinic cholinergic antagonist, dihydro-beta-erythroidine, to rat brain tissue. J Neurosci 4 2906-2911 Witkin JM, Dykstra LA, Carter RB (1982) Acute tolerance to the discriminative stimulus properties of morphine. Pharmacol Biochem Behav 17 223-228 Wooters TE, Bardo MT (2007) The monoamine oxidase inhibitor phenelzine enhances the discriminative stimulus effect of nicotine in rats. Behav Pharmacol 18 601-608 Wright JM Jr, Vann RE, Gamage TE, Damaj MI, WUey JL (2006) Comparative effects of dextromethorphan and dextrorphan on nicotine discrimination in rats. Pharmacol Biochem Behav 85 507-513... [Pg.332]

Agatsuma S, Lee M, Zhu H, Chen K, Shih 1C, Seif I, Hiroi N (2006) Monoamine oxidase A knockout mice exhibit impaired nicotine preference but normal responses to novel stimuli. Hum Mol Genet 15 2721-2731... [Pg.357]

Guillem K, VouiUac C, Azar MR, Parsons LH, Koob GF, Cador M, Stinus L (2005) Monoamine oxidase inhibition dramatically increases the motivation to self-administer nicotine in rats. J Neu-rosci 25 8593-8600... [Pg.360]


See other pages where Nicotine oxidase is mentioned: [Pg.77]    [Pg.78]    [Pg.231]    [Pg.232]    [Pg.27]    [Pg.49]    [Pg.77]    [Pg.78]    [Pg.231]    [Pg.232]    [Pg.27]    [Pg.49]    [Pg.228]    [Pg.334]    [Pg.312]    [Pg.42]    [Pg.45]    [Pg.449]    [Pg.472]    [Pg.966]    [Pg.42]    [Pg.44]    [Pg.122]    [Pg.140]    [Pg.146]    [Pg.160]    [Pg.165]    [Pg.210]    [Pg.230]    [Pg.236]    [Pg.236]    [Pg.252]    [Pg.256]    [Pg.257]    [Pg.346]    [Pg.350]    [Pg.357]    [Pg.359]   
See also in sourсe #XX -- [ Pg.132 ]




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