Steady-state concentration of cotinine as a measure of nicotine-intake by smokers

Galeazzi, Renato L.; Daenens, P.; Gugger, Mathias

doi:10.1007/bf00543327

Cited by 58 publications

(24 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, cotinine has been recommended as a parameter for nicotine consumption or abstinence (e. g. Benowitz et al 1983) and it has been demonstrated that plasma concentrations of cotinine are related to nicotine intake in man (Galeazzi et al 1985). Cotinine, which is a long-lived metabolite of nicotine, may enter secondary metabolic pathways leading to cotinine-N-oxide, norcotinine and trans-3'-hydroxycotinine (Wada et al 1961;Bowman and McKennis 1962;Dagne and Castagnoli 1972;Hibbert and Gorrod 1985).…”

Section: Discussionmentioning

confidence: 97%

“…Usually, cotinine is present in the plasma of smokers in concentrations exceeding those of nicotine and it remains there longer than nicotine after cessation of smoking (Benowitz et al 1983;Galeazzi et al 1985). Thus, cotinine has been recommended as a parameter for nicotine consumption or abstinence (e. g. Benowitz et al 1983) and it has been demonstrated that plasma concentrations of cotinine are related to nicotine intake in man (Galeazzi et al 1985).…”

Section: Discussionmentioning

confidence: 98%

See 1 more Smart Citation

Nicotine metabolism in isolated perfused lung and liver of phenobarbital- and benzoflavone-treated rats

et al. 1991

View full text Add to dashboard Cite

The kinetics of nicotine elimination was investigated in isolated perfused lung and liver of phenobarbital (PB)- and 5,6-benzoflavone (BF)-pretreated rats. The estimated kinetic parameters demonstrated a high nicotine elimination rate in rat lung approaching the capacity of liver when both organs were in an uninduced state. The concentration-time profiles of cotinine as the main metabolite were almost identical for isolated lung and liver. In both organs the cotinine plasma concentrations reached a plateau level after 60 min of perfusion. Pretreatment of rats with 5,6-benzoflavone did not affect the rate of nicotine elimination and cotinine formation either in the lung or in the liver. Phenobarbital treatment, however, induced nicotine clearance in lung approximately 2-fold. This effect is quantitatively lower than the PB-related 8-fold induction of hepatic nicotine elimination observed in a previous study. The present results also indicate that the turnover of cotinine is markedly enhanced after PB induction. The elimination half-lives and clearance values for cotinine as the substrate were approximately 10-fold increased in rat liver after PB pretreatment. Thus, an important contribution of extrahepatic tissues to nicotine metabolism in rats has to be assumed. Moreover, since cotinine elimination is significantly increased after PB induction it is questionable whether cotinine plasma concentrations can further be used as suitable parameter for nicotine consumption.

show abstract

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 98%

Nicotine metabolism in isolated perfused lung and liver of phenobarbital- and benzoflavone-treated rats

et al. 1991

View full text Add to dashboard Cite

show abstract

“…To quantify ETS exposure, we measured plasma cotinine, a good indicator of exposure to cigarette smoke (17). Because lifestyle factors can also influence oxidative DNA damage, we also investigated the effect of physical activity, body mass index, alcohol, and tea and coffee consumption.…”

Section: Introductionmentioning

confidence: 99%

Active and Passive Smoking and Lifestyle Determinants of 8-Oxo-7,8-Dihydro-2′-Deoxyguanosine Levels in Human Leukocyte DNA

Lodovici¹,

Caldini²,

Luceri³

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

View full text Add to dashboard Cite

We investigated the effects of smoking and exposure to environmental tobacco smoke (ETS) on oxidative DNA damage by measuring 8-oxo-7,8-dihydro-2V -deoxyguanosine (8-oxodGuo) levels in DNA of leukocytes of healthy donors (30 smokers, 29 nonsmokers, and 28 ETS-exposed subjects). Nonsmokers had lower 8-oxodGuo levels compared with smokers (5.94 F 0.87 Â 10 À6 and 19.85 F 4.75 Â 10 À62-deoxyguanosine, respectively, means F SE, P = 0.00007). Subjects exposed to ETS had higher mean value of 8-oxodGuo compared with nonsmokers (9.18 F 1.53 Â 10 À6 2-deoxyguanosine, mean F SE), nonsignificant by univariate analysis (P = 0.074). Multiregression analysis indicated that the increase of 8-oxodGuo levels induced by ETS was significant (P = 0.045) and that coffee and tea consumption reduced DNA oxidation (P = 0.0053). Oxidative leukocyte DNA damage was positively correlated with plasma cotinine levels in ETS-exposed subjects (r = 0.47, P < 0.01, n = 28) and was increased by age in nonsmokers and ETS-exposed subjects (P = 0.049

show abstract

“…Usually, cotinine is present in the plasma of smokers in concentrations exceeding those of nicotine and it remains there longer than nicotine after cessation of smoking [2,12]. It has been demonstrated that the plasma concentrations of cotinine are closely related to nicotine intake [12] and that the elimination kinetics of cotinine from plasma are directly proportional to the corresponding values in saliva [6,21]. Therefore, cotinine has been recommended as a biomarker for nicotine intake [2,6,21,33], although there are some limitations to this approach [19].…”

Section: Discussionmentioning

confidence: 99%

Increased cotinine elimination and cotinine-N-oxide formation by phenobarbital induction in rat and mouse

Foth¹,

Aubrecht²,

Höhne³

et al. 1992

Clin Investig

View full text Add to dashboard Cite

The metabolic fate of cotinine, the major metabolite of nicotine, was studied in phenobarbital-induced and non-induced isolated perfused rat lung and liver and in isolated hepatocytes of rats and mice. The non-induced lung tissue showed low cotinine metabolizing capacity while the perfused liver was approximately four times more active. After phenobarbital pretreatment the metabolism of cotinine was increased eight-fold in the intact liver. A substantial increase in cotinine metabolism was also found in isolated hepatocytes from PB-induced rats and in cultured mouse hepatocytes grown in a medium supplemented with PB. This was paralleled by an increased formation of cotinine-N-oxide which could be inhibited by 100 microM metyrapone. In contrast, the pulmonary elimination of cotinine was not affected by PB. A dominant role of primary N-oxidation of nicotine compared to C-oxidation was apparent in non-induced rat liver. After PB treatment the rate of nicotine-N'-oxide formation dropped markedly while the cotinine related pathways were increased causing an inversion of the N- to C-oxidation ratio. In the lung, cotinine formation was the preferred metabolic pathway of nicotine already in non-induced organs. The pattern of nicotine metabolites was not altered by PB induction. In conscious PB-induced rats receiving nicotine orally or intravenously, 3'-hydroxycotinine was found as the main urinary metabolite of nicotine while only a small fraction was excreted as cotinine-N-oxide. This discrepancy between the profile of nicotine metabolites in perfused liver and lung and in the urine in vivo indicates that extrahepatic organs other than the lung may be important sites of cotinine metabolism.

show abstract

Steady-state concentration of cotinine as a measure of nicotine-intake by smokers

Cited by 58 publications

References 9 publications

Nicotine metabolism in isolated perfused lung and liver of phenobarbital- and benzoflavone-treated rats

Nicotine metabolism in isolated perfused lung and liver of phenobarbital- and benzoflavone-treated rats

Active and Passive Smoking and Lifestyle Determinants of 8-Oxo-7,8-Dihydro-2′-Deoxyguanosine Levels in Human Leukocyte DNA

Increased cotinine elimination and cotinine-N-oxide formation by phenobarbital induction in rat and mouse

Contact Info

Product

Resources

About