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Kyerematen, Gabriel A.; Morgan, Monica L; Chattopadhyay, Balaka; deBethizy, J Donald; Vesell, Elliot S.

doi:10.1038/clpt.1991.166

Cited by 9 publications

(11 citation statements)

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“…As females represent a significant proportion of the current vaping population (USDHHS, 2016), studies examining the impact of nicotine vapor exposure in female subjects are important and warranted. Previous studies in rats have demonstrated sex differences in nicotine metabolism (Kyerematen et al, 1988) and the effects of nicotine on anxiety-like behaviors (Torres et al, 2013). A recent study examining nicotine vapor self-administration in male and female rats identified that while both males and female rats will self-administer nicotine vapor in roughly equivalent levels, passive vapor exposure produced significantly lower serum cotinine levels in females as compared to males (Lallai et al, 2021).…”

Section: Discussionmentioning

confidence: 97%

Electronic Nicotine Vapor Exposure Produces Differential Changes in Central Amygdala Neuronal Activity, Thermoregulation and Locomotor Behavior in Male Mice

Zhu

Sanchez

Douglass

et al. 2021

eNeuro

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Nicotine is an addictive substance historically consumed through smoking and more recently through the use of electronic vapor devices. The increasing prevalence and popularity of vaping prompts the need for preclinical rodent models of nicotine vapor exposure and an improved understanding of the impact of vaping on specific brain regions, bodily functions, and behaviors. We used a rodent model of electronic SIGNIFICANCE STATEMENTNicotine vaping is increasing, prompting the need for an improved understanding of the impact of electronic nicotine vapor exposure on specific brain regions and relevant physiological functions and behaviors. The present study used a mouse model of nicotine vapor exposure to examine the cellular and behavioral consequences of acute and repeated exposure to nicotine vapor. We found that acute, but not repeated, exposure to nicotine vapor increased activity in the central amygdala and that acute and repeated exposure produced differential effects on body temperature and movement.These findings demonstrate that nicotine vaping alters brain function in the central amygdala and produces dysregulation of normal body functions like thermoregulation and locomotion.

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Section: Discussionmentioning

confidence: 97%

Electronic Nicotine Vapor Exposure Produces Differential Changes in Central Amygdala Neuronal Activity, Thermoregulation and Locomotor Behavior in Male Mice

Zhu

Sanchez

Douglass

et al. 2021

eNeuro

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“…Fur ther, smoking accelerates the elimination of cotinine faster than that of 3-HCG. There fore, it has been suggested that 3-HCG is a more sensitive and discriminating marker of passive smoking [ 13]. However, the toxicolog ical aspects of 3-HCG have yet to be investi gated to evaluate the risk factors for its long retention in the body, especially after the use of smokeless tobacco products.…”

Section: Changes In Concentrations O F Nicotine and Cotinine In The Hmentioning

confidence: 99%

“…Among the eight metabo lites of nicotine in humans, besides cotinine, two other metabolites, i.e., 3-hydroxycotinine glucuronide (3-HCG, metabolite A) and demethylcotinine A2 •v-enamine (DMCE, me tabolite G), are considered to be of special interest due to their long plasma half-lives [13,16]. They persist longer than cotinine in smokers, and 3-HCG tends to persist longer than cotinine even in nonsmokers [13]. Fur ther, smoking accelerates the elimination of cotinine faster than that of 3-HCG.…”

Section: Changes In Concentrations O F Nicotine and Cotinine In The Hmentioning

confidence: 99%

Distribution and Retention of Nicotine and Its Metabolite, Cotinine, in the Rat as a Function of Time

Sastry¹,

Chance²,

Singh

et al. 1995

Pharmacology

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Nicotine is oxidized to its major metabolite, cotinine, which has a long biological half-life (19–24 h). The plasma concentration of cotinine has been used as an index of tobacco smoke exposure. Cotinine possibly increases the turnover rate of platelet-activating factor (PAF) because it is a potent activator of PAF hydrolase, and it may play a significant role in tobacco-induced arterial thrombosis. Therefore, we studied the distribution and retention of nicotine as it was metabolized to cotinine in the rat. Nicotine (1 mg/kg, 5 µCi/kg) was administered into the femoral vein of male Sprague-Dawley rats under nembutal anesthesia. At different times (5–60 min) after nicotine administration, nicotine and its metabolite, cotinine, were determined by HPLC in plasma, liver, kidney, heart and brain. Within 5–10 min after administration, nicotine concentrations reached peak values in plasma (2,160 pmol/ml) and the organs analyzed. The plasma level of nicotine decreased by 50% within 20 min (half-time) after its intravenous administration. The half-time of nicotine in the brain was about 50 min. The half-times of nicotine for the other organs were about 20–25 min. The major metabolite, cotinine, accumulated in plasma, and by about 30 min the concentrations of nicotine and cotinine in plasma were about equal (890–1,000 pmol/ml). While cotinine accumulated in plasma, nicotine was eliminated by the kidney. While the nicotine concentrations decreased with time in all organs, cotinine concentrations remained constant. These observations indicate that nicotine is renally eliminated or metabolized to cotinine while cotinine exhibits a long retention time and accumulates in plasma. This plasma accumulation may contribute to activation of PAF turnover rate and to thrombosis.

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“…Nicotine (NIC) and its major metabolite cotinine (COT) have been used as markers for assessment of prenatal tobacco smoke exposure [11,12]. Generally, COT rather than NIC is preferred for assessing exposure because its half-life (about 15-20 h) [13][14][15] in blood or urine is substantially longer than that of NIC's (0.5-3 h) [15][16][17]. Another NIC metabolite, trans-3 -hydroxycotinine (OHCOT), is also abundant in urine [18,19], with an effective half-life similar to that of COT from which it is formed.…”

Section: Introductionmentioning

confidence: 99%

Measurement of nicotine, cotinine and trans-3′-hydroxycotinine in meconium by liquid chromatography–tandem mass spectrometry

Yang

Alexander

et al. 2011

Journal of Chromatography B

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Abstract: Clinical Pharmacology and Therapeutics (1991) 50, 462–464; doi:

Cited by 9 publications

References 0 publications

Electronic Nicotine Vapor Exposure Produces Differential Changes in Central Amygdala Neuronal Activity, Thermoregulation and Locomotor Behavior in Male Mice

Electronic Nicotine Vapor Exposure Produces Differential Changes in Central Amygdala Neuronal Activity, Thermoregulation and Locomotor Behavior in Male Mice

Distribution and Retention of Nicotine and Its Metabolite, Cotinine, in the Rat as a Function of Time

Measurement of nicotine, cotinine and trans-3′-hydroxycotinine in meconium by liquid chromatography–tandem mass spectrometry

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