Prenatal cigarette smoke exposure: Pregnancy outcome and gestational changes in plasma nicotine concentration, hematocrit, and carboxyhemoglobin in a newly standardized rat model

Farkas, Svetlana; Hussein, Jabeen; Ariano, Robert E.; Sitar, Daniel S.; Hasan, Shabih U.

doi:10.1016/j.taap.2005.12.010

Cited by 18 publications

(17 citation statements)

References 43 publications

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“…Rodent models of cigarette exposure have been used widely to study tobacco smoke toxicology, particularly carcinogenesis [13, 14]. Much less attention has been directed at using smoke exposure systems to study nicotine pharmacology or pharmacokinetics, and most such studies have not measured serum or tissue concentrations of nicotine to determine how they relate to the exposures of cigarette smokers, or carboxyhemoglobin concentrations to assure lack of toxicity from carbon monoxide exposure.…”

Section: Discussionmentioning

confidence: 99%

“…Cigarette smoke exposure of rodents has been used widely for studying smoke toxicology [13, 14] but its use to investigate nicotine pharmacokinetics or tobacco addiction has been quite limited [15–19], and no studies to date have used rodent smoke exposure to investigate pharmacotherapies for tobacco addiction. In the current study rats were exposed to cigarette smoke under well defined conditions modeling the smoking of 1 cigarette over 10 min or the smoking of multiple cigarettes over 2 hr, as well to as i.v.…”

Section: Introductionmentioning

confidence: 99%

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Vaccination against nicotine alters the distribution of nicotine delivered via cigarette smoke inhalation to rats

Pravetoni¹,

Keyler²,

Raleigh³

et al. 2011

Biochemical Pharmacology

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Preclinical models of nicotine vaccine pharmacology have relied on i.v. or s.c. administration of nicotine. Models using cigarette smoke inhalation might more accurately simulate nicotine exposure in smokers. Nicotine vaccine effects were examined in rats using two cigarette smoke exposure models: a 10 minute nose-only exposure (NSE) producing serum nicotine levels equivalent to the nicotine boost from 1 cigarette in a smoker, and a two hour whole-body exposure (WBE) producing serum nicotine levels similar to those associated with regular midday smoking. Vaccination prior to 10 min smoke NSE reduced nicotine distribution to brain by 90%, comparable to its effect on nicotine administered i.v. Vaccination prior to 2 hr smoke WBE reduced nicotine distribution to brain by 35%. The nicotine concentration in broncheoalveolar lavage (BAL) fluid obtained after 2 hr WBE was increased by 230% in vaccinated rats but was also increased in rats passively immunized with a nicotine-specific monoclonal antibody, and so was likely due to transfer of antibody from serum rather than local production at the pulmonary mucosa. Nicotine-specific IgA was not detectable in BAL fluid, but titers in serum were appreciable at 21–25% of the IgG titer and could contribute to vaccine efficacy. Both vaccination and passive immunization are effective in reducing nicotine distribution to brain in rats when nicotine is delivered via inhaled cigarette smoke. These data validate results previously obtained in rodents for nicotine vaccines using i.v. or s.c. nicotine dosing and provide a quantitative method for studying aspects of nicotine exposure which are unique to cigarette smoke inhalation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Vaccination against nicotine alters the distribution of nicotine delivered via cigarette smoke inhalation to rats

Pravetoni¹,

Keyler²,

Raleigh³

et al. 2011

Biochemical Pharmacology

View full text Add to dashboard Cite

show abstract

“…In addition, laboratory animals exposed to cigarette smoke have also exhibited reduced fecundity, as evidenced by reduced litter size and increased resorptions [Izzotti et al 2003;Khan et al 2008], poor embryo quality [Huang et al 2008], low fetal weight [Esposito et al 2008]), and fetal demise [Farkas et al 2006]. Early evidence connecting smoking during pregnancy with the risk of spontaneous miscarriage was controversial, with some groups reporting a positive association [Himmelberger et al 1978;Kline et al 1977] and others reporting no association [Harlap and Shiono 1980].…”

Section: Smoking and Spontaneous Abortionmentioning

confidence: 99%

Embryonic Resorption and Polycyclic Aromatic Hydrocarbons: Putative Immune-mediated Mechanisms

Detmar

Jurisicova

2010

Systems Biology in Reproductive Medicine

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Polycyclic aromatic hydrocarbons (PAHs) are released into the environment as a result of incomplete fossil fuel combustion from industrial furnaces, woodburning stoves, and automobile exhaust fumes; however, the primary source of human exposure to these compounds is cigarette smoke. Embryonic and fetal loss after treatment with high doses of PAHs have been well documented in animal studies; however, few studies have addressed the reproductive consequences of long-term, low-level exposure to these chemicals. We previously reported that low doses of PAHs administered to ICR mice over a period of 9 weeks prior to conception resulted in early embryonic resorptions, whereby treated dams lost approximately 50% of their litter. During the course of these studies, we observed greater numbers of infiltrating uterine natural killer (uNK) cells into the placenta of PAH-exposed conceptuses. While exposure to high levels of PAHs has been shown to be immunosuppressive, increasing evidence suggests that chronic, low-dose exposure to PAHs may stimulate immune cells. Thus, we hypothesized that low-dose, chronic PAH exposure in our mouse model is mediating embryonic resorption by hyperstimulating maternal immune cells. In this review of the literature, we outline the rationale of our argument and present preliminary data, focussing upon PAH-mediated alterations in uNK cell dynamics and how these changes may be linked to early embryonic resorptions.

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“…Cigarette smoke inhalation systems involving either nose-only exposure (NOE) or whole-body exposure (WBE) have been used extensively to study tobacco carcinogenicity and toxicity in animals (Coggins, 2007; Farkas et al, 2006; Hecht, 2005), but only a few preclinical studies have examined the behavioral effects of smoke. Similar to pure nicotine administered parenterally (e.g., Sahley and Berntson, 1979), NOE or WBE to cigarette smoke produced diminished pain sensitivity (analgesia) in rats, with the development of tolerance following repeated exposures (Anderson et al, 2004; Mousa et al, 1988; Simons et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Comparison of the behavioral effects of cigarette smoke and pure nicotine in rats

Harris

Mattson

LeSage

et al. 2010

Pharmacology Biochemistry and Behavior

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Animal models of tobacco dependence typically rely on parenteral administration of pure nicotine. Models using cigarette smoke inhalation might more accurately simulate nicotine exposure in smokers. The primary goal of this study was to validate methods for administering cigarette smoke to rats using exposure conditions that were clinically relevant and also produced brain nicotine levels similar to those produced by behaviorally active doses of pure nicotine. A secondary goal was to begin examining the behavioral effects of smoke. Nose-only exposure (NOE) to smoke for 10-45 min or whole-body exposure (WBE) to smoke for 1-4 hr produced serum nicotine concentrations similar to those in smokers (14-55 ng/ml), without excessive carbon monoxide exposure. Daily nicotine (0.1 mg/kg, s.c.) induced locomotor sensitization whereas 45-min NOE producing brain nicotine levels within the same range did not. Nicotine 0.125 mg/kg s.c. reversed withdrawal from a chronic nicotine infusion as measured by elevations in intracranial self-stimulation thresholds whereas 4-hr WBE producing similar brain nicotine levels did not. These data demonstrate the feasibility of delivering cigarette smoke to rats at clinically relevant doses, and provide preliminary evidence that the behavioral effects of nicotine delivered in smoke may differ from those of pure nicotine.

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Prenatal cigarette smoke exposure: Pregnancy outcome and gestational changes in plasma nicotine concentration, hematocrit, and carboxyhemoglobin in a newly standardized rat model

Cited by 18 publications

References 43 publications

Vaccination against nicotine alters the distribution of nicotine delivered via cigarette smoke inhalation to rats

Vaccination against nicotine alters the distribution of nicotine delivered via cigarette smoke inhalation to rats

Embryonic Resorption and Polycyclic Aromatic Hydrocarbons: Putative Immune-mediated Mechanisms

Comparison of the behavioral effects of cigarette smoke and pure nicotine in rats

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