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Early Life Exposure to E-cigarettes ...

Lauterstein, Dana.

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Early Life Exposure to E-cigarettes Induces CNS Modifications Associated with Adverse Neurobiological and Neurobehavioral Outcomes.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Early Life Exposure to E-cigarettes Induces CNS Modifications Associated with Adverse Neurobiological and Neurobehavioral Outcomes./
作者:	Lauterstein, Dana.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2016,
面頁冊數:	243 p.
附註:	Source: Dissertation Abstracts International, Volume: 78-05(E), Section: B.
Contained By:	Dissertation Abstracts International78-05B(E).
標題:	Toxicology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10191922
ISBN:	9781369332506

Early Life Exposure to E-cigarettes Induces CNS Modifications Associated with Adverse Neurobiological and Neurobehavioral Outcomes.
Lauterstein, Dana.

Early Life Exposure to E-cigarettes Induces CNS Modifications Associated with Adverse Neurobiological and Neurobehavioral Outcomes. - Ann Arbor : ProQuest Dissertations & Theses, 2016 - 243 p.

Source: Dissertation Abstracts International, Volume: 78-05(E), Section: B.

Thesis (Ph.D.)--New York University, 2016.

Early life exposure to cigarette smoke is associated with adverse neurocognitive and neurobehavioral outcomes including decreases in general intellectual ability, development of conduct disorders, and increased hyperactivity-impulsivity behaviors. While there have been major declines in conventional cigarette usage over the past decade, recent epidemiological data indicate that the popularity of electronic cigarettes (e-cigarettes), and consequently nicotine use, is rising in both adolescent and adult populations on a global scale. As nicotine is a known developmental neurotoxin, these products present a potential threat for the developing central nervous system (CNS). The aim of this study was to evaluate whether developmental neurotoxicity and later life behavioral changes associated with early life exposure to cigarette smoke are also affected by early life exposure to e-cigarette aerosols. This study also investigated if nicotine was the primary e-cigarette component inducing adverse effects, or if other constituents emitted from e-cigarettes could produce neurotoxicity. To accomplish this pregnant C57BL/6 mice were exposed daily (by whole body inhalation) throughout gestation (3 hr/day; 5 day/week) to aerosols produced from e-cigarettes either with (13--16 mg/mL) or without nicotine; following birth, pups and dams were exposed together to e-cigarette aerosols throughout lactation beginning at postnatal day (PND) 4--6 using the same exposure conditions employed during prenatal exposure. Following exposure cessation, a subset of female and male juvenile offspring (1-mo-of-age) was evaluated for transcriptome changes (via RNA-sequencing) in the frontal cortex, as well as selected gene expression changes (via qRT-PCR) and markers of neuroinflammation (via fluorescent microscopy) in the frontal cortex and the hippocampus. In adulthood another subset of female and male offspring (4-mo-of-age) were tested for persistence of gene expression changes in the same brain regions, as well as for behavioral outcomes.

ISBN: 9781369332506Subjects--Topical Terms:

556884
Toxicology.

Early Life Exposure to E-cigarettes Induces CNS Modifications Associated with Adverse Neurobiological and Neurobehavioral Outcomes.
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520 $a Early life exposure to cigarette smoke is associated with adverse neurocognitive and neurobehavioral outcomes including decreases in general intellectual ability, development of conduct disorders, and increased hyperactivity-impulsivity behaviors. While there have been major declines in conventional cigarette usage over the past decade, recent epidemiological data indicate that the popularity of electronic cigarettes (e-cigarettes), and consequently nicotine use, is rising in both adolescent and adult populations on a global scale. As nicotine is a known developmental neurotoxin, these products present a potential threat for the developing central nervous system (CNS). The aim of this study was to evaluate whether developmental neurotoxicity and later life behavioral changes associated with early life exposure to cigarette smoke are also affected by early life exposure to e-cigarette aerosols. This study also investigated if nicotine was the primary e-cigarette component inducing adverse effects, or if other constituents emitted from e-cigarettes could produce neurotoxicity. To accomplish this pregnant C57BL/6 mice were exposed daily (by whole body inhalation) throughout gestation (3 hr/day; 5 day/week) to aerosols produced from e-cigarettes either with (13--16 mg/mL) or without nicotine; following birth, pups and dams were exposed together to e-cigarette aerosols throughout lactation beginning at postnatal day (PND) 4--6 using the same exposure conditions employed during prenatal exposure. Following exposure cessation, a subset of female and male juvenile offspring (1-mo-of-age) was evaluated for transcriptome changes (via RNA-sequencing) in the frontal cortex, as well as selected gene expression changes (via qRT-PCR) and markers of neuroinflammation (via fluorescent microscopy) in the frontal cortex and the hippocampus. In adulthood another subset of female and male offspring (4-mo-of-age) were tested for persistence of gene expression changes in the same brain regions, as well as for behavioral outcomes.
520 $a Frontal cortex transcriptome sequencing revealed that e-cigarettes, both with and without nicotine, induced sex-dependent gene expression changes associated with predicted adverse neurobiological and neurobehavioral outcomes. In addition, a greater number of significant gene expression changes were observed in offspring exposed to e-cigarette aerosols without nicotine compared to those exposed to nicotine-containing aerosols. Persistence of gene expression alterations for selected genes examined in the frontal cortex and hippocampus of 1-mo- and 4-mo-old offspring revealed variations based on brain region, sex, and e-cigarette aerosol treatment type (i.e., with or without nicotine). Results from microscopy studies indicated that only offspring exposed to e-cigarette aerosols without nicotine early in life exhibited enhanced expression of Iba-1, a specific marker of microglia, in the CA1 region of the hippocampus. Lastly, behavioral analyses demonstrated significant locomotor activity increases in adult offspring exposed to both e-cigarette aerosols with and without nicotine early in life.
520 $a Overall, results indicate that exposure to e-cigarette aerosols, with and without nicotine, pose a considerable risk to the developing CNS. Additionally, nicotine does not appear to be the driving factor for the examined biological effects, as similar or more extensive effects were seen in offspring exposed to e-cigarette aerosols without nicotine for all parameters (when compared to offspring exposed to e-cigarette aerosols that contained nicotine). These results contribute to the limited toxicological database on e-cigarettes and emphasize the need for studies examining early life exposure to these products and development of later life disease.
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