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Maternal Electronic Cigarette Use Can Enhance Offspring Susceptibility to Hypoxic‐Ischemic Brain Injury
Author(s) -
Sifat Ali Ehsan,
Nozohouri Saeideh,
Villalba Heidi,
Vaidya Bhuvaneshwar,
Abbruscato Thomas
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.813.2
Subject(s) - nicotine , medicine , fetus , offspring , brain damage , hypoxic ischemic encephalopathy , population , electronic cigarette , hypoxia (environmental) , ischemia , pregnancy , anesthesia , encephalopathy , physiology , pathology , biology , chemistry , oxygen , genetics , environmental health , organic chemistry
Prenatal exposure to tobacco smoke and nicotine is believed to interfere with fetal brain development predisposing offspring to different neurobehavioral and neuropsychological disorders. Included in this is increased neonatal vulnerability to hypoxic‐ischemic encephalopathy (HIE) which is a major cause of neonatal death and child disability in the US. These effects could be, in part, mediated by fetal nicotine exposure. Use of electronic cigarettes (e‐Cigs), commonly known as vaping, has been rapidly increasing in recent times in the general population, including women of reproductive age. E‐Cig use during pregnancy is also increasing because of the addictive properties of nicotine along with the perception of the relative safety of e‐Cigs. In this study, we aimed to investigate the effects of maternal e‐Cig use on neonatal brain development and HIE utilizing a combination of in vitro and in vivo models. Pregnant CD1 mice were exposed to e‐Cig vapor (2.4% nicotine). Primary cortical neurons were isolated from e‐Cig exposed fetus and cultured for seven days with subsequent exposure to oxygen‐glucose deprivation followed by reoxygenation (OGD/R) to mimic ischemia‐reperfusion injury. Hypoxic‐ischemic brain injury was induced in 8–9 days old mouse pups by a combination of left common carotid artery ligation and 15 minutes exposure to 8% oxygen. We found that e‐Cig exposed cortical neurons demonstrated decreased cell viability and increased caspase‐3 expression in OGD/R condition. These effects were accompanied by a decrease in neurite formation, mitochondrial dysfunctions, and decreased glucose uptake & glucose transporter expression in OGD/R condition. Our preliminary data also indicate increased sensitivity to HI brain injury in prenatally e‐Cig exposed mouse pups. Additionally, in utero e‐Cig exposed mice offspring displayed a significantly increased level of hyperactivity at postnatal day 45 in open field test. These results indicate that maternal e‐Cig exposure could lead to offspring behavioral abnormalities and enhance HI brain injury. Further studies are needed to demonstrate the long‐term anatomical and behavioral effects of HI brain injury in e‐Cig exposed offspring pups. This study is instrumental in elucidating the possible deleterious effects of maternal e‐Cig use in the general population. Support or Funding Information R01 DA029121 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .