Abstract

Almost ¼ of the world population suffers from anemia, a condition characterized by an insufficient number of red blood cells or oxygen‐carrying capacity within the blood. Anemia is associated with fatigue, weakness, and dizziness, and when it occurs early in life it may alter the course of behavioral and cognitive development in human and murine populations causing decreased physical activity and responsiveness. Pregnant women and children are particularly vulnerable to anemia as are individuals who use nicotine. Despite the link between adverse birth outcomes of pre‐ and perinatal nicotine exposure, 11% of US women continue smoking or using alternative nicotine products throughout pregnancy. We hypothesize that in utero exposure to nicotine will result in post‐natal anemia precipitating a characteristic abnormal bone phenotype. To test this hypothesis, wild type C57BL6 males and females were utilized to produce in utero nicotine exposed litters. Drinking water for pregnant dams was supplemented with nicotine. Pups were grown to 15 days postnatal then sacrificed. Blood and whole skulls were collected for complete blood count, micro‐computed tomography (μCT), and histological analyses. Complete blood count data comparing nicotine exposed pups to unexposed controls indicated increased mean corpuscular volume indicative of macrocytic anemia in nicotine exposed mice. Additionally, nicotine exposed pups presented with low platelet counts also associated with anemia. μCT analysis of bone surface compared to bone volume indicated a greater ratio in individuals exposed to nicotine, which suggests weaker pitted bone also associated with anemia. Histological investigation of osteoclast activity indicated greater osteoclast activity in individuals exposed to nicotine. Together, these data indicate that exposure to nicotine in utero precipitates a negative bone phenotype associated with nutritional deficiency and anemia.Support or Funding InformationThis research was supported by the National Institutes of Health (NIH) National Institute of Dental and Craniofacial Research (NIDCR) [R03DE026192, 5T32DE017551 F31DE026684], National Center for Advancing Translational Sciences [UL1TR000062], and Plastic Surgery Foundation [Pilot Award 512114]. This study utilized the facilities and resources of the Medical University of South Carolina Center for Oral Health Research supported by the NIH/NIGM [P30GM103331].This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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