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Alternative Title

How PAHs (polycyclic aromatic hydrocarbons) impact craniofacial development

Publication Date

2017-5

First Advisor

Michael J.F. Barresi

Document Type

Honors Project

Degree Name

Bachelor of Arts

Department

Biological Sciences

Keywords

Napthalene, Polycyclic aromatic hydrocarbons, Birth defects, Teratogenesis, Environmental science, Developmental biology, Chemistry, Polycyclic aromatic hydrocarbons-Physiological effect, Head-Abnormalities, Face-Abnormalities

Abstract

Craniofacial anomalies encompass a variety of structural and sensory defects of the lip, jaw, head cartilage, and bone (n.a., 2017). Many craniofacial anomalies have been linked to prenatal exposure to teratogens: environmental factors that lead to embryonic defects (GilbertBarness, 2010). During embryonic development, proper formation of the pharyngeal system, including arches, pouches, and placodes, is crucial for craniofacial development, as it generates the craniofacial structures and associated sensory neurons (Holzchuh, et al., 2005). In zebrafish, development of the pharyngeal arches and placodes rely upon the initiation and growth of pharyngeal pouches, which occurs when the pharyngeal endoderm receives various cellular regulatory signals to undergo actin web-assisted migration (Berg, 2016).

It has been demonstrated that the development of craniofacial structures are sensitive to environmental teratogens, such as the main fossil fuel chemical, polycyclic aromatic hydrocarbons [PAHs]. We have shown that zebrafish embryos exposed to either water accommodated fractions of crude oil or individual PAHs result in the malformation of craniofacial structures (De Soysa, et al.; 2012, Chen, 2014; Berg, 2016). More specifically, naphthalene, a ubiquitously found PAH, caused a loss in the most posterior cartilage elements. However, it had been unknown what aspects of the pharyngeal system are impacted by naphthalene exposure. We showed previously that naphthalene may be first interfering with the formation of the pharyngeal pouches, which leads to a failure in the proper separation of the last two arches. The aforementioned naphthalene-treated embryos have disorganized pouches that lack proper slit-like morphology and a loss of the posterior-most arch. Staining for F-actin filaments revealed that naphthalene caused disorganized actin webs within the pouch endoderm. In contrast, gene and protein marker analyses of placode development suggested that placode development was overall normal. The results suggested that naphthalene-induced craniofacial teratogenesis is primarily due to malformations in pouch development.

Language

English

Comments

80 pages : illustrations (chiefly color). Includes bibliographical references (pages 74-80)

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