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Assessing the Role of Estrogen Signaling in the Developmental Toxicity of Oil in Fish

Abstract

Oil spills are one of the primary sources of polycyclic aromatic hydrocarbons (PAHs) in marine environments. PAHs are subject to biotic and abiotic weathering that can alter their physical and chemical characteristics. Due to photochemical reactions and microbial activity PAHs can undergo oxidation forming oxygenated products that can have severe effects on marine life and the environment. Previous studies have indicated that weathered oil can cause greater developmental toxicity than source oil. Among the PAHs found in crude oil, chrysene is one of the most persistent in the water column and can undergo photo-oxidation to produce oxygenated derivatives such as 2-hydroxychrysene and 6-hydroxychrysene, which possess respective estrogenic and antiestrogenic properties. The endocrine system regulates many signaling processes that control the development of cardiovascular immune, reproductive and central nervous systems. The integrated role of various biological systems and the interaction between organs can make it difficult to assess the effects of endocrine disrupting compounds (EDCs) especially when a series of signaling events need to occur in a precise spatio-temporal manner during embryogenesis. To assess the role of estrogen signaling in the effects of hydroxychrysene, estradiol toxicity was first characterized using zebrafish. Here we showed that although disruption of estrogen signaling can result in significant malformations, the toxic effects of 2-hydroxychrysene and 6-hydroxychrysene were not directly mediated through this pathway. Additionally, studies evaluating microRNA regulation of mRNA expression, indicated disruption of ion transport may be critical step in the cardiovascular toxicity caused by oil. These findings raise the need to utilize genomic and epigenomic tools to identify mechanisms that are involved in the toxicity of these compounds to assess the potential risks of oil spills on fish populations.

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