G5 Doctoral dissertation (article)
A multi-omics approach to understand PAH toxicity in rainbow trout (Oncorhynchus mykiss) alevins (2022)
Omiikat apuna PAH-yhdisteiden toksisuusmekanismien selvittämiseen kirjolohen (Oncorhynchus mykiss) poikasissa

Eriksson, A. (2022). A multi-omics approach to understand PAH toxicity in rainbow trout (Oncorhynchus mykiss) alevins [Doctoral dissertation]. University of Jyväskylä. JYU Dissertations, 523. http://urn.fi/URN:ISBN:978-951-39-9159-3

JYU authors or editors

Publication details

All authors or editors: Eriksson, Andreas

eISBN: 978-951-39-9159-3

Journal or series: JYU Dissertations

eISSN: 2489-9003

Publication year: 2022

Number in series: 523

Number of pages in the book: 1 verkkoaineisto (111 sivua, 26 sivua useina numerointijaksoina, 19 numeroimatonta sivua)

Publisher: University of Jyväskylä

Place of Publication: Jyväskylä

Publication country: Finland

Publication language: English

Persistent website address: http://urn.fi/URN:ISBN:978-951-39-9159-3

Publication open access: Openly available

Publication channel open access: Open Access channel

Abstract

Polycyclic aromatic hydrocarbons (PAHs) are a group of environmental contaminants originating from incomplete combustion or pyrolysis of organic material, as well as intentional or accidental release of crude oil or industrial spillage and effluents. Exposure to PAHs is known to cause toxicity in developing fish larvae, which includes reduced heart rate, increased occurrence of blue sac disease (BSD) symptoms, as well as altered morphology and behavior. The exact mechanisms of PAH-mediated toxicity, in fish larvae, are still not fully understood, even after decades of research. In this doctoral thesis, the toxicity of two PAHs, with different modes of action (retene: an aryl hydrocarbon receptor 2, Ahr2, agonist; and fluoranthene: a weaker Ahr2 agonist and a cytochrome P450a1, Cyp1a, inhibitor), either alone or as a mixture, were investigated in newly hatched rainbow trout (Oncorhynchus mykiss) alevins. Multiple endpoints, including development and growth, BSD, heart function and PAH accumulation, were investigated in relation to how the cardiac transcriptome, proteome, and metabolome responded. Each treatment resulted a unique toxicity profile, while that the mixture was more potent at inducing toxicity than the components. The transcriptome, proteome and metabolome responded in an exposure specific manner. Alterations in heart function and accumulation of the PAHs were a direct consequence of, and could be explained by, changes in the exposure specific upregulations and enrichments. Additionally, we found a specific metabolite, known as FICZ (an Ahr2 agonist that causes PAH and dioxin-like toxicity), which could contribute to toxicity, accumulated following exposure to the mixture. Restrictions in energy availability is implied as per numerous enrichments and upregulations, suggesting impaired yolk consumption, which in turn could influence growth and development negatively. These findings, as presented within this doctoral thesis, extend our understanding of how PAH, alone or as a mixture, induces toxicity in developing rainbow trout alevins.

Keywords: environmental toxins; PAH compounds; toxicity; rainbow trout; animal young; growth disorders; genomics; proteomics; developmental biology; ecotoxicology; doctoral dissertations

Free keywords: cardiotoxicity; PAHs; proteome; rainbow trout; transcriptome; metabolome

Contributing organizations

Ministry reporting: Yes

Reporting Year: 2022