A multi-omics approach to understand PAH toxicity in rainbow trout (Oncorhynchus mykiss) alevins
Julkaistu sarjassa
JYU dissertationsTekijät
Päivämäärä
2022Tekijänoikeudet
© The Author & University of Jyväskylä
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: Cardiotoxicity; metabolome; mixture; PAHs; proteome; rainbow trout; transcriptome
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Julkaisija
Jyväskylän yliopistoISBN
978-951-39-9159-3ISSN Hae Julkaisufoorumista
2489-9003Julkaisuun sisältyy osajulkaisuja
- Artikkeli I: Eriksson, A. N., Rigaud, C., Krasnov, A., Wincent, E., & Vehniäinen, E.-R. (2022). Exposure to retene, fluoranthene, and their binary mixture causes distinct transcriptomic and apical outcomes in rainbow trout (Oncorhynchus mykiss) yolk sac alevins. Aquatic Toxicology, 244, Article 106083. DOI: 10.1016/j.aquatox.2022.106083
- Artikkeli II: Eriksson, A. N., Rigaud, C., Rokka, A., Skaugen, M., Lihavainen, J. H., & Vehniäinen, E.-R. (2022). Changes in cardiac proteome and metabolome following exposure to the PAHs retene and fluoranthene and their mixture in developing rainbow trout alevins. Science of the Total Environment, 830, Article 154846. DOI: 10.1016/j.scitotenv.2022.154846
- Artikkeli III: Eriksson A.N.M., Rigaud C., Wincent E., Pakkanen H., Salone n P. & Vehniäinen E-R. Endogenous AhR agonist FICZ accumulates in rainbow trout ( Oncorhynchus mykiss ) alevins exposed to a mixture of two PAHs, retene and fluoranthene. Submitted manuscript.
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Endogenous AhR agonist FICZ accumulates in rainbow trout (Oncorhynchus mykiss) alevins exposed to a mixture of two PAHs, retene and fluoranthene
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