A1 Journal article (refereed)
Exposure to retene, fluoranthene, and their binary mixture causes distinct transcriptomic and apical outcomes in rainbow trout (Oncorhynchus mykiss) yolk sac alevins (2022)

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. https://doi.org/10.1016/j.aquatox.2022.106083

JYU authors or editors

Publication details

All authors or editorsEriksson, Andreas N.M.; Rigaud, Cyril; Krasnov, Aleksei; Wincent, Emma; Vehniäinen, Eeva-Riikka

Journal or seriesAquatic Toxicology



Publication year2022


Article number106083


Publication countryNetherlands

Publication languageEnglish


Publication open accessOpenly available

Publication channel open accessPartially open access channel

Publication is parallel published (JYX)https://jyx.jyu.fi/handle/123456789/79608


Polycyclic aromatic hydrocarbons (PAHs) are widely spread environmental contaminants which affect developing organisms. It is known that improper activation of the aryl hydrocarbon receptor (AhR) by some PAHs contributes to toxicity, while other PAHs can disrupt cellular membrane function. The exact downstream mechanisms of AhR activation remain unresolved, especially with regard to cardiotoxicity. By exposing newly hatched rainbow trout alevins (Oncorhynchus mykiss) semi-statically to retene (32 µg l−1; AhR agonist), fluoranthene (50 µg l−1; weak AhR agonist and CYP1a inhibitor) and their binary mixture for 1, 3, 7 and 14 days, we aimed to uncover novel mechanisms of cardiotoxicity using a targeted microarray approach. At the end of the exposure, standard length, yolk area, blue sac disease (BSD) index and PAH body burden were measured, while the hearts were prepared for microarray analysis. Each exposure produced a unique toxicity profile. We observed that retene and the mixture, but not fluoranthene, significantly reduced growth by Day 14 compared to the control, while exposure to the mixture increased the BSD-index significantly from Day 3 onward. Body burden profiles were PAH-specific and correlated well with the exposure-specific upregulations of genes encoding for phase I and II enzymes. Exposure to the mixture over-represented pathways related to growth, amino acid and xenobiotic metabolism and oxidative stress responses. Alevins exposed to the individual PAHs displayed over-represented pathways involved in receptor signaling: retene downregulated genes with a role in G-protein signaling, while fluoranthene upregulated those involved in GABA signaling. Furthermore, exposure to retene and fluoranthene altered the expression of genes encoding for proteins involved in calcium- and potassium ion channels, which suggests affected heart structure and function. This study provides deeper understanding of the complexity of PAH toxicity and the necessity of investigating PAHs as mixtures and not as individual components.

Keywordsenvironmental toxinsPAH compoundsmixturesembryogenesistranscriptomerainbow troutecotoxicology

Free keywordsMixture; Retene; Fluoranthene; PAH; Oncorhynchus mykiss; Early life development

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Ministry reportingYes

Reporting Year2022

JUFO rating1

Last updated on 2024-14-06 at 23:25