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Expression of aryl hydrocarbon receptor–regulated genes and superoxide dismutase in the Antarctic eelpout Pachycara brachycephalum exposed to benzo[a]pyrene

Strobel, Anneli, Mark, Felix C., Segner, Helmut, Burkhardt‐Holm, Patricia
Environmental toxicology and chemistry 2018 v.37 no.5 pp. 1487-1495
Pachycara, adverse effects, benzo(a)pyrene, biotransformation, body weight, exposure duration, fish, gene expression, genes, liver, metabolism, oxidative stress, pollutants, quantitative polymerase chain reaction, superoxide dismutase, xenobiotics, Antarctic region
The aryl hydrocarbon receptor (AhR) pathway mediates many, if not all, responses of fish to dioxin‐like compounds. The Southern Ocean is progressively exposed to increasing concentrations of anthropogenic pollutants. Antarctic fish are known to accumulate those pollutants, yet nothing is known about their capability to induce chemical biotransformation via the AhR pathway. The objective of the present study was to investigate whether Antarctic eelpout, Pachycara brachycephalum, respond to anthropogenic pollutants by activation of the AhR and its target gene cytochrome P4501A (CYP1A), and of superoxide dismutase (SOD), which served as a representative for oxidative stress. We exposed P. brachycephalum to 10 and 100 mg benzo[a]pyrene (BaP)/kg body weight for 10 d and measured the expression of AhR, CYP1A, and SOD in liver tissue via quantitative polymerase chain reaction. We identified two distinct AhR isoforms in the liver of P. brachycephalum. Antarctic eelpout responded to both BaP exposures by an up‐regulation of AhR and SOD, and by a particularly strong induction of CYP1A expression, which remained high until day 10 of the exposure time. Our data suggest that P. brachycephalum possesses the potential to up‐regulate xenobiotic biotransformation pathways, at least at the gene expression level. The time course of the AhR and CYP1A response points to an efficient but slow xenobiotics metabolism. Moreover, BaP exposure could include adverse effects such as oxidative stress. Environ Toxicol Chem 2018;37:1487–1495. © 2018 SETAC