Abstract

A luciferase reporter gene-based bioassay battery consisting of stress-activated receptors from fish, complemented with traditional fish cell-based bioassays, were used to assess the toxicity of marine sediment samples from the Byfjorden area around the city of Bergen (Norway). The reporter assays covered a wide range of cellular signalling and metabolic pathways, representing different molecular initiating events in the adverse outcome pathway framework. Cytotoxicity, generation of reactive oxygen-species, and induction of 7-ethoxyresorufin-O-deethylase activity were analysed using fish liver and gill cell lines. Chemical analyses of the sediment extracts revealed complex contamination profiles, especially at the innermost stations, which contained a wide array of persistent organic pollutants, polycyclic aromatic hydrocarbons, and metals. Sediment extracts from these sites were more potent in activating the stress-activated receptors than the other extracts, reflecting their toxicant profiles. Importantly, receptor- and cell-based bioassays complemented the chemical analyses and provided important data for future environmental risk assessments of urban marine sediments.

Highlights

  • The marine environment has been a sink for environmental pollut­ ants originating from anthropogenic activities for generations

  • Traditional fish cell-based bioassays were com­ plemented with luciferase-based reporter gene assays using a battery of stress-activated receptors from Atlantic cod and zebrafish to investigate the presence of bio-active pollutants in sediments from contaminated sites within the Bergen Byfjorden area

  • Previous analyses have demonstrated that Bergen Byfjorden contains high levels of poly­ cyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCB), and heavy metals such as lead, mercury and cadmium, and is regarded as a polluted fjord according to the Water Framework Directive (WFD) (Jartun et al, 2009; Jartun and Pettersen, 2010)

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Summary

Introduction

The marine environment has been a sink for environmental pollut­ ants originating from anthropogenic activities for generations. Chemical analyses cannot be used as the only strategy to evaluate environmental quality as current methodolo­ gies are not able to identify every single chemical present, nor the bioavailability of pollutants, and importantly, possible biological ef­ fects, including additive, synergistic, potentiating, or antagonistic in­ teractions that may occur when organisms are exposed to mixtures of compounds (Chapman, 2007). Responses taking place at these levels are considered the first manifes­ tation of toxicity. They often involve stress-activated transcription fac­ tors such as the aryl hydrocarbon receptor (AHR) or nuclear receptors (NRs), which can be used in the development of molecular tools that can be applied for the early and sensitive detection of chemical exposures (Fent, 2001). Different receptor and cell-based bioassays, using fish and human cell models, have previously been successfully used to estimate the biological activity of sediment-bound pollutants, integrating their interactions and covering endpoints such as acute and long-term toxicity, oxidative-stress, bioaccumulation, and endocrine disrupting effects (Creusot et al, 2010; Schnell et al, 2013; Fernandes et al, 2014; Perez-Albaladejo et al, 2016; Blanco et al, 2018)

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