Department Environmental Toxicology

Fish play a key role in the environmental risk assessment of chemicals, with impacts on survival and growth being measured in laboratory experiments as a proxy for fish population health. However, laboratory animal experiments are ethically problematic, very resource intensive in terms of manpower, time, testing volumes, etc., and a significant bottleneck in chemical risk assessment, a fact that is increasingly recognized by regulatory agencies worldwide. Fish cell-based model strategies that use permanent fish cell lines can significantly reduce, if not eliminate, the need for animal experimentation.

In this project, we wish to shed light on the molecular response networks activated inside fish cells upon chemical exposure and leading to reduced cell population growth. For this purpose, we make use of the permanent, epithelia-like RTgill-W1 cell line, which was shown by our research group to be an excellent proxy for reduced fish growth. A well-rounded systems toxicology approach is applied to achieve our objectives. This approach combines chemical exposure of cells, followed by cell-based morphological and functional high-throughput profiling and genome-wide gene expression analysis as building blocks for mechanistic networks.

The following research objectives have been set:

To identify molecular pathways leading to reduced fish cell population growth upon exposure to different chemicals

To identify at which level (transcriptional, translational, phenotype) these pathways converge to cause reduced fish cell population growth

To establish whether the same molecular pathways are also active in growth retardation in fish in vivo.