Abstract
Chemotherapeutics, such as the chitin synthesis inhibitor teflubenzuron, are widely used in marine aquaculture to control parasitic salmon lice. However, these compounds may also harm non-target species like Calanus finmarchicus, a keystone copepod in Arctic and boreal ecosystems. With growing environmental stress from climate change and pollution, it is critical to understand the mechanisms behind such impacts to improve ecological risk assessments.
This study explored the effects of teflubenzuron on C. finmarchicus, using Adverse Outcome Pathway (AOP) 360, “Inhibition of chitin synthase 1 leading to increased mortality,” as a knowledge organizing framework. Over a seven-day sub-acute exposure, we assessed mortality, development, morphology, and gene expression linked to molting processes in the copepod.
Teflubenzuron exposure at ≥0.012 µg/L caused significant mortality, disrupted development, and led to visible deformities. It also altered the expression of genes involved in molting and chitin metabolism. However, no significant changes in chs1 gene expression were detected at concentrations between 0.001 and 0.012 µg/L. Thus, we could not directly link chs1 inhibition to the observed effects as described in AOP 360.
Further studies are needed to clarify molecular mechanisms related to teflubenzuron toxicity and validate AOP 360’s relevance for C. finmarchicus.