The benzoylurea
chitin synthesis inhibitor
teflubenzuron, widely used against sea lice in North Atlantic aquaculture, may pose an environmental threat to non-targeted crustaceans. In this experiment, laboratory acclimated pink shrimp (Pandalus montagui), a species found in fjords with Atlantic salmon farming, were exposed to dietary
teflubenzuron for 46 days (control; low dose: 0.01 μg/g; high dose: 0.1 μg/g). The exposure doses represent 0.1% and 1% of a standard treatment dose for Atlantic salmon. Mortality and prevalence of
deformities, pharmacokinetics, oxidative stress and transcriptomic and metabolomic profiling were used to assess the response to
teflubenzuron exposure. Mortality in the high-dose group was 25% (five of 20 individuals). No control or low-dose group shrimps died. Phenotypic responses,i.e., leg
deformities (0 control, 6 low, 8 high) and cloudy eyes (0 control, 3 low, 7 high), were observed in some surviving shrimps (control n = 15, low n = 17, high n = 15). Accumulated levels of
teflubenzuron in shrimps from the high-dose group ranged from 4.7 to 369 ng/g wet weight. Transcriptomic profiling showed very few significantly altered genes in the exposed shrimps.
Teflubenzuron-induced changes to the metabolome pointed to well-known effects of benzoylurea agents, with reduced levels of
N-acetylglucosamine indicating an effect on
chitin synthesis. The metabolomic profiling showed that
teflubenzuron exposure was associated with reduced energy metabolism. Some metabolites pointed to increased
necrosis and/or bacterial overgrowth in the
teflubenzuron-exposed shrimps. In conclusion, this study shows that
teflubenzuron causes phenotypic effects in P. montagui exposed to 0.1% of the treatment dose given to Atlantic salmon.