Whole-animal accumulation, oxidative stress, transcriptomic and metabolomic responses in the pink shrimp (Pandalus montagui) exposed to teflubenzuron.

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.

Mortality and deformities in European lobster (Homarus gammarus) juveniles exposed to the anti-parasitic drug teflubenzuron.

This study describes experiments carried out to examine effects of the antiparasitic drug teflubenzuron, used in delousing farmed salmon, on a non-target species, the European lobster (Homarus gammarus). Juvenile lobsters were fed two doses of teflubenzuron, 10 and 20mg/kg successively for 7 days corresponding to a standard medication of the fish (10mg/kg day) and twice the standard dose (20mg/kg day). Monitoring lasted 3 months to include at least one moulting period for all individuals. Cumulative mortality was higher in all replicates given medicated feed compared with the control group. Mean cumulative mortality for each dosing was 41 ± 13% for 10mg/kg and 38 ± 8% for 20mg/kg, i.e. no difference. Drug residue was analysed in all juveniles that died, in addition to 12 juveniles at day 8 and the first 12 surviving lobsters. A decline in concentration of teflubenzuron from over 8,000 ng/g (day 5) to 14 ng/g (day 70) was observed in the juveniles that died during the experiment. Twelve individuals that died contained 82 ng/g or less whereas the mean concentration in the first 12 lobsters that survived moulting was 152 ng/g. Following a single oral administration, the half-life of teflubenzuron in lobster was estimated to 3.4 days and the initial concentration (C0) to 515 ng/g at time t0. At the end of the study a considerable number of juvenile lobsters were observed with deformities in various organs; carapace, walking legs, cheliped, tail fan, abdomen and antenna. The occurrence of observed deformities varied from 0 to 15% in treated replicates and will most likely affect ability to locate and consume food (antenna, claw and walking legs), respiration (carapace) and ability to move/swim (walking legs, tail fan and abdomen). In total, the mortality and senescent damages were close to 50% in all replicates. Juveniles that survived medication without deformities however, moulted and increased in size at each moult equally well as the unmedicated controls.