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The proliferation of sea lice (Lepeophtheirus salmonis) represents a major challenge for the salmonid aquaculture industry in Norway. Hydrogen peroxide (H 2 O 2 ) is a chemotherapeutant frequently used on Norwegian farms, however, its toxicity to non-target benthic species and habitats remains poorly understood. Maerl beds are constructed by the accumulation of non-geniculate coralline algae and provide important ecological functions. Due to the rapid expansion of aquaculture in Norway and the continued use of H 2 O 2 as an anti-sea lice treatment, it is crucial to understand the impact of H 2 O 2 on the physiology of maerl-forming species. The effects of a 1 h exposure to H 2 O 2 on the photophysiology and bleaching of the coralline alga Lithothamnion soriferum were examined here through a controlled time-course experiment. PAM fluorimetry measurements showed that H 2 O 2 concentrations ≥ 200 mg l -1 negatively affected photosystem II (PSII) in thalli immediately after exposure, which was observed through a significant decline in maximum photochemical efficiency (F v /F m ) and relative electron transport rate (rETR). The negative effects on PSII induced by oxidative stress, however, appear to be reversible, and full recovery of photosynthetic characteristics was observed 48 h to 28 days after exposure to 200 mg H 2 O 2 l -1 and 2000 mg H 2 O 2 l -1 , respectively. At 28 days after exposure, there was evidence of two- to four-times more bleaching in thalli treated with concentrations ≥ 200 mg H 2 O 2 l -1 compared to those in the control. This indicates that despite the recovery of PSII, persistent damages can occur on the structural integrity of thalli, which may considerably increase the vulnerability of coralline algae to further exposure to H 2 O 2 and other chemical effluents from salmonid farms., (Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.)

Increasing use of pharmaceutical drugs to delouse farmed salmon raises environmental concerns. This study describes an experiment carried out to elucidate the molecular mechanisms of the antiparasitic drug teflubenzuron on a non-target species, the European lobster. Juvenile lobsters (10.3±0.9 mm carapace length) were fed two environmentally relevant doses of teflubenzuron, corresponding to 5 and 20% of a standard salmon medication (10 mg/kg day), termed low and high dose in this study. After 114 days of dietary exposure, whole-animal accumulation of teflubenzuron was determined. One claw from each animal was collected for transcriptional analysis. Overall, exposed animals showed low cumulative mortality. Six animals, two from the low dose treatment and four from the high dose, showed exoskeletal abnormalities (claw deformities or stiff walking legs). Residual levels of teflubenzuron in juvenile lobster were 2.7-fold higher in the high dose (282 ng/g) compared to the low dose treatment (103 ng/g). The transcriptional examination showed significant effects of teflubenzuron on 21 out of 39 studied genes. At the transcriptional level, environmentally relevant levels of the anti-salmon lice drug impacted genes linked to drug detoxification (cyp3a, cyp6a2, cyp302a, sult1b1, abcc4), cellular stress (hsp70, hsp90, chh), oxidative stress (cat, gpx3) and DNA damage (p53), as well as molting and exoskeleton regulation (chi3l1, ecr, jhl1, chs1, ctbs, gap65, jhel-ces1) in claw tissue (muscle and exoskeleton). In conclusion, teflubenzuron at sub-lethal levels can affect many molecular mechanisms in European lobster claws., (Copyright © 2015 Elsevier B.V. All rights reserved.)

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., (Copyright © 2014 The Authors. Published by Elsevier B.V. All rights reserved.)