title: Physiology and mRNA expression in rainbow trout (Oncorhynchus mykiss) after long-term exposure to the new antifoulant medetomidine.
abstract: Medetomidine is under evaluation for use as an antifouling agent, and its effects on non-target aquatic organisms are therefore of interest. In this study, rainbow trout was exposed to low (0.5 and 5.0nM) concentrations of medetomidine for up to 54 days. Recently we have reported on effects on paleness and melanophore aggregation of medetomidine in these fish. Here, specific growth rates were investigated together with a broad set of physiological parameters including plasma levels of growth hormone (GH), insulin-like growth factor-I (IGF-I) and leptin, glucose and haemoglobin (Hb), hematocrit (Ht), condition factor, liver and heart somatic indexes (LSI, HSI). Hepatic enzyme activities of CYP1A (EROD activity), glutathione S-transferases (GST) and glutathione reductase (GR) were also measured. Additionally, hepatic mRNA expression was analysed through microarray and quantitative PCR in fish sampled after 31 days of exposure. Medetomidine at both concentrations significantly lowered blood glucose levels and the higher concentration significantly reduced the LSI. The mRNA expression analysis revealed few differentially expressed genes in the liver and the false discovery rate was high. Taken together, the results suggest that medetomidine at investigated concentrations could interfere with carbohydrate metabolism of exposed fish but without any clear consequences for growth.
authors.affiliation: Department of Zoology/Zoophysiology, University of Gothenburg, Sweden. anna.lennquist@zool.gu.se
authors.forename: Anna
authors.initials: A
authors.lastname: Lennquist
authors.forename: Noomi
authors.initials: N
authors.lastname: Asker
authors.forename: Erik
authors.initials: E
authors.lastname: Kristiansson
authors.forename: Adam
authors.initials: A
authors.lastname: Brenthel
authors.forename: Björn Thrandur
authors.initials: BT
authors.lastname: Björnsson
authors.forename: Peter
authors.initials: P
authors.lastname: Kling
authors.forename: Maria
authors.initials: M
authors.lastname: Hultman
authors.forename: D G Joakim
authors.initials: DG
authors.lastname: Larsson
authors.forename: Lars
authors.initials: L
authors.lastname: Förlin
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D019363:Cytochrome P-450 CYP1A1 / Q000235:genetics; D004305:Dose-Response Relationship, Drug; D004781:Environmental Exposure; D015870:Gene Expression / Q000187:drug effects; D005980:Glutathione Reductase / Q000235:genetics; D005982:Glutathione Transferase / Q000235:genetics; D013006:Growth Hormone / Q000097:blood; D006400:Hematocrit; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D020738:Leptin / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D020926:Medetomidine / Q000633:toxicity*; D017686:Oncorhynchus mykiss / Q000235:genetics / Q000254:growth & development / Q000502:physiology*; D012333:RNA, Messenger; D014874:Water Pollutants, Chemical / Q000633:toxicity
chemical_list: D001786:Blood Glucose; D020738:Leptin; D012333:RNA, Messenger; D014874:Water Pollutants, Chemical; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D019363:Cytochrome P-450 CYP1A1; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D020926:Medetomidine