title: Water-borne diclofenac affects kidney and gill integrity and selected immune parameters in brown trout (Salmo trutta f. fario).
abstract: The detection of residues of various pharmaceuticals in surface waters during the last two decades has prompted concerns about possible adverse effects of this kind of pollution on aquatic organisms. The objective of the present study was to investigate effects of the non-steroidal anti-inflammatory drug diclofenac, one of the pharmaceuticals most prevalent in surface waters, on brown trout (Salmo trutta f. fario), a salmonid species native to German rivers. Brown trout were exposed to 0.5, 5 and 50 microg/L diclofenac for 7, 14 and 21 days, whereby the lowest exposure concentration is comparable with concentrations commonly found in the aquatic environment. Fish exposed to diclofenac displayed significantly reduced haematocrit levels after 7 and 14 days of exposure. After 21 days, trout were examined for histopathological alterations, whereby diclofenac exposure resulted in increased monocyte infiltration in the liver, telangiectasis in gills, and the occurrence of interstitial hyaline droplets, interstitial proteinaceous fluid and mild tubular necrosis in trunk kidney. Concurrent immunohistological analysis revealed an increase of granulocyte numbers in primary gill filaments, as well as granulocyte accumulation and increased major histocompatibility complex (MHC) II expression in kidney, suggestive of an inflammatory process in these organs. Moreover, the ability of diclofenac to hinder the stimulation of prostaglandin E2 synthesis was shown in head kidney macrophages of brown trout in vitro. These findings support the hypothesis that environmental exposure of fish to diclofenac provokes the same mechanism of action in these non-target organisms as previously described for mammalian species and can thus lead to similar (possibly adverse) effects. In general, the present study suggests that exposure of brown trout to diclofenac in concentration ranges commonly found in the environment can result in adverse effects in various organs and possibly compromise the health of affected fish populations.
authors.affiliation: Environmental Toxicology, University of Konstanz, Konstanz, Germany.
authors.forename: Birgit
authors.initials: B
authors.lastname: Hoeger
authors.forename: Bernd
authors.initials: B
authors.lastname: Köllner
authors.forename: Daniel R
authors.initials: DR
authors.lastname: Dietrich
authors.forename: Bettina
authors.initials: B
authors.lastname: Hitzfeld
mesh_terms: D000818:Animals; D004008:Diclofenac / Q000633:toxicity*; D015232:Dinoprostone / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004781:Environmental Exposure; D004797:Enzyme-Linked Immunosorbent Assay; D005786:Gene Expression Regulation / Q000187:drug effects*; D005802:Genes, MHC Class II / Q000235:genetics; D005858:Germany; D005880:Gills / Q000187:drug effects*; D006098:Granulocytes / Q000187:drug effects; D007150:Immunohistochemistry; D007668:Kidney / Q000187:drug effects*; D009113:Muramidase / Q000097:blood; D045483:Rivers; D014337:Trout / Q000276:immunology / Q000378:metabolism*; D014874:Water Pollutants, Chemical / Q000633:toxicity*
chemical_list: D014874:Water Pollutants, Chemical; D004008:Diclofenac; D009113:Muramidase; D015232:Dinoprostone