title: Biomarker responses and disease susceptibility in juvenile rainbow trout Oncorhynchus mykiss fed a high molecular weight PAH mixture.
abstract: Juvenile rainbow trout were fed a diet containing an environmentally relevant mixture of 10 high molecular weight polycyclic aromatic hydrocarbons (PAHs) at a dose of 0.66 or 7.82 µg PAH · g fish(-1) · d(-1). At 3, 7, 14, and 28 d, biomarkers of aryl hydrocarbon receptor activation (AHR), hepatic microsomal ethoxyresorufin-O-deethylase (EROD) activity, and cytochrome P4501A (CYP1A)-associated staining increased 14- to 26-fold and 6- to 14-fold, respectively, in fish fed 7.82 µg PAH · g fish (-1) · d(-1). Cytochrome P4501A-associated staining increased 2- to 9-fold on days 3, 7, and 28 in fish fed 0.66 µg PAH · g fish(-1) · d(-1). Bile fluorescent aromatic compounds served as a biomarker of exposure and confirmed that PAH exposure was consistent over 50 d. DNA damage in blood cells, protein oxidation, and lipid peroxidation in the kidney were biomarkers of oxidative stress and all increased in fish fed 7.82 µg PAH · g fish(-1) · d(-1). Fish fed 0.66 µg PAH · g fish(-1) · d(-1) had elevated DNA damage in blood cells but increased protein oxidation or lipid peroxidation in the kidney were not observed. Challenge with Aeromonas salmonicida, at lethal concentration (LC) 20, decreased survival in fish previously fed either 0.66 µg PAH · g fish(-1) · d(-1) or 7.82 µg PAH · g fish(-1) · d(-1) relative to fish fed the control diet. In general, biomarkers of both AHR activation and oxidative stress peaked at 3 to 14 d then declined at 28 to 50 d of PAH exposure and an increase in susceptibility to disease was observed at 50 d. These results link PAH exposure to biomarker responses that may be useful as early indicators of population level responses, such as mortality resulting from an increase in disease susceptibility.
authors.affiliation: Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, Oregon, USA. claudia.f.bravo@gmail.com
authors.forename: C F
authors.initials: CF
authors.lastname: Bravo
authors.forename: L R
authors.initials: LR
authors.lastname: Curtis
authors.forename: M S
authors.initials: MS
authors.lastname: Myers
authors.forename: J P
authors.initials: JP
authors.lastname: Meador
authors.forename: L L
authors.initials: LL
authors.lastname: Johnson
authors.forename: J
authors.initials: J
authors.lastname: Buzitis
authors.forename: T K
authors.initials: TK
authors.lastname: Collier
authors.forename: J D
authors.initials: JD
authors.lastname: Morrow
authors.forename: C A
authors.initials: CA
authors.lastname: Laetz
authors.forename: F J
authors.initials: FJ
authors.lastname: Loge
authors.forename: M R
authors.initials: MR
authors.lastname: Arkoosh
mesh_terms: D048409:Aeromonas salmonicida; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D019363:Cytochrome P-450 CYP1A1 / Q000378:metabolism; D004198:Disease Susceptibility; D004305:Dose-Response Relationship, Drug; D004784:Environmental Monitoring; D062665:Epidemiological Monitoring; D028441:F2-Isoprostanes / Q000378:metabolism; D005393:Fish Diseases / Q000453:epidemiology* / Q000378:metabolism / Q000382:microbiology; D016905:Gram-Negative Bacterial Infections / Q000453:epidemiology* / Q000378:metabolism; D017686:Oncorhynchus mykiss / Q000378:metabolism* / Q000382:microbiology; D011084:Polycyclic Aromatic Hydrocarbons / Q000008:administration & dosage / Q000378:metabolism / Q000633:toxicity*; D018336:Receptors, Aryl Hydrocarbon / Q000378:metabolism; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism; D014874:Water Pollutants, Chemical / Q000008:administration & dosage / Q000378:metabolism / Q000633:toxicity*
chemical_list: D015415:Biomarkers; D028441:F2-Isoprostanes; D011084:Polycyclic Aromatic Hydrocarbons; D018336:Receptors, Aryl Hydrocarbon; D014874:Water Pollutants, Chemical; C002744:3-nitrotyrosine; D014443:Tyrosine; D019363:Cytochrome P-450 CYP1A1