Effects of 3,3′,4,4′,5,5′‐hexachlorobiphenyl on cytochrome P4501A and estrogen‐induced vitellogenesis in rainbow trout (<i>Oncorhynchus mykiss</i>)

Donohoe, Regina M.; Wang-Buhler, Jun-Lan; Buhler, Donald R.; Curtis, Lawrence R.

doi:10.1002/etc.5620180532

Cited by 7 publications

(3 citation statements)

References 48 publications

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“…Bile fluorescent aromatic compounds confirmed PAH exposure. Induction of EROD activity and CYP1A protein [22] were selected to assess AHR activation. Oxidative damage to DNA, protein, and lipids was assessed with the comet assay, tissue 3-nitrotyrosine content (3-NT), and F 2 -isoprostanes, respectively.…”

Section: Introductionmentioning

confidence: 99%

Biomarker responses and disease susceptibility in juvenile rainbow trout Oncorhynchus mykiss fed a high molecular weight PAH mixture

Bravo

Curtis

Myers

et al. 2011

Enviro Toxic and Chemistry

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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.

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Section: Introductionmentioning

confidence: 99%

Biomarker responses and disease susceptibility in juvenile rainbow trout Oncorhynchus mykiss fed a high molecular weight PAH mixture

Bravo

Curtis

Myers

et al. 2011

Enviro Toxic and Chemistry

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“…In juvenile rainbow trout treated with a range of PCB 169 doses, the LSI increased almost progressively with the administered doses. The exception was the lowest dose of 250 g/kg, which did not produce LSI change [28]. Similarly, in white perch treated with a high dose of PCB 77, the ovarian development was so severely affected by the contaminant that fewer females matured, and those fish that reached maturity had lower GSI than control females.…”

Section: Pcb 126 Effect On Gsi and Lsimentioning

confidence: 94%

Hepatic P4501a Activity, Plasma Sex Steroids, and Gonadal Steroidogenesis in Vitro in Yellow Perch Exposed to 3,3′,4,4′,5-Pentachlorobiphenyl

Dabrowska¹,

Fisher²,

Ciereszko³

et al. 2000

Environ Toxicol Chem

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Abstract-Yellow perch were given a single intraperitoneal injection of polychlorinated biphenyl (PCB) 126 dissolved in corn oil at nominal concentrations of 0, 10, 100, and 500 g/kg body weight. Following the injection, the fish were held for four weeks under photothermal conditions characteristic for Ohio, USA, and fed a commercial fish food. Thereafter, they were sacrificed to examine the PCB 126 concentrations in the liver and to assess the contaminant effects on hepatic P4501A activity, reproductive hormones in plasma, and steroidogenic potential of gonads. The administered doses resulted in liver concentrations of 0.8 (corn oil control), 12.1, 38.9, and 174.5 g/kg wet tissue weight. Hepatic P4501A indices were differentially affected depending on both the PCB 126 dose and fish gender. In untreated fish, the P4501A protein and ethoxyresorufin-O-deethylase activity were several times lower in females than in males. In treated males, the hepatic P4501A was inhibited by all three PCB 126 doses. In females, a significant P4501A induction occurred in those dosed with 10 g/kg, while no changes were found in the two higher-dosed female groups in comparison to controls. A significant negative correlation was observed between hepatic P4501A indices and gonad somatic indexes values and plasma estradiol concentrations. The PCB 126 administration produced alterations in concentrations of plasma sex hormones in females but not in males. The in vitro steroidogenic potential of the female and male gonads was not affected by the in vivo PCB 126 treatment.

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“…Note: Rank of potential in vitro risk is the product of ͑Estradiol equivalent͒ x ͑Mean effluent concentration͒ whereas rank of potential in vivo effect is the product of ͑Estradiol equivalent in trout vitellogenin response͒ x ͑Mean effluent concentration͒. Harries et al 1996Harries et al , 1997Routledge et al 1998;Allen et al 1999;Noaksson et al 2001͒ • Gonadosomatic index: ͑Harries et al 1997Gibbons et al 1998aGibbons et al , 1998bNoaksson et al 2001;Sepulveda et al 2003;Sheahan et al 2002a͒ • Hepatosomatic index: ͑Gibbons et al 1998a, 1998bAllen et al 1999;Donohoe et al 1999;Sheahan et al 2002a, 2003͒ • Estrogen: ͑Williams et al 1998Nichols et al 1999;Sepulveda et al 2003͒ • Testosterone: ͑Folmar et al 1996Williams et al 1998;Nichols et al 1999;Dube and MacLatchy 2000;Sepulveda et al 2003͒ • Egg fecundity: ͑Gibbons et al 1998bWesterlund et al 2000;Sepulveda et al 2003͒ • Size: ͑Gibbons et al 1998aKarels et al 2001;Noaksson et al 2001͒ • Physical abnormalities: ͑Kelly and Di Giulio 2000; Noaksson et al 2001;Sepulveda et al 2003͒ • Development: ͑Allen et al 1999Metcalfe et al 2000Metcalfe et al , 2001Noaksson et al 2001͒ • Response compared to control samples. Although the production of VTG and the alterations in GSI and HSI are widely used as biomarkers for endocrine disruption, to what degree they adversely affect organismal characteristics and higher organizational levels remain unclear.…”

Section: Occurrence and Biological Effects In The Environmentmentioning

confidence: 99%

Occurrence and Effects of Endocrine Disrupting Chemicals in the Environment

Huang

Elrod

2003

Pract. Period. Hazard. Toxic Radioact. Waste Manage.

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This review focuses on environmental chemicals that mimic the activity of the endogenous estrogen, 17␤-estradiol ͑E2͒, and their effects on wildlife, because it is the most studied area of endocrine disruption. The potential human health impact of endocrine disruptors is beyond the scope of this paper and readers should refer to other publications as reported by Crisp et al. in 1998 and Safe in 1995. The concentrations of endocrine disrupting chemicals in effluents from sewage treatment plants ͑STPs͒ are summarized and compared. By utilizing in vitro and in vivo assays, environmental estrogens from STPs and other point source pollutants have been shown to induce reproductive abnormalities in fish and wildlife. Though treatment systems of sewage facilities can reduce the amounts of endocrine disrupting chemicals, the removal efficiency can still be improved to further reduce estrogenic effects upon aquatic organisms. Up to date, a lack of comprehensive research impedes the ability to correlate estrogenic chemicals to community-and ecosystem-level effects. Thus, total ecosystem evaluations such as species diversity and impact on keystone species and understudied nonpoint source pollution should be two primary focuses of future research.

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Effects of 3,3′,4,4′,5,5′‐hexachlorobiphenyl on cytochrome P4501A and estrogen‐induced vitellogenesis in rainbow trout (Oncorhynchus mykiss)

Cited by 7 publications

References 48 publications

Biomarker responses and disease susceptibility in juvenile rainbow trout Oncorhynchus mykiss fed a high molecular weight PAH mixture

Biomarker responses and disease susceptibility in juvenile rainbow trout Oncorhynchus mykiss fed a high molecular weight PAH mixture

Hepatic P4501a Activity, Plasma Sex Steroids, and Gonadal Steroidogenesis in Vitro in Yellow Perch Exposed to 3,3′,4,4′,5-Pentachlorobiphenyl

Occurrence and Effects of Endocrine Disrupting Chemicals in the Environment

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