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Träfflista för sökning "WFRF:(Förlin Lars 1950 ) ;pers:(Celander Malin C. 1962)"

Sökning: WFRF:(Förlin Lars 1950 ) > Celander Malin C. 1962

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1.
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2.
  • Lennquist, Anna, 1978, et al. (författare)
  • Effects of medetomidine on hepatic EROD activity in three species of fish
  • 2008
  • Ingår i: Ecotoxicology and Environmental Safety. - : Elsevier BV. - 0147-6513. ; 69:1, s. 74-79
  • Tidskriftsartikel (refereegranskat)abstract
    • Medetomidine, an antifouling candidate, was investigated for its effects on cytochrome P4501A (CYP1A) activity in fish. Rainbow trout (Oncorhynchus mykiss), turbot (Psetta maxima), and Atlantic cod (Gadus morhua) were exposed to medetomidine either via i.p. injection (o5 mmol (1 mg)/kg) or via water (o50 nM). Enzyme activity was measured as ethoxyresorufin-O-deethylase (EROD) activity in liver microsomes. There was a small (2–7-fold) increase in EROD activity in rainbow trout. In turbot, EROD activity increased (4- fold) after injection, while a non-significant (50%) decrease was observed after water exposure. No effects on EROD activities were observed in Atlantic cod. In vitro inhibition studies of EROD activities in liver microsomes from all three species showed that medetomidine was a very potent CYP1A inhibitor. Thus, median inhibition values (IC50) were 35710nM for rainbow trout, 47717nM for turbot, and 111770nM for Atlantic cod. These observed effects suggest that medetomidine interferes with CYP1A-dependent metabolism of xenobiotics in these fish species.
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3.
  • Stephensen, Eiríkur, et al. (författare)
  • Biomarker responses and chemical analyses in fish indicate leakage of polycyclic aromatic hydrocarbons and other compounds from car tire rubber
  • 2003
  • Ingår i: Environmental Toxicology and Chemistry. - : Wiley. - 0730-7268 .- 1552-8618. ; 22:12, s. 2926-2931
  • Tidskriftsartikel (refereegranskat)abstract
    • Rubber tire material contains toxic compounds including oils rich in polycyclic aromatic hydrocarbons (PAH), so-called highly aromatic (HA) oils, as well as other reactive additives used as antioxidants, antiozonants, and vulcanization accelerators. The toxicity of rubber tire leachates to aquatic organisms has been demonstrated before. However, previous Studies have focused on lethal rather than sublethal effects. We kept rainbow trout (Oncorhynchus mykiss) in tanks with two types of fires: a tire containing HA oils in the tread or a tire free of HA oils in the tread. After 1 d of exposure. an induction of cytochrome P4501A1 (CYP1A1) was evident in both exposed groups, measured as elevated ethoxyresorufin-O-deethylase (EROD) activity and increased CYP1A1 mRNA levels. After two weeks of exposure, EROD activity and CYP1A1 mRNA were still high in fish exposed to leachate from HA oil-containing tire, whereas the effect was somewhat lower in fish exposed to leachate from HA oil-free tread tire. Compounds in the tire leachates also affected antioxidant parameters. Total glutathione concentration in liver as well as hepatic glutathione reductase, glutathione S-transferase, and glucose-6-phosphate dehydrogenase activities were markedly elevated after two weeks of exposure in both groups. The responses were greater in the group exposed to leachate from HA oil-free tread tire. Vitellogenin measurements did not indicate leakage of estrogenic compounds from the tires. Chemical analyses of bile from exposed fish revealed the presence of hydroxylated PAH as well as aromatic nitrogen compounds indicating uptake of these compounds by the fish.
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4.
  • Sturve, Joachim, 1966, et al. (författare)
  • Effects of North Sea oil and alkylphenols on biomarker responses in juvenile Atlantic cod (Gadus morhua)
  • 2006
  • Ingår i: Aquatic Toxicology. - : Elsevier BV. - 0166-445X. ; 78, s. S73-S78
  • Tidskriftsartikel (refereegranskat)abstract
    • A consequence of oil drilling at sea is the release of produced water contaminated with e.g. polycyclic aromatic hydrocarbons (PAH) and alkylphenols. In the present study, juvenile Atlantic cod were exposed to North Sea oil, nonylphenol and a combination of the North Sea oil and an alkylphenol mixture in a flow-through system. A suite of hepatic biomarkers were analysed. Exposure to North Sea oil resulted in strong induction of CYPIA protein levels and EROD activities. Exposure to nonylphenol, on the other hand, resulted in decreased CYPIA levels and EROD activities. Thus, nonylphenol appears to down-regulate CYPIA expression in Atlantic cod. Combined exposure to North Sea oil with an alkylphenol mixture resulted in lower EROD induction, compared to that in fish exposed to North Sea oil alone. This difference was not statistically significant. but still we believe that the alkylphenols have inhibited CYPIA activities in the fish which may have compromised CYPIA mediated metabolism of other xenobiotics, including PAH. CYP3A protein levels were lower, compared to controls, in fish exposed to nonylphenol and the combination of North Sea oil and alkylphenol mixture. In contrast. the oil alone had no effect on CYP3A protein content. North Sea oil exposure, alone or in combination with alkylphenols, caused oxidative stress observed as elevated levels of GSSG content and GR and CAT activities. Interestingly. exposure to nonylphenol resulted in a marked depletion of total glutathione levels. This apparent depletion may be a consequence of increased conjugation of glutathione to nonylphenol followed by excretion. An increase in conjugation enzyme GST activity was observed in the nonylphenol exposed group, although the difference was not significant. No sign of oxidative damage, measured as lipid peroxidation, was observed in any of the exposures experiments. This study suggests that North Sea oil may lead to oxidative stress and altered CYP1A and CYP3A expression. Alkylphenols, present in produced water, resulted in decreased CYP1A and CYP3A protein expression in Atlantic cod. (c) 2006 Elsevier B.V. All rights reserved.
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