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Modulation of antioxidant defence system in brain of rainbow trout (Oncorhynchus mykiss) after chronic carbamazepine treatment
University of South Bohemia in Ceske Budejovice, Faculty of Fisheries and Protection of Waters, Research Institute of Fish Culture and Hydrobiology, Zatisi 728/II, 389 25 Vodnany, Czech Republic.
University of South Bohemia in Ceske Budejovice, Faculty of Fisheries and Protection of Waters, Research Institute of Fish Culture and Hydrobiology, Zatisi 728/II, 389 25 Vodnany, Czech Republic.
University of South Bohemia in Ceske Budejovice, Faculty of Fisheries and Protection of Waters, Research Institute of Fish Culture and Hydrobiology, Zatisi 728/II, 389 25 Vodnany, Czech Republic.
Umeå University, Faculty of Science and Technology, Department of Chemistry. (University of South Bohemia in Ceske Budejovice, Faculty of Fisheries and Protection of Waters, Research Institute of Fish Culture and Hydrobiology, Zatisi 728/II, 389 25 Vodnany, Czech Republic)
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2010 (English)In: Comparative Biochemistry and Physiology - Part C: Toxicology & Pharmacology, ISSN 1532-0456, E-ISSN 1878-1659, Vol. 151, no 1, 137-41 p.Article in journal (Refereed) Published
Abstract [en]

We investigated the effect of long-term exposure to CBZ on the antioxidant system in brain tissue of rainbow trout. Fish were exposed to sublethal concentrations of CBZ (1.0mug/L, 0.2mg/L or 2.0mg/L) for 7, 21, and 42days. Oxidative stress indices (LPO and CP) and activities of antioxidant enzymes (SOD, CAT, GPx and GR) in fish brain were measured. In addition, non-enzymatic antioxidant (GSH) was determined after 42days exposure. Carbamazepine exposure at 0.2mg/L led to significant increases (p<0.05) of LPO and CP after 42days and, at 2.0mg/L, after 21days. Activities of the antioxidant enzymes SOD, CAT, and GPx in CBZ-treated groups slightly increased during the first period (7days). However, activities of all measured antioxidant enzymes were significantly inhibited (p<0.05) at 0.2mg/L exposure after 42days and after 21days at 2.0mg/L. After 42days, the content of GSH in fish brain was significantly lower (p<0.05) in groups exposed to CBZ at 0.2mg/L and 2.0mg/L than in other groups. Prolonged exposure to CBZ resulted in excess reactive oxygen species formation, finally resulting in oxidative damage to lipids and proteins and inhibited antioxidant capacities in fish brain. In short, a low level of oxidative stress could induce the adaptive responses of antioxidant enzymes, but long-term exposure to CBZ could lead to serious oxidative damage in fish brain.

Place, publisher, year, edition, pages
2010. Vol. 151, no 1, 137-41 p.
Keyword [en]
Oxidative stress, Fish, Brain damage, Residual pharmaceutical
National Category
Chemical Sciences
Identifiers
URN: urn:nbn:se:umu:diva-30037DOI: 10.1016/j.cbpc.2009.09.006ISI: 000273152400017PubMedID: 19778632OAI: oai:DiVA.org:umu-30037DiVA: diva2:278996
Available from: 2009-12-01 Created: 2009-12-01 Last updated: 2017-12-12Bibliographically approved

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