Modulation of antioxidant defence system in brain of rainbow trout (Oncorhynchus mykiss) after chronic carbamazepine treatment
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
19778632
DOI
10.1016/j.cbpc.2009.09.006
PII: S1532-0456(09)00209-9
Knihovny.cz E-resources
- MeSH
- Antioxidants metabolism MeSH
- Time Factors MeSH
- Water Pollutants, Chemical toxicity MeSH
- Glutathione metabolism MeSH
- Glutathione Peroxidase metabolism MeSH
- Glutathione Reductase metabolism MeSH
- Carbamazepine toxicity MeSH
- Protein Carbonylation drug effects MeSH
- Catalase metabolism MeSH
- Thiobarbituric Acid Reactive Substances metabolism MeSH
- Brain drug effects enzymology MeSH
- Oncorhynchus mykiss metabolism MeSH
- Oxidative Stress drug effects MeSH
- Lipid Peroxidation drug effects MeSH
- Reactive Oxygen Species metabolism MeSH
- Fish Proteins metabolism MeSH
- Superoxide Dismutase metabolism MeSH
- Dose-Response Relationship, Drug MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Antioxidants MeSH
- Water Pollutants, Chemical MeSH
- Glutathione MeSH
- Glutathione Peroxidase MeSH
- Glutathione Reductase MeSH
- Carbamazepine MeSH
- Catalase MeSH
- Thiobarbituric Acid Reactive Substances MeSH
- Reactive Oxygen Species MeSH
- Fish Proteins MeSH
- Superoxide Dismutase MeSH
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 (1.0 microg/L, 0.2mg/L or 2.0mg/L) for 7, 21, and 42 days. 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 42 days exposure. Carbamazepine exposure at 0.2mg/L led to significant increases (p<0.05) of LPO and CP after 42 days and, at 2.0mg/L, after 21 days. Activities of the antioxidant enzymes SOD, CAT, and GPx in CBZ-treated groups slightly increased during the first period (7 days). However, activities of all measured antioxidant enzymes were significantly inhibited (p<0.05) at 0.2mg/L exposure after 42 days and after 21 days at 2.0mg/L. After 42 days, 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.
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