Major distinctions in the antioxidant responses in liver and kidney of Cd2+-treated common carp (Cyprinus carpio)
Autor: | Ágnes Ferencz, Zsanett Jancsó, Edit Hermesz, Renáta Juhász, Krisztina N. Dugmonits |
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Rok vydání: | 2013 |
Předmět: |
Anions
Fish Proteins medicine.medical_specialty Carps Antioxidant Physiology Health Toxicology and Mutagenesis medicine.medical_treatment Molecular Sequence Data Glutathione reductase Kidney Toxicology Biochemistry Antioxidants Gene Expression Regulation Enzymologic Glutathione Synthase Lipid peroxidation Superoxide dismutase chemistry.chemical_compound Glutathione Peroxidase GPX1 Peroxynitrous Acid Internal medicine medicine Animals chemistry.chemical_classification Glutathione Peroxidase Glutathione Disulfide biology Reverse Transcriptase Polymerase Chain Reaction Superoxide Dismutase Glutathione peroxidase Hydrogen Peroxide Cell Biology General Medicine Glutathione Catalase Glutathione synthetase Glutathione Reductase Endocrinology Liver chemistry biology.protein Water Pollutants Chemical Cadmium |
Zdroj: | Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology. 158:225-230 |
ISSN: | 1532-0456 |
DOI: | 10.1016/j.cbpc.2013.07.005 |
Popis: | This study is related to the accumulation of Cd(2+), its effects on oxidative stress biomarkers and its role in macromolecule damage in liver and kidney of common carp. We present evidence of an increased ratio of reduced to oxidized glutathione (GSH/GSSG) in both organs after 10 mg/L Cd(2+) exposure, with different underlying biological mechanisms and consequences. In the liver, the expressions and/or activities of superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase increased to cope with the Cd(2+)-generated toxic effects during the first 48 h of treatment. In contrast, none of these selected antioxidant markers was significantly altered in the kidney, whereas the expression of glutathione synthetase was upregulated. These results suggest that the major defense mechanism provoked by Cd(2+) exposure involves the regeneration of GSH in the liver, while its de novo synthesis predominates in the kidney. High levels of accumulation of Cd(2+) and peroxynitrite anion (ONOO(-)) were detected in the kidney; the major consequences of ONOO(-) toxicity were enhanced lipid peroxidation and GSH depletion. The accumulation of ONOO(-) in the kidney suggests intensive production of NO and the development of nitrosative stress. In the liver the level of hydrogen peroxide was elevated. |
Databáze: | OpenAIRE |
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