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
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