Genotoxic, hematoxic, pathological, and biochemical effects of hexane on Swiss albino rats
| Autor: | Unal Egeli, Rahmi Bilaloglu, Gulsah Cecener, Taci Cangül, Çigdem Çimen, Hasan Batmaz, Müfit Kahraman, Pinar Tuncel, Berrin Tunca, Gurler Akpinar, Betül Sevinir |
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| Rok vydání: | 2000 |
| Předmět: |
Male
medicine.medical_specialty Pathology Erythrocytes Health Toxicology and Mutagenesis Bone Marrow Cells Biology Toxicology medicine.disease_cause Lipid peroxidation chemistry.chemical_compound Internal medicine Genetics medicine Animals Hexanes Rats Wistar Mean corpuscular volume Genetics (clinical) Whole blood Chromosome Aberrations medicine.diagnostic_test Bone Marrow Examination Glutathione Catalase Blood Cell Count Rats Bone marrow examination medicine.anatomical_structure Endocrinology Liver Oncology chemistry Toxicity Female Lipid Peroxidation Bone marrow Genotoxicity Mutagens |
| Zdroj: | Teratogenesis, Carcinogenesis, and Mutagenesis. 20:329-340 |
| ISSN: | 1520-6866 0270-3211 |
| DOI: | 10.1002/1520-6866(2000)20:6<329::aid-tcm2>3.0.co;2-m |
| Popis: | In the present study, the genotoxic, hematoxic effects, and their relation with pathological and biochemical parameters of hexane were investigated. Cytogenetic evaluation performed on the bone marrow indicated that chromosome aberrations increased at both hexane doses in relation to the negative controls. Decreased hematocrit, hemoglobin concentrations, and mean corpuscular volume were observed on the whole blood counts. Conjugated dienes (CD), glutathione (GSH), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and catalase (CAT) were increased. Histological examinations showed intracytoplasmic vacuolisation, nuclei with lower chromatin, and parenchymatous degenerations in the dose groups. In the bone marrow slides, depletion of the erythroid series were observed. In conclusion, hexane seems to be a genotoxic and hematoxic agent leading to degeneration and lipid peroxidation in exposed groups. Teratogenesis Carcinog. Mutagen. 20:329-340, 2000. (C) 2000 Wiley-Liss, Inc. |
| Databáze: | OpenAIRE |
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