دورية أكاديمية
Aroclor 1254 induced cytotoxicity and mitochondrial dysfunction in isolated rat hepatocytes.
| العنوان: | Aroclor 1254 induced cytotoxicity and mitochondrial dysfunction in isolated rat hepatocytes. |
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| المؤلفون: | Aly, Hamdy A A, Domenech Cabrera, Oscar |
| المساهمون: | UCL - MD/FSIO - Département de physiologie et pharmacologie |
| المصدر: | Toxicology, Vol. 262, no. 3, p. 175-83 (2009) |
| سنة النشر: | 2009 |
| المجموعة: | DIAL@UCL (Université catholique de Louvain) |
| مصطلحات موضوعية: | Toxicity Tests, Rats, Oxidative Stress, Mitochondria, Liver, Membrane Potential, Mitochondrial, Male, Lipid Peroxidation, L-Lactate Dehydrogenase, Hepatocytes, Glutathione, Electron Transport Complex III, Electron Transport Complex I, Dose-Response Relationship, Drug, Chlorodiphenyl (54% Chlorine), Cell Survival, Animals |
| الوصف: | Polychlorinated biphenyls (PCBs) are widespread persistent environmental contaminants that display a complex spectrum of toxicological properties, including hepatotoxicity. Although Aroclor 1254 is ubiquitous in the environment, its potential cytotoxic effect on rat hepatocytes and the mechanism underlines its cytotoxicity are not fully investigated. Therefore, the present study was conducted to investigate: (1) the potential cytotoxicity of Aroclor 1254 in rat hepatocytes, and (2) characterization of the molecular mechanisms involved in the Aroclor 1254-induced hepatotoxicity, particularly the role of mitochondria, possibly a primary target in such event, could greatly explain the cytotoxic effect of Aroclor 1254 in rat hepatocytes. Hepatocytes were isolated from adult male albino rats and incubated for 24h in a fresh media containing 0, 20, 30, 40, 50 or 60muM of Aroclor 1254. At the end of incubation, hepatocytes and hepatocyte mitochondria were used for the assay. Our results showed cytotoxicity of Aroclor 1254 in rat hepatocytes starting at a concentration of 30muM as manifested by increased lactate dehydrogenase (LDH) leakage, decreased cell viability (MTT assay) and increased lipid peroxidation. As mitochondria are known to be one possible site of the cell damage, the effects of Aroclor 1254 on hepatocyte mitochondria was investigated. Aroclor 1254 induced reactive oxygen species (ROS) generation in hepatocyte mitochondria, inhibited mitochondrial respiratory chain complexes I and III and beta-oxidation of free fatty acids, depletion of mitochondrial antioxidant enzymes GPx and GR and the non-enzymatic antioxidant reduced glutathione, inhibited mitochondrial membrane potential (Deltapsi(m)), decreased mitochondrial aconitase and cardiolipin content, and elevated levels of cytochrome P450 subfamily, CYP1A and CYP2B activities as indicated by ethoxyresorufin O-deethylase (EROD) and pentoxyresorufin O-deethylase (PROD). Therefore, we can conclude that Aroclor 1254 induced rat hepatocyte toxicity and our ... |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| تدمد: | 0300-483X 1879-3185 |
| العلاقة: | boreal:23052; http://hdl.handle.net/2078.1/23052Test; info:pmid/19486918; urn:ISSN:0300-483X; urn:EISSN:1879-3185 |
| DOI: | 10.1016/j.tox.2009.05.018 |
| الإتاحة: | https://doi.org/10.1016/j.tox.2009.05.018Test http://hdl.handle.net/2078.1/23052Test |
| حقوق: | info:eu-repo/semantics/restrictedAccess |
| رقم الانضمام: | edsbas.9FF1C521 |
| قاعدة البيانات: | BASE |
| تدمد: | 0300483X 18793185 |
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| DOI: | 10.1016/j.tox.2009.05.018 |