Unconjugated bilirubin differentially affects the redox status of neuronal and astroglial cells

التفاصيل البيبلوغرافية
العنوان: Unconjugated bilirubin differentially affects the redox status of neuronal and astroglial cells
المؤلفون: Adelaide Fernandes, Ana S. Falcão, Rui F.M. Silva, D. Allan Butterfield, Maria Alexandra Brito, Dora Brites, Alexandra Isabel Rosa
المساهمون: Repositório da Universidade de Lisboa
المصدر: Neurobiology of Disease, Vol 29, Iss 1, Pp 30-40 (2008)
Repositório Científico de Acesso Aberto de Portugal
Repositório Científico de Acesso Aberto de Portugal (RCAAP)
instacron:RCAAP
بيانات النشر: Elsevier, 2008.
سنة النشر: 2008
مصطلحات موضوعية: Cell death, Programmed cell death, Lipid peroxidation, Protein oxidation, medicine.disease_cause, Antioxidants, lcsh:RC321-571, chemistry.chemical_compound, fluids and secretions, Pregnancy, medicine, Animals, Buthionine sulfoximine, Drug Interactions, Rats, Wistar, Cell damage, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Cells, Cultured, chemistry.chemical_classification, Cerebral Cortex, Neurons, Reactive oxygen species, Cell-type vulnerability, Dose-Response Relationship, Drug, L-Lactate Dehydrogenase, Chemistry, Neurotoxicity, Neurosciences, Bilirubin, Glutathione, medicine.disease, Embryo, Mammalian, Cell biology, Acetylcysteine, Rats, Neurology, Biochemistry, nervous system, Astrocytes, embryonic structures, Female, Reactive Oxygen Species, Oxidation-Reduction, Oxidative stress
الوصف: We investigated whether nerve cell damage by unconjugated bilirubin (UCB) is mediated by oxidative stress and ascertained the neuronal and astroglial susceptibility to injury. Several oxidative stress biomarkers and cell death were determined following incubation of neurons and astrocytes isolated from rat cortical cerebrum with UCB (0.01-1.0 microM). We show that UCB induces a dose-dependent increase in neuronal death in parallel with the oxidation of cell components and a decrease in the intracellular glutathione content. Comparison of the results obtained in both cell types demonstrates that neurons are more vulnerable than astrocytes to oxidative injury by UCB, for which accounts the lower glutathione stores in neuronal cells. Moreover, neuronal oxidative injury is prevented by supplementation with N-acetylcysteine, a glutathione precursor, whereas astroglial sensitivity to UCB is enhanced by inhibition of glutathione synthesis, using buthionine sulfoximine. Collectively, we demonstrate that oxidative stress is involved in UCB neurotoxicity and depict a new therapeutic approach for UCB-induced oxidative damage.
وصف الملف: application/pdf
اللغة: English
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::711f0e437ebe7410b7b89ad03b30f0adTest
http://www.sciencedirect.com/science/article/pii/S096999610700174XTest
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....711f0e437ebe7410b7b89ad03b30f0ad
قاعدة البيانات: OpenAIRE