β-Amyloid-Induced Cytotoxicity, Peroxide Generation and Blockade of Glutamate Uptake in Cultured Astrocytes
-
Maria L. de Ceballos
Abstract
β-Amyloid (βA) is cytotoxic to neurons in culture by increasing hydrogen peroxide and altering calcium homeostasis. We have evaluated βA-induced cytotoxicity, peroxide generation and glutamate (Glu) uptake in cultured astrocytes. Twenty-four hours after a single addition of either βA25–35 or βA1–40 there was a concentration-dependentdecrease in viability. Catalase or vitamin E showed no protective effect against βA25–35. Dithiothreitol (DTT), N-acetylcysteine (NAC) and cyclosporine A significantly prevented the toxic effects of both βA25–35 and peroxide, while inhibition of peroxide detoxifying enzymes enhanced toxicity. Exposure to βA25–35 or βA1–40 increased peroxides at 2 h and 24 h, which was prevented by DTT and NAC, but not vitamin E. βA25–35 inhibited Glu uptake in astrocytes and neurons in culture. Following exposure of neurons to βA for 24 h there was decreased uptake and increased Glu levels in the culture medium, that resulted in gradual excitotoxicity.
Copyright © 2001 by Walter de Gruyter GmbH & Co. KG
Articles in the same Issue
- IFCC/ Beckman Coulter Inc. Conference Frontiers in Molecular Basis of Diseases: Cell Biology of Neuronal Dysfunction, Paris, October 12-13, 2000
- Distribution of Cellular Prion Protein in Normal Human Cerebral Cortex – Does It Have Relevance to Creutzfeldt-Jakob Disease?
- Caspase-3 Apoptotic Signaling Following Injury to the Central Nervous System
- Parkinsons Disease and other α-Synucleinopathies
- Aggregation-Dependent Interaction of the Alzheimers β-Amyloid and Microglia
- β-Amyloid-Induced Cytotoxicity, Peroxide Generation and Blockade of Glutamate Uptake in Cultured Astrocytes
- Protein S-100B: A Serum Marker for Ischemic and Infectious Injury of Cerebral Tissue
- Reporting Cerebrospinal Fluid Data: Knowledge Base and Interpretation Software
- The Intrathecal Humoral Immune Response: Laboratory Analysis and Clinical Relevance
- Source of Endothelin-1 in Subarachnoid Hemorraghe
- Polymorphism of Apoprotein E (APOE), Methylenetetrahydrofolate Reductase (MTHFR) and Paraoxonase (PON1) Genes in Patients with Cerebrovascular Disease
- Neurotrophic Factor Therapy – Prospects and Problems
- Cell Therapy and Transplantation in Parkinsons Disease
- Matrix Metalloproteinases: Potential Therapeutic Target in Spinal Cord Injury
Articles in the same Issue
- IFCC/ Beckman Coulter Inc. Conference Frontiers in Molecular Basis of Diseases: Cell Biology of Neuronal Dysfunction, Paris, October 12-13, 2000
- Distribution of Cellular Prion Protein in Normal Human Cerebral Cortex – Does It Have Relevance to Creutzfeldt-Jakob Disease?
- Caspase-3 Apoptotic Signaling Following Injury to the Central Nervous System
- Parkinsons Disease and other α-Synucleinopathies
- Aggregation-Dependent Interaction of the Alzheimers β-Amyloid and Microglia
- β-Amyloid-Induced Cytotoxicity, Peroxide Generation and Blockade of Glutamate Uptake in Cultured Astrocytes
- Protein S-100B: A Serum Marker for Ischemic and Infectious Injury of Cerebral Tissue
- Reporting Cerebrospinal Fluid Data: Knowledge Base and Interpretation Software
- The Intrathecal Humoral Immune Response: Laboratory Analysis and Clinical Relevance
- Source of Endothelin-1 in Subarachnoid Hemorraghe
- Polymorphism of Apoprotein E (APOE), Methylenetetrahydrofolate Reductase (MTHFR) and Paraoxonase (PON1) Genes in Patients with Cerebrovascular Disease
- Neurotrophic Factor Therapy – Prospects and Problems
- Cell Therapy and Transplantation in Parkinsons Disease
- Matrix Metalloproteinases: Potential Therapeutic Target in Spinal Cord Injury
