β-Amyloid-Induced Cytotoxicity, Peroxide Generation and Blockade of Glutamate Uptake in Cultured Astrocytes
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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
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- The Intrathecal Humoral Immune Response: Laboratory Analysis and Clinical Relevance
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