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• W2016384227 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 βA 25–35 or βA 1–40 there was a concentration-dependentdecrease in viability. Catalase or vitamin E showed no protective effect against βA 25–35 . Dithiothreitol (DTT), N-acetylcysteine (NAC) and cyclosporine A significantly prevented the toxic effects of both βA 25–35 and peroxide, while inhibition of peroxide detoxifying enzymes enhanced toxicity. Exposure to βA 25–35 or βA 1–40 increased peroxides at 2 h and 24 h, which was prevented by DTT and NAC, but not vitamin E. βA 25–35 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." @default.
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• W2016384227 date "2001-01-25" @default.
• W2016384227 modified "2023-09-26" @default.
• W2016384227 title "β-Amyloid-Induced Cytotoxicity, Peroxide Generation and Blockade of Glutamate Uptake in Cultured Astrocytes" @default.
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• W2016384227 doi "https://doi.org/10.1515/cclm.2001.049" @default.
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