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beta-amyloid peptides are cytotoxic to astrocytes in culture: a role for oxidative stress.

Abstract：

:beta-Amyloid is cytotoxic to neurons in culture by increasing hydrogen peroxide and altering calcium homeostasis. We have evaluated the cytotoxicty of beta-amyloid peptides (betaA(25-35) and betaA(1-40)) and generation of hydrogen peroxide on cortical cultured astrocytes. Twenty-four hours after a single addition of either betaA(25-35) or betaA(1-40) there was a concentration-dependent decrease in viability. This toxicity never exceeded 50% of the population independently of exposure time and concentrations. The subpopulation of astrocytes resistant to betaA(25-35) effects were also insensitive to peroxide. Catalase or vitamin E showed no protective effect against betaA(25-35) toxicity. Dithiothreitol (DTT), N-acetylcysteine (NAC), and cyclosporine A significantly prevented the toxic effects of both betaA(25-35) and peroxide. Inhibition of peroxide detoxifying enzymes increased betaA(25-35) and peroxide toxicity. Exposure to betaA(25-35) or betaA(1-40) increased peroxide production at 2 and 24 h, which was prevented by DTT and NAC, but not vitamin E. Despite the inability of added catalase to reduce betaA toxicity, these results suggest that betaA-induced cytotoxicity to astrocytes in culture is, as in neurons, mediated by generation of hydrogen peroxide.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Brera B,Serrano A,de Ceballos ML

doi

10.1006/nbdi.2000.0313

keywords:

subject

Has Abstract

pub_date

2000-08-01 00:00:00

pages

395-405

issue

4

eissn

0969-9961

issn

1095-953X

pii

S0969996100903139

journal_volume

7

pub_type

杂志文章

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